Biopsychology Lecture Notes PDF

Lecture 1 - Neurons and Action Potentials -4 kinds of explanations in Biology Physiological: what is the physiological cause? Functional: what is the fuction? Does it have a bene!t? Ontogenetic: how behavior appears/develops? Evolutionairy: where does it...

Lecture 1 - Neurons and Action Potentials -4 kinds of explanations in Biology Physiological: what is the physiological cause? Functional: what is the fuction? Does it have a bene!t? Ontogenetic: how behavior appears/develops? Evolutionairy: where does it come from? Evolutionary orgins -Mind-Body problem Monistic view: mind and body are one Dualistic view: mind and body are separated -Animal Research Animals share many genes and physiological mechanisms with humans → used as "models" for healthy human brain and to develop understanding and treatment for various diseases we need to balance human su"ering vs the animal discomfort -Neurons Neurons have some common characteristics but also come in many di"erent shapes (that are related with their functions) Types of Neurons: a) Purkinje ce# (cerebe#um) → important for precise timing of movements b) Sensory neuron → eg. touch, pressure, pain receptors in our skin c) Pyramidal ce# → found in the cortical tissue (gray matter) → communication within the brain (from lower to higher levels) d) Bipolar ce# (retina) → important for precise coding -Structure of Neurons Soma (ce# body): contains nucleus, ribosomes and mitochondria Axon: channel with microtubules that sends the impulse Myelin sheath: insulation of axon, speeds up the information transmission and reduces needed energy Node of Ranvier: sma# unmyelinated segments of the axon Dendrites and dendritic spines: where a neurou receives inputs from other neurons (greater area of dendrites = more inputs and stronger connections) Ce# membrane: insulates the ce# from the environment, has selective permability + ion chanels -Glial Ce#s Astrocytes: control the dilation of our blood vessels (+ synchronizing function as have many branches) Oligodendrocyte: create myelin sheaths in the central nervous system Schwann ce#s: create myelin sheaths in the peripheral nervous system Microglia: part of the brains immune system (like white blood ce#s in blood) -Blood-Brain barrier Its rea#y hard for chemicals to pass through it to protect the brain from dangerous chemicals and viruses because neurons are not replaced (we are born with a# of our neurons) some chemicals can pass (through active and passive transport) -Action Potential Electrical signals that are produced by nerve ce#s in the brain and that enable one nerve ce# to activate or inhibit another ce# Optogenetics: a research method that a#ows for selective activation or inhibition of nerve ce#s by inducing or preventing the occurrence of an action potential -Action Potential: The Mechanism 1. resting potenential - neuron is "at rest" - a di"erence between the inside and outside of the neuron (-70mV) - inner is more negatively charged (anions are inside of the ce#) - outside is more positively charged - a# channels are closed (Na, K, and Cl ions) 2. Threshold is reached - ions are voltage-gated -> only work when a certain threshold is reached (-65mV) - Sodium channels open 3. Depolarisation - Decreasing the di"erence in the ce# interior - potassium channels open 4. Reaching top - sodium channels close 5. Repolarisation - increasing the di"erence (reinstating) - potassium channels close 6. Hyperpolarisation - when the action potential is lower than resting potential - extrace#ular $uid - positively charged compared to interce#ular $uid - interce#ular $uid - negatively charged compared to extrace#ular $uid  Lecture 2 - Synapses -The Synapse Synapse = the space between the axon terminal and postsynaptic neuron Transmits the impulse as chemical energy using neurotransmitters -Neurotransmission: the mechanism 1. Synthesis of neurotransmitters (ce# body and axon terminal) 2. Storage of neurotransmitters (in axon terminals as vesicles) or transport from ce# body to terminals 3. Exocytosis: the release of neurotransmitters into the synaptic cleft 4. Binding to receptors on the postsynaptic neuron (after traveling through the synaptic cleft) 5. Some receptors activate ligand-gated ion channels (they open when the neurotransmitter binds) 6. The post-synaptic neuron releases retrograde transmitters (to con!rm receiving of the message + stop further release of neurotransmitters) 7. Neurotransmitters separate from the receptors and are broken down or reuptaken -Exocytosis 1. Action potential reaches axon terminal 2. Calcium ion channels open, a#owing Ca2+ ions in 3. Calcium causes synaptic vesicles to release from microtubules 4. Synaptic vesicles fuse with axon membrane at release site 5. Resides open, releasing neurotransmitters into synaptic gap 6. Vesicle material is recycled 7. Vesicles either are reuptaken or re!#ed at axon terminal -Receptors Receptor: molecular structure attached to the ce# body and dendrites that has a structure that wi# only a#ow ore chemical to bind (key and lock model) A"inity: based on shape and molecular properties, a receptor has an a"inity for a certain type of neurotransmitters (only binds to our type of neurotransmitters) -Ionotropic Receptors: Ligand-gated channels: receptors that are connected to an ion channel that opens when a neurotransmitter binds Graded post-synaptic potentials: ligand - gated channels can lead to excitatory (depolarizing) or inhibitory (hyperpolarizing) e"ects on the post -synaptic ce#'s membrane potential Depolarizing e"ects: channels a#owing for entry of positive ions into post-synaptic ce# (eg. glutamine and acetylcholine receptors) Hyperpolarizing e"ects: channels a#ow entry of negative ions (chloride) and out$ow of positive (potassium) ions (eg. GABA receptors) -Electrophysiology Discoveries through electrophysiology: excitatory and inhibitory post-synaptic potentials summation e"ects  -Temporal Summation By summing up the potentials we can achieve the threshold potential (which wouldn't be possible with just one neuron) the order matters !!! -Neurotransmitters 1. Dopamine → movement, reinforcement, planning → substantial nigra and ventral tegmental area 2. Norepinephrine → arousal, vigilance, mood 3. Serotonin → sleep, apetite, mood → raphe nuclei (brain stem) 4. Glutamate → excitation, long-term memory 5. GABA → inhibition, mood, seizure threshold -Where neurotransmitters come from? 1. Synthesized by brain ce#s acetyl + choline → acetylcholine phenylalaline (from diet) → dopamine → norepinephrine → epinephrine tryptophan (from diet) → serotonin 2. From psychoactive drugs usua#y found in nature eg. co"ee, tobacco , cocaine, opium -Mechanism of psychoactive drugs Possible e"ects of psychoactive drugs on synaptic communication: increase release of neurotransmitters E decrease reuptake of neurotransmitter agonist block breakdown of neurotransmitter into inactive chemicals directly stimulate postsynaptic receptors antagonist cause vesicles to leak neurotransmitters block postsynaptic receptor -Types of drugs and their e"ects Dopamine Amphetamine → increases release of dopamine cocaine, amphetamine, Ritalin → inhibit dopamine reuptake apomorphine → stimulates dopamine receptors (antagonistic) schizophrenia medication → block dopamine receptors Serotonin MDMA (ectasy) → increases serotonin release MDMA + SSRIs → inhibit seratonin reuptake MAO inhibitors → interfere with breakdown of monoamines (including serotonin) within the axon terminal (antagonistic) negative symptoms of schizophrenia → drugs that block serotonin receptors -Drugs binding to receptors Opiates (heroin and morphine) → endorphin receptors Nicotine → nicotinic acetylcholine receptors THC → anamide and 2-AG receptors on presynaptic neurons (reduces neurotransmitter release)  Lecture 3 - Anatomy -Planes Horizontal plane: top Sagittal plane: through midline (side view) Coronal plane: front view view -Neuroaxis Axis that aligns with the central nervous system names of organs and areas are given with regard to the neuroaxis -Anatomical terms relating to direction -Parts of the nervous system Gray matter: ce# bodies of neurons White matter: axons of neurons corpus ca#ous: connect the right and left hemisphere -Peripheral Nervous System Everything outside the brain and spinal cord Divides into: Somatic: control voluntary muscles and conveys sensory information to the central nervous system Autonomic: controls involuntary muscles → Sympathetic (!ght or $ight): expends energy → Parasympathetic (rest and digest): conserves energy  -Central Nervous System Consists of brain and spinal cord Spinal cord has cranial nerves (12 pairs) dorsal side → sensory input ventral side → motor output Brain → grey matter outside Spinal cord → white matter outside -Ventricles Ventricle system → irrigation system of the brain tissue helps with bringing nutrients to the brain Cerebrospinal $uid $ows from fourth ventricle into the subarachnoid space (space between the membrane surrounding the brain and the sku#) → to protect our brain better -CNS: hindbrain, midbrain, forebrain Hindbrain: Midbrain Cerebe#um (balance, motor coordination, timing, cross modal Superior co#iculus attention) Inferior co#iculus The Brainstem → ! Medu#a ! (part of hindbrain): produces Tectum neurotransmitters + opiate receptors + basic life activities Tegmentum (eg. respiration) Pons: sends information to the opposite (contralateral) side of the brain -Forebrain Starts in brainstem → thalamus (important for conveying impulses from the senses to the places of processing (true for a# senses except olfaction)) The Limbic System: involved in motivated behaviors (e.g. drinking when thirsty) emotion, drives and aggression olfactory bulb → sense of sme# = olfaction hypothalamus → aggression, regulation of hunger, thirst, sex, temperature, cicardian rhythms, hormones hippocampus → memory amygdala → fear, aggression cingulate gyrus → decision making, error detection, pain, empathy, eye movements, spatial orientation basal ganglia → movement, procedural learning The Cerebral Cortex: folded top area of the brain folds increase the surface area = more neurons = better thinking processes and inte#igent behaviour frontal lobe → movement planning, recent memory, some emotion temporal lobe → hearing, advanced visual processing precentral gyrus = primary motor cortex postcentral gyrus = primary somato sensory cortex parietal lobe → body sensations occipital lobe → vision Prefrontal Cortex: sensory integration, rule-based behavior, working memory, abstract thinking and planning -Research methods for studying the brain 1. Correlate brain anatomy with behavior (e.g. Music training) 2. Examine the e"ects of brain damage 3. Record brain activity during behavior (by using fMRI and EEG) 4. Examine the e"ects of stimulating parts of the brain (e.g. by using Transcravial Magnetic Stimulation (TMS)) Sadly a# of them are just correlational  Lecture 4 - Genetics and Evolution -Deoxribonucleic Acid (DNA) A# living organisms on earth have DNA DNA → double helix has a sugar phosphate backbone nucleotides form "ladder" (adenine - thymine; cytosine - guanine) -Human Genome Project Project dedicated to determine now many genes humans have about 25000 were found right now we sti# haven't found the fu# number of genes we have -Chromosomes tightly coiled DNA structures in the nucleus of every ce# we have 23 pairs of chromosomes most chromosomes → autosomal (+ has autosomal genes on itself) genes on the chromosomes can be homozygous (the same) or heterozygous (di"rent) 23 pair of chromosomes → sex chromosomes sex-linked genes = genes on the 23rd pair of chromosomes -Epigenetics Gene expression: a process in which genes are acitaved or repressed by environmental factors everything you do changes your gene expression -Heritability vs. Environment Methods used in heritability research: twin studies adoption studies gene - identi!cation studies: candidate gene approach genome-wide association studies Findings of heritability research: a# psychological traits show signi!cant and substantial genetic in$uence no trait is 100% heritable heritable it is caused by many genes of sma# e"ect -Evolution Evolution: a change in frequency of various genes in population over generations Fitness: the number of copies of one's genes that endure in later generations Evolution happens when there is variation, natural selection and heridity -Development of the brain Steps of development: 1. Proliferation (neurogenesis) → production of new ce#s 2. Migration →movement towards target destination 3. Di"erentiation → development of - more specialized ce# types from stem ce#s 4. Myelination → axon becomes myelinated -Path!nding by axons How axons know where to connect? research on amphebians → turning eye around → axons growing back to exact same spots axons are attracted or repe#ed by chemicals on the surface of other ce#s -Competition between axons Neural Darwinism: postsynaptic ce#s streghten connection with some ce#s and eliminate connections with others best understood for peripheral nervous system (PNS) Neurotrophins: chemicals promoting the survival of nerve ce#s Axons that are not exposed to neurotrophius undergo apoptosis (= programmed death of the ce#) -Vulnerability of developing brain Early stages of brain development are critical for normal development later in life mutation on one gene can lead to many defects chemical distortions in the brain during early development can cause signi!cant impairment and developmental problems Fetal Alcochol Syndrome caused by drinking during pregnancy reduces dendritic branching in an o"spring suppression of glutamate and enhancing of GABA → less excitation to neurons → apoptosis can lead to: hyperactivity, impulsiveness, mental retardation, heart e"ects etc... -Further development we are born with most of our neurons neurogenesis continues in regions related to memory (basal ganglia and hippocampus) new olfactory receptors and neurons in a factory bulb -Plasticity new connections can be made based on new experience axons and dendrites continue to modify their structure and connections throughout the lifetime -Phantom limb e"ect Phantom limb: the continuation of sensation of an amputated body part cortex reorganizes itself after the amputation by becoming responsive to other parts of the body original axons degenerate leaving vacant synapses into which others axons sprout  Lecture 5 - Vision -Senses Olfaction (sme#) -> olfactory bulb (frontal lobe) Audition (sound) -> auditory (temporal lobe) Vision -> visual (occipital) Somesthesis -> motor + somesthetic (parietal) -Law of specy!c nerve energies Brain somehow interprets the action potentials from the auditory nerve as sound and from optic nerve as vision -Vision Functions: localise and identify predators, food, partners Evolution: evolved in several ways (depending on what the species needed) Humans: are guided by vision (we use 2/3 of our brain to process visual input Computional power: human brain outperforms computer-vision algorithms Vision has been studied for years and in detail → we want to reach this level of understanding for other processes -Electrophysiology Method of studying vision 1. Electrode is inserted in a single ce# in an animal brain 2. Action potentials are recorded by the electrode 3. A#ows to see what stimuli makes t he ce#s active -The Stimuli - Light white light = a# wavelengths = consists of a# colors Light can be both absorbed and re$ected objects we perceive → re$ect light light give us information about physical properties (eg. movement, shape, size, depth, color, luminance, texture) -The Eye: Retinae and Receptors Outside: Inside: Iris (colored area) Retina Pupil Optic nerve Cornea Fovea Lens Blind spot -Retina consists of layers Amacrine ce# - modulate activation of ganglion ce# # Axons of Ganglion ce#s - send information to brain Gangliou ce#s Bipolar ce#s Receptors - transduction = light → action potential Horisontal ce# - modulate activation of ganglion ce# -Optic disc = Blind spot = place where optic nerve leaves the eye = no receptors there -Fovea Responsible for seeing detail (e.g. reading) we see more detail and color when we !xate our eyes on something (an object) Each bipolar ce# receives input from only one cone and transmits it to just one ganglion ce#= hence low sensitivity to dim light -Periphery Each bipolar ce# receives input from many rods (and cones) = hence high sensitivity to dim light and low visual acuity (summation) -Receptors 2 kinds 1. Cones - responsible for seeing in detail and color in good light conditions (in fovea) come in 3 types : short, medium and long wavelenght types 2. Rods - responsible for seeing in low light conditions (in periphery) -Receptive Field region of the visual space where the light needs to come from in order to hit the right receptors on the retina combined receptive !eld of the gaugliou ce# = a# receptors that were hit by light - and are responding to the same gaugliou ce# ( is larger than single receptor !eld) -Three Theories of Color Perception A# are right but focus on di"rent domains of perceiving color 1. Trichromatic theory 2. Opponent - process theory 3. Retainex theory -Trichromatic theory ( Young-Helmholtz) If you take 3 colors (red, green and blue) you can mix them up to any and a# existing colors → each of these colors have own receptors (sensitive to di"rent wavelengths ) color is determined via relative rates of response of these receptors ratio of receptor activity = color perceived -Opponent Process theory (Hering) Problems with trichromatic theory: de!cits in color perception sometimes concern pairs of color (e.g. red-green color blindness) color aftere"ects (seeing opposite color after staring at another one for a long time) How the aftere"ects work? we have receptors of di"erent colors R G B these receptors respond to lightwaves from a speci!c location (receptive !eld) receptors are a subject to adaptation: they become tired opponent - process theory bipolar ce#s respond to colors along dimensions (blue→ye#ow, red →green) hyperpolarization: ye#ow depolarization: blue -Retinex theory The brain decides which color we perceive input from the retrua is interpreted based on what the brain knows and predicts about color of the object (e.g. rubics cube in di"erent lights) brain is making inferences —Edge Detection The starting point for discerning objects from their surrounding background lies in center-surround receptive !eld of bipolar and ganglion ce#s (activated by receptors in the center, inhibited by receptors in the surround or vice versa) Lateral inhibition: reduction in activity of a neuron by stimulation of neighboring neurons lateral inhibition enhances edges (retinal processing) -Brain Light → receptors → brain visual input → thalamus → primary visual cortex -Primary Visual Cortex (V1) First recipient of the visual stimuli Retinotopy: mapping between brain and physical space Electrophysiology: single-ce# recordings of neurons in V1 recording electrode inserted into the visual area of the brain electrical signal from the brain is being recorded and measured -Ventral Stream Ventral Stream: towards the stomach (passing through inferior temporal lobe) the "what" pathaway → conscious recognition of objects and people and ability to name them damage to ventral pathaway = visual aguosia = inability to recognize objects -Dorsal Stream Dorsal Stream: through the parietal lobe (towards the top of the head) the "where" pathaway → responsible for perception and motor movements connected to the object we are looking at intact dorsal stream = intact visuo-motor coordination -Medial Temporal Lobe Fusiform gyrus → mediates face recognition Prosopagnosia: inability to recognize faces (can stem from damage to fusiform gyrus) -Percieving Motion MT= middle temporal area MST = medial superior temporal area MT and MST are responsible for perceiving movement -Fi#ing In Our brains try to make sense of the input we percieve what the brain thinks is the most likely interpretation secondary visual cortex (V2) responds to i#usory contours  Lecture 6 - Other Sensory Systems -Audition Functions: localization and identi!cation of objects and animals communication and speech (in humans and other animals) -Soundwaves Periodic compression and decompression of air can be determined and described by frequency (how lightly is the wave packed) and amplitude (the di"erence between the top and bottom of the wave) di"erent species can near di"erent ranges of frequencies (bigger animals → better with low frequencies) our ability to hear high frequencies decreases with age -Sound Localisation brain interprets the sound and localizes it based on loudness, time of arrival and soundwave phase Usua#y sound wi# arrive to one ear earlier that to the other moment in the sound wave is di"erent when it reaches ears at di"rent times sound shadow: the sound passes through something (e.g. head) and appears to be more disturbed and/or quiter -The Sensory System: The Ear Outer Ear Summary of work of cochlea Middle Ear Inner Ear I Cochlea -Action Potentials Sounds of di"erent frequencies translate to di"erent pitches the basilar membrane has a tonotopic coding (which frequency activates which part) the base is thick and in$exible → wi# vibrate only to highest frequencies -Hair Ce#s When at rest approximately 15% of potassium channels are open the hair ce#s are not bent When stimulated hair ce#s bend potassium channels open hair ce# at rest hair ce# stimulated -Primary (A1) and Secondary (A2) Auditory Cortex Tonotopy (from basilar membrane) is re$ected in the primary auditory cortex = di"erent regions become activated by di"erent frequencies secondary auditory cortex → higher level conceptual recognition/processing of sound (eg. What is generating that sound?) -Mechanical Senses Respond to pressure, bending and other phisical/mechanical distortions of a receptor (action potential occurs due to mechanical changes of the receptor) Audition Vestibular sensation Touch Pain Other body sensations -Vestibular sensation Detects position and movement of the head directs compensatory movements of the eye and helps to maintain balance Vestibular organs (the semicircular canals) are located adjacent to the cochlea -Somatosensation: feeling your body Eg. Shape identi!cation, deep pressure, cold-warmth, pain, itch, tickle, position and movement we have di"erent types of receptors for di"erent sensations we have di"erent types of axons for di"erent sensations Touch → travels on ipsilatelar side of the body Pain → travels on the contralateral side of the body dermatomes → regions of the body corresponding to one of 31 sets of nerves -Somatosensation: Tactile I#usion I#usion of being touched "cutaneus rabbit i#usion" → when you touch someone on the wrist and then immediately after on the elbow, the person wi# experience i#usion of touch in the midpoint between wrist and elbow -Pain pain serves to warn us that something is wrong depressed people → more sensitive to pain pain receptors with bare nerve endings alfa-delta !bers → sharp pain (glutamate + substance P) c-!bers → mild, du# pain (glutamate) managing pain opioids and endorphins (ease pain) prolonged experience of pain = no function (we know something is wrong) → natural pain ki#er is used (endorphins) endorphins bind to opiate receptors (pain signals are inhibited) -Emotional and Physical pain centers in the brain pain is experienced in somatosensory cortex activation is seen in cingulate cortex, anygdala, hippocampus and hypothalamus → are implicated in emotional pain -Chemical Senses Taste Olfaction Pheromones Syntesia -Olfaction Sense of sme# → ability to sense airborne chemicals (odorants) used by most life forms for guidance towards good things and away from danger Chemosensation is the oldest form of communication Odors are: 1. Environmental (e.g. food) 2. Ale#ochemical: odors from other species (eg. predators or prey) 3. Pheromones: chemicals used to communicate information between conspeci!cs (animals of the same species) -Human Olfactory system olfactory stimuli is reported directly to olfactory bulb (not passing through thalamus as in other senses) neurogenesis continues into the adult life  Lecture 7 - Movement -Muscles 3 categories: Smooth muscles: control digestive system and other organs Striated muscles: control movement of the body Cardiac muscles: heart muscles that have properties of skeletal and smooth muscles Striated muscles divide into: Fast -twich → rely on anaerobic energy, fatigue quickly (short and strong bursts of energy) Slow -twich → rely on aerobic energy, don't fatigue Myostatin gene inhibits development of muscles -Nervous system and movement Neuromuscular junction: synapse between a motor neuron axon and a muscle !ber Motor neurons release acetylcholine: excitatory neurotransmitter that causes a muscle to contract (there is no inhibition of muscles = cannot "relax" a muscle ) Axon-muscle ratio: 1 muscle !ber is contro#ed by 1 motor neuron but 1 motor neuron can control many muscle !bers -Antagonistic muscles We have both $exor and extensor muscles on each body part to be able to make movements in di"erent directions Flexor muscles: lower leg up, lower arm towards shoulder (e.g. biceps) Extensor muscles: lower leg straight, straighten arm (e.g. triceps) -Proprioceptors We need feedback from muscles to know if we need to stop the movement or continue it stronger Proprioceptors: operate as a direct feedback system, sensors that register muscle contractions, stretches, tension and activate antagonistic muscles to counter these e"ects Muscle spindles: counter the sudden streak of a muscle by activating the antagonistic muscle Golgi tendons: respond to increases in muscle tension preventing them from being contracted too strongly -Units of movement Involuntary and voluntary movements Ba#istic movements: unstoppable once initiated rapid sequences of movements ( eg. paw licking mouse) motor programs: !xed sequences of di"erent movements -Complexity of Movement most of our movements are aimed at achieving a goal (e.g. picking up a bottle of water) even simple movements involve a complex coordination of what we see, location of our body and hands I and a# of the many muscles that we need to perform the action -Brain and Movement Cerebral cortex: "planning" of movement Basal ganglia: initiation of movement Cerebe#um: timing/duration of movements -Cerebral cortex Primary motor cortex same mapping as in somatosensory cortex but actual muscles are connected (can produce movement) axons send impulses to motor neurons in the brain stem and spinal cord brief stimulation of the primary motor cortex generates simple movements, longer stimulation generates complex movements motor cortex "orders" an outcome but other areas move muscles Posterior parietal cortex part of dorsal pathaway (vision for action → guiding the movement) monitors the position of the body relative to its environment involved in "planning a movement” if stimulated we feel an urge to move (sometimes even believing that a movement was made) Supplementary motor cortex involved in planning and organizing movements inhibiting habitual movements detecting errors in movement one of the location for mirror neurons Premotor cortex active immediately before movement receives and integrates information about the movement target and about the position and posture of the body organizes the direction of the movement in space Prefrontal cortex stores sensory information relevant to movement (a#owing the movement to be executed after delay) anticipating outcomes of a movement if damaged: conceptual movement errors / i#ogical errors -Basal ganglia Triggers the initiation of a voluntary movement by ceasing to inhibit the movement plan inhibits other movements at the same time to ensure that only the planned movement is Basal ganglia pathaway -1 -1 Cerebral cortex → activates striatum → striatum inhibits globus pa#idius → globus pa#idius inhibits thalamus → +1 thalamus excites cortex (overa# the score is at 1 (multiplication)) -Cerebe#um Contains more neurons than the rest of the brain combined (many synapses) very important for aiming and timing action potentials in parrarel !bers → excite Purkinje ce#s → more parrarel !bers active = more Purkinje ce#s activated = longer response time -Parkinson’s disease -Huntington’s disease Neurodegenerative disorder (loss of brain ce#s) Also neurodegenerative symptoms: di"iculty initiating voluntary movement, symptoms: arm jerks, facial twitches, di"iculty walking, tremors, rigidity, cognitive de!cits (due to dopamine voluntary movements and speech, depression and apathy, de!ciency) ha#ucinations and delusions, sexual disorders heritable - 28 genes identi!ed as risk factors cause: autosomal dominant gene ou chromosome 23 risk factors - exposure to pesticides used in farming based on the number of C-A-G repeats → predictive of smokers and co"ee drinkers have lower probability of developing Parkinson's age onset L - dopa as treatment experimental treatment- tissue transplant  Lecture 8 - Wakefulness and Sleep -Circannual Rythm Rhythm fo!owing the yearly orbit of the earth around the sun examples of behaviors depending on the year rhythm - seasons → produce variation in lightning - seasonal migratory behavior in birds (regulated by hormones, not by external conditions) - calorie intake in humans → higher in fa! and winter -Cicardian Rythm Rhythm fo!owing the 24h turn around earths axis (day and night cycle) a! living creatures show regular rhythmic "uctuations in internal and external behaviors during the 24h cycle cicardian rhythm in humans: an overview our bodily variables "uctuate over the day so do our observable behaviors e.g. Wakefulness and sleep -Endogenous Control "Things" that are generated from inside of an organism For example - sleep-wake cycle → hard to deviate from the 24h cycle by changing environmental factors - the presence of sunlight (overa! time) impacts our sleep-wake cycle (e.g. Germany east and west) persistence of cicardian rhythm in absence of light cues suggest that we have an internal biological clock clock appears to synchronize with sunlight (zeitgeber → things in our environment that we use as biological cues to know what time it is) -The internal clock: suprachiasmatic nucleus the suprachiasmatic nucleus (SCN) → neural substrate of the biological clock - shows changing activity within 24h cycle - SCN retains its rhythm even when in petri dish ( e.g. In-vitro ) SCN neurons: protein synthesis through mRNA transcription, the genes that lead to the synthesis of the PER and TIM proteins are silenced by high concentrations of PER and TIM producing A self-regulatory (endogenous) rhythm with 24h duration how the sunlight impacts the clock? - light sensitive ganglion ce!s send action potentials directly to SCN through retino-hypothalamic pathaway - intrinsica!y photosensitive retinal ganglion ce!s: receive input from a! receptors but also respond to light directly (react most strongly to bluish light -Brain areas and neurotransmitters that regulate wakefulness and sleep FRINre  Orexin → responsible for maintaining wakefulness narcolepsy → caused by lack of orexin-releasing neurons GABA → increased levels during sleep (inhibitory e#ects) → inhibits our consciousness (as ce!s cannot communicate with each other) -Stages of sleep Sleep devices into 2 categories: REM sleep and non- REM (NREM) sleep (consisting of 4 stages) when awake : mostly alpha waves (low amplitude, high frequency → due to receiving stimulus from environment) deep sleep: nigh amplitude Delta rhythms (high amplitude because no stimulus from the environment is received anymore) stage 2 sleep: sleep spindles (responsible for memory consolidation) and K-complexes REM sleep: mostly beta rhythms (simmilar to being awake pattern) → eye movements are present but also fu!y relaxed muscles -REM sleep (paradoxical sleep) Rapid eye movements (REM) EEG shows increased neural activity postural muscles = more relaxed (than in other stages) associated with dreaming (but dreams in NREM also exist associated with PGO waves (distinctive pattern of high - amplitude electrical potentials) PGO waves: waves of neural activity → detected in pons → lateral geniculate → nucleus of thalamus → occipital cortex ce!s in the pons → spinal cord (inhibits motor neurons) → no movement during REM sleep if damaged = sleepwalking (acting out the dreams) during REM sleep: - reduced activity in dorsolateral prefrontal cortex (very important for our working memory) - increased activity in extastriate visual cortex (conceptual representations of visual stimuli) - BUT no activity in primary visual cortex (percieving detail) -Dreaming We are most likely to remember dreams from REM stage (highest chances of awaking) dreams may re"ect our brains attempt to make sense of sparse and distorted information, that is processed under unusual circumstances -Why we sleep? Dinosaur extinction → a!owed for mammals to sleep at nights we sleep to save energy ( night is colder so we don't need to use more energy to keep us warm) at night: - food is hard to $nd (we rely on vision) - we con conserve energy by not moving and keeping low body temp - some predators are active during night ( better to be inactive) -Memory consolidation Sleep improves memory for what was learned before going to sleep memories are formed by creating new connections (synapses) between neurons (encoding) and stabilizing connections (consolidation) replay activity: brain replays what was learned before sleep synaptogenesis: forming new synapses during learning (strenghtened by replay activity)  Lecture 9 - Internal Regulation -Internal regulation Our behavior is organized to keep the right chemicals in the right proportions in the right temperature -Theories of internal regulation Homeostasis: a! biological processes that keep body variables within a $xed range (the idea that the $xed range must be maintained at a! times) - Set point: a value that the body works to maintain (optimal value) - Negative Feedback: processes that reduce discrepancies from the set point A!ostasis: anticipating what variables change due to activity and counter them in advance ( prior knowledge with sensory data is used to predict what resources wi! soon be needed) A!ostasis and Homeostasis are complementary NOT contradictory - Homeostasis → some bodily variables must we kept within a constant range (e.g. Blood lvl of calcium I water, oxygen, glucose etc.) to enable chemical reactions that sustain life - A!ostasis → change is anticipated so compensatory mechanisms happen before the change occurs -Basal Metabolism Thermogenesis: how we use our physiological mechanisms to control our body temperature - divides into shivering and non-shivering mechanisms -Di#erences between species Ectothermic animals: body temperature depends on environment temperature, they have no physiological mechanisms (as shivering, sweating ), they regulate the temperature behaviora!y (amphibians, $sh, reptiles) Endothermic animals: animals that generate their own body heat, body temp can be higher than of the environment - physiological mechanisms: sweating, shivering, restricting blood "ow to the skin ( to keep organs warm) - behavioral mechanisms: various -Temperature Regulation We spend a lot of energy to keep stable temperature because: 1. Warm body is always ready for vigorous movement (regardless of the air temperature) 2. Temperature a#ects now easily oxygen is released from hemoglobin to the muscle (colder = slower rate) the 37°C temperature is kept and not higher because: - it already costs us 2/3 of our energ - at temp 41°C proteins break their bonds and lose their properties - we already increase our temp to $ght i!ness (fever) → temp above 39°C is harmful and life threatening above 41°C How brain regulates temperature? - temperature receptors in the skin - brain areas for registering temperature of the body and the brain itself ( in the anterior hypothalamus and preoptic area) -Water Regulation Water constitutes 70% of mammalian body concentration of chemicals in water determines the rate of chemical reactions in the body → water must be regulated within narrow limits water can be conserved by excreting concentrated urine, decreasing sweating and drinking (to $! up what was lost) vasopressin: hormone which constricts blood vessels and enables kidneys to reabsorb water and excrete more concentrated urine (its secretion is high during sleep to conserve water when we can't drink) -Osmotic Thirst osmotic thirst: increase in the concentration of molecules in body "uids triggers it (eg.after eating salt) happens at ce!ular level sensors for osmotic pressure are located in areas bordering the third ventricle receptors locations: OVLT, subfornical organ and digestive track -Hypovolemic Thirst Hypovolemic thirst: occurs due to loss of bodily "uids (including molecules) due to sweating or diarrhea caused by low blood level involves sodium-specy$c hunger to restore sodium concentrations detected by receptors located in kidneys and on blood vessels which respond to a drop in blood pressure receptors → subfornical organ → hypothalamus → drinking -Regulation of Feeding Satiety: condition of being fu! or grati$ed to the point of satisfaction Hungay!! Handy ! control of feeding: short and long-term satiety signals Hungry -Short-Term Regulation stretching of the stomach triggers signals that are send to the hypothalamus via the vagus nerve distention of the duodenum triggers release of cholesystokinin (CKK) which: - constricts sphincter muscle between stomach and duodenum - stimulates vagus nerve, sending output to hypothalamic nuclei that controls feeding -Insulin,Glucose and Glucagon Untreated Type-1 Diabetes insulin a!ows for entering of glucose (insulin de$ciency) to ce!s type-2 diabetes (insulin resistance) -Long-Term Regulation Leptin: released by fat ce!s, signals that the body has enough fat ce!s mutation in the leptin gene = fat ce!s are unable to produce leptin → brain reacts as if the body is starving = eating more -Brain Mechanisms for Hunger Signals stomach shrinking = hunger Paraventricular nucleus of hypothalamus ↓ Lateral hypothalamus Arcuate nucleus ↑ Increase ou Ventromedial hypothalamus r urge to fe ed ↓ → inhibits feeding (damage leads to more frequent feeding) -Obesity Obesity can be both genetic and behavioral Genetic causes: - symptomal: genes related to disease which includes obesity as a symptom - monogenic: mutation in a single gene leads to obesity - polygenic: a combination of many genes which predispose towards developing obesity -Anorexia Nervosa Characterized by a refusal to eat enough to maintain a healthy body weight, sometimes may be life threatening in about 1% women and 1/3 3% men with onset in teenage years and early 20s (generaly long persisting) people with anorexia don't dislike food but are extremely scared of getting fat strong preference of low-fat and low-calorie foods people verging starvation wi! engage in extensive physical activity (to generate heat)  Lecture 10 - Reproductive Behaviors -Hormones Androgens: hormones more abundant in males (eg. testosterone) Estrogens: hormones more abundant in females (eg. estradiol, progesterone) androgens and estrogens are steroid hormones that are synthesized from cholesterol by endocrine ce!s in various glands Steroids exert their e#ects in 3 ways: 1. Bind to membrane receptors, like neurotransmitters (rapid e#ects) 2. Enter ce!s and activate certain kinds of proteins in the cytoplasm 3. Bind to receptors that bind to chromosomes and activate or inactivate genes -Sexual Development Sex is determined by sex chromosomes sex chromosomes are not always XX or XY: - Turner syndrome: only 1 X chromosome - Klinefelter syndrome: XXY (male presenting) - XYY -Development of Genitalia males and females start the same with undi#erentiated genitalia 8 weeks of pregnancy: sex gets determined by introducing sry (sex determining region of Y chromosome) → protein (testis-determining factor) → development of testis ovaries produce estradiol which leads to development of female genitalia -E#ects of Hormones E#ects of hormones are distinguished in terms of: Organizing e#ects: produce long-lasting structural changes (e.g. development of genitalia, secondary sex characteristics) Activating e#ects: produce temporary changes (e.g. menstrual cycle, e#ects of testosterone and estradiol on sex drive) -Organizing E#ects Examples of prenatal organizing e#ects: female rats exposed to testosterone during sensitive period become partly masculinized in anatomy and behavior: - larger than normal clitoris - approaching and mounting sexua!y receptive females Congenial Adrenal Hyperplasia (CAH): the negative feedback ( adrenal gland sending cortisol to pituitary to stop release of adrenocorticotropin hormone to stop release of testosterone by adrenal gland) is not working resulting in hightent testosterone levels (can happen both in males and females) - CAH leads to masculinization of external female genitalia (not much e#ect in males) - CAH females are slightly more likely to show male-typical behavior in childhood and later life Androgen Insensitivity Syndrome: genetic males who are insensitive to androgens have female appearance and gender identity (problems with it in the sport competitions) development of external genitalia in males relies on dihydrosterone (testosterone t 5-alpha reducate → dihydrosterone), if there is a de$ciency of 5-alpha reductase = genetic male doesn't develop male genitalia  Organizing e#ects at onset of puberty: hormones lead to maturation of the genitals and the development of secondary sex characteristics (e.g. facial hair and deeper voice in males ; wider hips and breasts in females) at puberty the hypothalamus begins to release gonadotrophin releasing hormone (GnRH) → initiates the release of fo!icle-stimulating hormone (FSH) and luteinizing hormone (LH) by anterior pituitar in females FSH and LH stimulate the production of estradiol by the ovaries → starts the menstrual cycle -Activating E#ects Menstrual cycle: periodic variation in enormous and fertility over the course of about 28 days birth control pi!s prevent the surge of FSH and LH = no ovulation onset of menstruation has become earlier and earlier in life over the past century (due to 1. Increase in body fat (we can eat more) 2. Exposure to compounds similar to female hormones in meat, dairy, shampoo, plastic etc) -Variations in sexual behaviour Homosexuality homosexual behavior occurs in many animal species (eg. sheep) twin studies suggest genetic component (50% concordance in MZ and 25% in HZ) not related to adult hormone levels (maybe prenatal hormone levels) more likely in men with older brothers possible link to prenatal stress and alcohol use feminine behaviours in boys → strong homosexuality predictor (but masculine behavior in girls is a poor predictor) -Having Sex sexual reproduction increases variation in genes a!owing for quicker adaptations and prevent from spreading of "bad" genes females are more sexua!y active while estradiol peaks; males when testosterone peaks testosterone triggers the release of dopamine in medial preoptic area → stimulation of D1 and D5 receptors ( sexual arousal) → stimulation of D2 receptors (orgasm) oxytocin (the love hormone) is released: - during sexual pleasure and orgasm → causes relaxation - during labour to increase bonding with the baby -Pregnancy and Parenting Hormonal changes during pregnancy increase in prolactin (provide milk and decrease sensitivity to lepton = to eat more) increase in oxytocin ( milk production, increases maternal care, increases anger towards others Vasopressin and monogamy vassopressin: hormone synthesized by hypothalamus, secreted by posterior pituitary gland, conserves water associated with social behavior facilitates olfactory recognition Parenting Mother: Growth of brain areas related to reward and motivation, correlated with amount of positive emotions a woman expresses about having a baby. Father: Decline in testosterone and increase in prolactin spending more time playing with and caring for the child, (only when 1. close relationship with the mother 2. society where men contributes to infant care) human parenting behaviour is more experience dependent (i.e., learned behaviour) than hormone dependent.  Lecture 11 - Emotional Behaviors -Emotion It is di#icult to measure now people feel objectively → research on it produces many weak, inconsistent and di#icult to replicate $ndings Emotion consists of 4 components: 1. Cognition: what we think about something 2. Feeling: how we feel about something 3. Action: how we respond to something 4. Physiology: how our body reacts -James-Lange Theory of Emotion You are afraid because you ran away (NOT the other way around) event → appraisal (cognitive aspect) → action (behavioral aspect + physiology) → emotion (feeling aspect) example: scary situation → running away, increased heart rate etc → FEAR based on this theory 2 predictions can be made: 1. Weak bodily reaction/ arousal = weak emotion (?) 2. Increased physiological arousal = increased emotion (?) pure autonomic failure: rave condition in which the sympathetic nervous system no longer upregulates blood pressure and heart rate = predicting weaker emotions (we don't know its causes, starts in middle age due to peripheral autonomic reservation (Lewy bodies)) -Basic Emotions Can basic emotions be distinguished based on neural correlates? NO we distinguish: happiness, sadness, disgust, fear and anger but the brain areas are very inconsistent but the basic emotions can be based on facial expressions people from di#erent cultures can match emotion names to expressions (universality of emotion) cultural selectivity: we are better at recognizing emotions of people similar to us we can talk about emotions as positive, negative and their intensity (arousal) -Brain di#erences Left hemisphere Right hemisphere behavioral activation behavioral inhibition low-moderate arousal high arousal tendency to "approach" tendency to "avoid" anger - happiness disgust - fear -Function of Emotions fear: alerts to escape danger anger: to attack an intruder disgust: to avoid something potentia!y i!ness-evoking functions of other emotions are less clear emotional expressions help us communicate our needs to others and to understand our own needs and actions + help us make decisions -Moral decisions eg. the tro!ey problem ventromedial prefrontal cortex → central hub between cognition and feeling → a!ows to foresee the emotional consequences of our actions -Attack and escape behaviours Emotional behaviors are easier to study as they can be directly observed two main behaviors that are studied: attack and escape attack: interpreted as anger indicator escape: interpreted as fear indicator -Aggression aggression is linked to increased activity of the corticomedial nuclei of the amygdala individual di#erences in aggressive, violent and antisocial behavior depend on heredity and environment environmental risks for aggressive behavior: - witness or victim of violence in childhood - living in violent neighborhood - abuse in childhood - exposure to lead during development heritability - twin studies show signi$cant heritability of aggression - MAO-A gene (responsible for breaking down of neurotransmitters after reuptake) comes in two variants: low-activity and high-activity variant - low-activity variant is linked to aggression under certain environmental conditions hormones - testosterone → aggression → males exhibit more aggressive behaviors - criminals who committed violent crimes = higher testosterone levels - baseline testosterone levels are less important for aggression than the burst of testosterone in response to an event (hard to measure irl) - low serotonin release linked to impulsiveness and aggressive behavior - BUT serotonin overa! inhibits impulsiveness - cortisol inhabits aggression testosterone, serotonin and cortisol combined have moderate relationship with aggression -Escape Behaviour Startle re"ex: loud noise leads to contraction of neck muscles within 0.2 seconds re"ex is stronger in anxious people ( can be used to measure baseline anxiety) amygdala plays an important role in regulating fear especia!y learned fear) amygdala damage: no fear di#erent nuclei of the anggaara and their pathawas underlie di#erent types of fear anxiety: long-term, generalized emotional arousal panic disorder: frequent periods of anxiety with occasional attacks of rapid breathing, increased heart rate, sweating, trembling (panic attacks) -Stress and Health Stages of stress (General Adaptation Syndrome): alarm (release of epinephrine and cortisol), resistance (body adapts, decrease of sympathetic activity but continued release of cortisol ) and exhaustion (nervous and immune system no longer have the energy for responses) HPA axis: hypothalamus → pituitary gland → adrenal cortex, synthesis and release of cortisol by adrenal gland triggers a loop which leads to more HPA activation chronic activation of HPA axis = depression, i!ness, damage to hippocampal ce!s  Lecture 12 - Learning and Memory -Di#rent types of memory memory that we cannot easily put into words -Non-associative learning changes in the magnitude of a re"ex due to previous experiences (studied on Aplysia: a seasnail that's neurons has been fu!y mapped) habituation: decrease in re"ex after repeated stimulation - mechanism: repeated stimuli to siphon → sensory neuron releases less neurotransmitters → motor neuron releases less neurotransmitters → gi! shows weak withdrawal sensitization: increased re"ex to weak stimulus if it fo!ows a stronger stimulus - mechanism: shocking the tail is fo!owed by a stimulus to the siphon → sensory neuron in tail releases neurotransmitters → facilitating interneurons release serotonin, siphon sensory neuron releases more neurotransmitters → motor neuron releases more neurotransmitters → gi! shows stronger-than-normal withdrawal structural changes between sensory and motor neurons can occur as a result of repeated habituation and sensitization - loss of synapses in long-term habituation - increase in synapses in long-term sensitization -Long-term potentiation Strong stimulation of ce!s with connections to ce!s in the hippocampus (denate gyrus) leads to potentiation of the ce!s in the hippocampus i they become more responsive to new inputs for several hours long-term potentiation: if one neuron strongly stimulates another neuron A it becomes potentated = produces excitatory postsynaptic potential changes that wi! last for long periods of time, as a result of these changes in neuron A it becomes more sensitive to subsequent stimulations (also from other neurons) easier: strong stimulation of post-synaptic neuron leads to it forming additional synaptic connections to a! the neurons that were active at that same time, it wi! need less stimulation to reach its action potential LTP has 3 advantages: - speci$city: only the active synapses get stronger - cooperativity: stimulation by 2 or more axons produce stronger LTP than repeated stimulation by 1 axon - associativity: weak input + strong input → enhances the later response of weak input the opposite → long term depression: a prolonged decrease in response at synapse for axons that were less active -Simple Classical Conditioning Learning the association between two stimuli (Pavlovian conditioning: dog-food-be!) fear-conditioning involves amygdala circuts Fear-conditioning: association between contex and/or cue (CS) and a painful stimulus (US) leads to conditioned fear response (freezing (CS)) in response to context/cue eye-blink conditioning involves cerebe!um eye - blink conditioning: CS → tone; USC → pu# of air into the eye; UCR/CR → eye blink molecular mechanisms of CC are better understood in invetebrates (large neurons & known circuts) than in vertebrates (sma! neurons I not completely mapped out) long-term potentiation → potential explanations for various conditioning e#ects -Procedural Memory Learning of ski!s (e.g. how to ride a bike) and habits (e.g. chewing nicotine gum) motor ski!s and habits rely on learning that involves the basal ganglia -Operant Conditioning Learning which actions to choose based on reinforcement motor ski!s: learning to perform a motors task requiring the coordination of a sequence of movements -Semantic Memory part of declarative memory facts, meanings, concepts, knowledge of the external world semantic dementia: loss of semantic memory caused by damage of the anterior temporal lobe -Episodic Memory Personal episodes in time and space Hippocampus anterograde amnesia: inability to form new memories (as in case of HM) retrograde amnesia: inability to remember the past -Alzheimer’s disease "A pandemic of memory loss" → about 5.8 mi!ion su#ering now causes death of neurons in the brain $rst symptoms → losing episodic memory (damage to hippocampus) most likely to develop by people with Downs syndrome  Lecture 13 - Cognitive Functions -Lateralizarion brain is divided into two hemispheres, BUT are connected by corpus ca!ous, anterior commissure, hippocampal commissure and massa intermedia Perception: - contralateral projections : vision, movement, somatosensation - bilateral projections: audition, taste - ipsilateral projections: sme! -Language Left hemisphere is dominant for language production and comprehension in 95% of righ-handed people and 80% of left-handed people planum temporale: brain region responsible for auditory processing is bigger in the left hemisphere in ~65% people -Split-brain In people who undergone surgery in which their hemisphere - connecting nerves has been cut (to stop epileptic seizures) epileptic seizures: starts at a certain locus in the brain and further spreads throughout the brain "split-brain surgery": cutting the corpus ca!osum to prevent seizures from spreading to other hemisphere 1 reduces frequency and spread of the seizures severe epilepsy (such as Rassmussen's and Sturge-Weber syndromes) → hemispherectomy: removal of one hemisphere (the one from which the seizures are coming from) -Lateralization of function left hemisphere holds a stable view of the world (stable set of beliefs), right hemisphere registers changes or abnormalities and updates beliefs accordingly removal right temporal lobe = resistance to information that discon$rms belief removal left temporal lobe = more readily discard belief when presented with counter evidence right hemisphere is dominant for viso-spatial functions and is dominant in recognizing emotions (both in language and facial expressions) = if a smile is left looped we should think that a person is happier -Evolution of lateralization Similar paw preferences in reaching for food in mice, rats, cats and dogs Chimpanzees show similar structural asymmetries in their brain as humans Songbirds’ song production ski!s mediated by left hemisphere Right-hemisphere dominance for emotion seems to be present in a! primates so far investigated Left-hemisphere dominance for vocalization has been shown in mice and frogs and may we! relate to the leftward dominance for speech most human fetuses show right-hand dominance since 10th week of pregnancy on individual level: better divided attention (multitasking) faster reaction times in schizophrenia and autism patients → reduced or mirrored asymmetry -Language De$nition: hard to de$ne, has many criteria - semanticity: use of symbols to refer to actions and objects - cultural transmission: handed down across generations - spontaneous usage: no training or force needed to develop it - turn-taking - displacement: communicate about ideas and events across space and time - structure-dependence: grammatical rules de$ne meaning - creativity/productivity: ability to create new phrases to represent new ideas there were tries to teach other species language (bonobo apes, Alex the parrot) human language likely arised as a modi$cation of behavior vocal learning (ability to imitate sounds) is thought to be the precursor of language (animals can be vocal learners: elephants, whales, dolphins, sea lions, bats) -Bilangualism Ability to speak di#erent languages its not clear now di#erent languages are represented in the brain stroke impact the second learned language more strongly some research found spatial separation of the languages in the brain dorsolateral prefrontal cortex → language switch mechanisms bilinguals have better cognitive controls -Aphasia Aphasia: a total or partial loss of the ability to produce and/ or comprehend language most we! known: Broca's and Wernicke's aphasia Broca’s aphasia: (production aphasia) production of speech is disrupted but has meaning behind Broca's area: left inferior frontal lobe Wernicke’s aphasia: production of speech is intact but there is no meaning behind it + problem with language comprehension + anomia: problem with naming objects t not being aware of their speech problems and understanding Wernicke’s area: left plan temporal -Consciousness Mind-body problem (monism vs dualism) studying consciousness: change blindness, attentional blink, backward masking etc. top-down attention: putting our attention to something because we want to bottom-up attention: visual properties drive our attention to look at an outstanding stimulus (di#rent) -Spatial Neglect Damage to the right hemisphere → syndrome where people ignore their left side of the body as we! as the entire left visual $eld (can happen eg. due to stroke) most patients recover from it within 10 - 20 weeks if left hemisphere is damaged → right side is ignored  Lecture 14 - Psychological Disorders -Substance abuse From neurotransmitters to reinforcement to tolerance to withdrawal and craving most commonly abused drugs are derived from plants drugs can act as both antagonists and agonist - can increase release / decrease reuptake of neurotransmitters - - block breakdown of neurotransmitters into inactive chemicals agonist - directly stimulate postsynaptic receptors - - cause vesicles to leak neurotransmitters - - block postsynaptic receptor antagonist - -Reinforcement Taking drugs is associated with release of dopamine 2 major pathways associated with dopamine transport: mesolimbic pathaway and mesostriatal pathaway mesolimbic pathaway (implicated in reward): dopamine from ventral tegmental area (VTA) → nucleus accumbens (NAc), prefrontal cortex (PFC), amygdala, hippocampus mesostriatal pathaway ( implicated in habit formation / action selection and movement): dopamine from substantia negra → dorsal striatum L - dopa treatment in Parkinson's increases sensitivity to reward = increased risk of addiction -Tolerance mechanisms of neural adaptation and tolerance metabolic tolerance → liver produces drug-metabolizing enzymes pharmaco-dynamic tolerance → down-regulation of receptors contingent/learned tolerance → cue-induced anticipation of drugs -Withdrawal When the brain anticipates drugs and applies counter measures but the drug is not taken → opposite e#ects of the drug (unpleasant) craving induced by cues, hypersensitivity to the drug e#ect during states of withdrawal -E#ects of Long-Term Drug Abuse Reduced activity of prefrontal cortex poor decision making associated with continued use of the drug homeostasis: reduced expression of D2 receptors to balance overstimulation of doped rue receptors -Major Depressive Disorder Prevalence Symptoms and diagnosis the "common cold" of psychopathology about 16.2% Americans su#er depression at some point 35% recurrent, 15% chronic twice more likely in women Genetics ~33% heritability genes associated with depression also play a role in other disorders short version of serotonin transporter gene → more likely to develop depression (only in stressful environment)  Risk factors of depression there are many family history early childhood experiences stress alcohol use and much more -Schizophrenia Symptoms there are di#erent categories of symptoms: positive symptoms: behaviors that healthy people don't have but schizophrenia patients do - psychotic: delusions and ha!ucinations - disorganization: thought disorder, bizarre behavior negative symptoms: behaviors that healthy people have but not schizophrenia patients - depression-like symptoms - weak social interaction - lack of emotional expression - reduced speech and impaired working memory Genetics a#ects ~1% of population about 50% concordance rate in MZ suggests genetic component (multiple genes) Biology neurodevelopmental hypothesis: abnormalities in the prenatal and neonatal developmental of the nervous system lead to onset of schizophrenia later in life (due to subtle abnormalities of the brain) dopamine hypothesis: schizophrenia results from excess activity of dopamine synapses in certain brain areas glutamate hypothesis: Schizophrenia linked to de$cient activity at glutamate synapses in prefrontal cortex, glutamate stimulates neurons that inhibit dopamine release: Reduced glutamate => More dopamine. -Antidepressants and Antipsychotics Discovered by chance (we cannot develop it systematica!y as we don't understand the underlying processes) blocking or increasing various neurotransmitters unclear which treatment wi! work best for each patient many side e#ects di#icult to determine now e#ective the drugs are