L7 - Perception Mechanism PDF

L7 - Perception Mechanism Inner Ear Hearing, Hearing loss. deafness E flows into Structure & Function...

L7 - Perception Mechanism Inner Ear Hearing, Hearing loss. deafness E flows into Structure & Function ampulla which Audition Semicircular canals Detects position n 1. Conductive or middle dear deafness have hair cells, Sound as a stimulus movement of head Diseases, infection, or tumorous bone the sensory Saccule growth, prevent middle ear form Physical stimulus involving movement Utricle Maintains balance receptor of V.S transmitting sound nerves Sets off waves of vibration: collisions Normal cochlea n auditory nerve bet neighboring/nearby molecules Cochlea Three tunnels Processes sound Can hear themselves clearly. Medium: air typically carries sound, sense sound travel through liquids, n Tunnels are Sends signals to 2. Nerve deafness, or inner-ear deafness At top each hair cell is collection of small solids filled with fluid nerve cells (to the Damage to the cochlea, hair cells, or “hairs” = stereocilia. Interacts with environment as it travels Hair cells brain) auditory nerve the movement of E causes movement of (receptor) Nerve cells to the perceiver Tinnitus -Frequent/ constant ringing in ear stereocilia = release neurotransmitter to Received through the ears and Pitch Perception Hearing loss send info abt the plane of mvmt to brain perceived as sound perception Place Theory Various situation that results with Ex: fabric absorbs sound n surface Each area along the basilar membrane hearing loss V.S uses 2 other organ reflect sound has hair cells sensitive to only one Old age (otolith organ) to detect Variation in sound waves determined by specific frequency of sound wave Trouble suppressing irrelevant sounds forward n backward mvmt n gravitational Amplitude (intensity) is the height of Frequency Theory Loss if inhibitory neurotransmitters force the wave n perceived as loudness. Basilar membrane vibrates in synchrony Attention High wave as loud n low wave as soft with the sound n causes auditory nerve 2 otolith in V.L: utricle Attending to name (detect mvmt in Frequency is the no. of wave cycles axons to produce action potentials at Attending to one person only per unit of time (Hertz; Hz) n perceived the same frequency. horizontal plane) & as pitch. low F as low-pitched Individual differences saccule (detect mvmt in Timbre (complexity) is the distant The current pitch theory combined modified versions of both the place theory n frequency theory: Amusia vertical plane) quality or uniqueness of sound. It is Low F sound best explained by the F theory “tone deafness” perceived as the “color”/”quality” of High F sounds best explained by P theory Normal auditory cortex, fewer Within the utricle and saccule, hair cells tones having = pitch n loudness. Pure connection to the frontal cortex detect movement when crystals of tones = single F, complex tones made Sound Localization Absolute pitch or perfect pitch calcium carbonate called otoconia shift up of several frequencies. Compare responses of the 2 ears Genetic predisposition, n early musical in response to it, leading to movement in Cues for sound localization: training the layers below the otoconia and Structure of the Ear Sound shadow displacement of hair cells. Common among individuals speaking Time of arrival tonal language Phase difference Somatosensation Mechanical Senses Sensation and movement. The Auditory Cortex Destination where auditory information Vestibular Sensation Discriminative touch, deep pressure, arrive in the temporal lobe of the brain Detects position and movement of head cold, warmth, pain, itch, tickle, and joints’ Results with compensatory eye position+movement movement Whose axons Vestibular Organs Receptor Location Respond to represent 95% of the cochlear nerve In the ear, adjacent to cochlear free nerve pain & Vestibular System any skin area ending temperature V. L continuous hair-follicle Ascending - info to brain with hair covered skin Mvmt of hairs Descending - from brain to elsewhere cochlea. receptor Outer Ear V. L contain Structure Ipsilateral = same side Contralateral = opposite side semicircular Meissner’s Mvmt across Pinna hairless area Most auditory info crosses over. how, each cerebral hemisphere canals (tube) corpuscles the skin Ear canal (auditory canal) processes stimuli from both the I &C Functions Advantages: Pacinian vibration / Brain damage in one any skin are Protection hemisphere has little effect on sense of hearing 3 tubes each situated in a plane (head corpuscles sudden touch Locate sound More processing can rotate) - detect head movement; Direct sound to middle ear Stops in ascending auditory path nodding, shaking and tilting right n left Merkel’s disk any skin area Static touch Organ of Corti - Cochlear Middle Ear nerve - Cochlear nucleus S. C filled with endolymph (when head Structure and function (cross over C) - primary second path - some stay at I rotate, causes movement of E through Ruffini endings any skin area Skin stretch Both cases, the neurons Tympanic membrane (ear drums) - synapse in superior olivary canal correspond to plane of complex (brainstem) movement Sound waves converts to vibrations by Signal continue to relay to the ear drums lateral lemniscus to inferior Krause end mostly hairless colliculus in midbrain Uncertain Ossicles: Inferior colliculus, the infor relay to medial geniculate of bulbs areas Malleus (hammer) Transmit waves Second primary thalamus Some stay at I n move into Incus (anvil) from middle to cortex auditory cortex The auditory cortex tucked Stapes (stirrups) inner ear through into lateral sulcus. Primary auditory cortex / A1 organized oval window tonotopically/ frequency Oval Window Somatosensation in the CNS Cannabinoids & Capsaicin Through the medulla (nucleus of the tractus solitarius; NTS) branches out L8 - Visual System Information from touch receptors in the Cannabinoids-block certain types of to various areas of the brain Structure pain, but produce problems such as head enters the CNS memory impairment. Somatosensory cortex: respond to Structure of the eye through the cranial Capsaicin-produces temporary touch information nerves. Insula is the primary taste cortex Information from burning sensation followed by a receptors below the longer period of decreased pain respond to taste information. head enters the spinal Placebos Variation in Taste Sensitivity cord and passes In medical research, the control group Genetic factors and hormone may toward the brain contribute to differences in taste through the spinal receives a placebo: drug/procedure nerves. with no pharmacological effects. sensitivity. Each spinal nerve is Shown to relieve pain, depression, and Related number of fungiform papillae connected to an area anxiety. near the tip of the tongue. of the body called a Taste Supertasters: higher sensitivity to all dermatome. tastes and mouth sensations. Touch experience is Has one function: decide to swallow or processed in the not. Tend to dislike strongly flavored primary Taste: stimulation of taste buds; food especially bitter somatosensory cortex. receptors on the tongue. Pregnant women have higher Flavor is a perception resulting from sensitivity Fibrous Tunic - superficial coat of the eyeball: combination of taste and smell. avascular Information from taste and smell Olfaction receptors are processed in the same Sense of smell Cornea area: endopiriform cortex. Response to chemicals that contact the transparent coat covers the colored iris membranes inside the nose. curved, helps focus light on the retina Pain Taste Receptors For most mammals: Taste receptors are modified skin cells. Finding food Sclera Pain sensation begins with bare nerve Taste receptors are replaced every 10-14 The “white” of the eye, layer of dense ending. Finding mates connective tissue days. Avoiding danger Pain sensitive cells in the spinal cord Papillae: structures on the surface of Covers the entire eyeball except cornea relay information to several sites in the the tongue Olfactory Receptors Gives shape to the eyeball makes it more brain. Each papillae may contain up to 10 or Olfactory cells: neurons responsible for rigid, protects its inner parts. The pain pathway crosses immediately more taste buds, and each taste bud smell, line the olfactory epithelium in the from receptors on one side of the body rear of the nasal air passages. Vascular tunic - middle layer of the eyeball contains about 50 receptors. Choroid - Provides nutrients to the posterior to a tract ascending the contralateral Traditional, there are four types of Olfactory cells has cilia, which has side of the spinal cord. (Touch olfactory receptors. surface of the retina receptors known: sweet, sour, salty, and information travels up the ipsilateral side bitter. Humans have several hundreds of Ciliary body of the spinal cord to the medulla, and Evidence for 5th type of taste receptor, olfactory receptors. Each receptor Ciliary process then crosses to the contralateral side.) umami. This receptor responds to responds to only a few stimuli. Pathway 1: receptor- spinal cord Contain blood capillaries that secrete glutamate. Olfactory Mechanism aqueous humor thalamus somatosensory cortex Suggested 6th type is oleogustus, taste Receptors activated by chemicals, will [Localization] Zonular Fibers: of fat. trigger changes in G protein, and G Extending from ciliary processes; Pathway 2: receptor spinal cord protein triggers chemical activities that thalamus hypothalamus, amygdala, Taste Mechanism lead to action potentials. Attached to lens hippocampus, prefrontal cortex and Salty: Saltiness receptor allows sodium Information from olfactory receptors Ciliary muscle anterior cingulate cortex. [emotion] ions to cross the membrane producing delivered to olfactory bulb. Circular band of smooth muscle that Pain relief action potential Olfactory bulb sends information to the alters the shape of the lens, adapting Sour: Sour receptors detect the cerebral cortex. it for near or far vision. Opioid mechanisms: presence of acid Olfactory Damage Iris - regulate the amount of light entering vitreous Opiate receptors in the spinal cord Sweet, bitter, umami: Molecule binds to Olfactory receptors are vulnerable chamber of the eyeball through the pupil (hole in and midbrain. receptor. Activation G protein that because they are exposed to the air the center of the iris) Endorphins are endogenous release a second messenger in the cell morphine. Bitter: Bitter taste; wide range of Average survival of over a month. Retina Stem cell matures into a new olfactory Brain produces several types of substance that are toxic. There are a cell in the same location as first and endorphins, and relieve different number of bitter receptors (30 or more) expresses the same receptor protein. types of pain. that are sensitive to various toxic If the entire olfactory surface is Gate theory: chemicals damaged: subject to permanent Spinal cords neurons receiving Taste Coding in the Brain impairment. messages from pain receptors also Taste information is sent to the brain via New receptors may fail to make the receive messages from touch receptors cranial nerves correct connections. and from axons descending from the brain. From anterior two-thirds of the Individual Differences These other inputs “close the gates” for tongue 7th cranial nerve Genetic differences. the pain messages, which is done partly From posterior tongue and throat Odor sensitivity declines with age. by releasing endorphins. Example: 9th & 10th cranial nerves rubbing can reduce sensation of pain Women detect odor more readily than men.  In humans, half of the axons from each Peripheral eye cross to the other side of the brain Characteristic Foveal vision vision Most ganglion cell axons go to the lateral geniculate nucleus, a smaller amount to Proportion of the superior colliculus, and fewer to rods increase other areas Receptors Cones only toward Primary Visual Cortex periphery aka area V1, located in the occipital cortex Each ganglion Each ganglion The primary visual cortex (area V1) Convergence of receives information from the lateral cell excited by a cell excited by input geniculate nucleus and is the area single cone many receptors responsible for the first stage of visual Optic Disc: site where optic nerve exits the eyeball; Responds well processing Pigmented layer damage: blindsight= ability to respond Distinguishes to dim light; Neural layer: Opponent-Process Theory in limited ways to visual information Brightness among bright poor for without perceiving it consciously. 3 layers of retinal neurons Suggests that we perceive color in terms sensitivity lights; responds distinguishing of paired opposites Unaware of visual input Photoreceptor layer: transduce light rays into receptor potentials: poorly to di light among bright The brain has a mechanism that Two possible explanation: lights perceives color on a continuum from red Presence of small area of healthy Photoreceptor layer: transduce to green and another from yellow to blue light rays into receptor tissue but not enough to provide potentials: Good details A possible mechanism for the theory conscious perceptions. vision because Poor detail is that bipolar cells are excited by one Thalamus sends visual input to other Rods: each retina has about set of wavelengths and inhibited by areas of the brain 120 mil each cone’s own visions because another Sensitivity to Ventral and Dorsal Paths Cones: each retina has about ganglion cell many receptors Limitations of Color Vision Theories 6 mil detail The secondary visual cortex (area V2) sends a converge their Both - Color constancy, the ability to receives information from area V1, Bipolar cell layer Ganglion cell layer message to the input onto recognize color despite changes in processes information further, and brain lighting, is not easily explained by these sends it to other areas Fovea / central fovea theories Information is transferred between area Contains only cones Good (many Poor (few Retinex Theory V1 and V2 in a reciprocal nature Area of highest visual acuity or Color vision The ventral stream refers to the path cones) cones) Retinex theory suggests the cortex resolution compares information from various that goes through temporal cortex Visual Coding Theories parts of the retina to determine the The “what” path Visual Coding: Color Vision brightness and color for each area Specialized for identifying and Fovea Area of highest visual acuity or The perception of color is dependent Color Vision Deficiency recognizing objects resolution upon the wavelength of the light An impairment in perceiving color The dorsal stream refers to the visual Each receptor in the fovea connects to a “Visible” wavelengths are dependent differences path in the parietal cortex single bipolar cell, which in turn upon the species’ receptors Gene responsible is contained on the X The “how” path connects to a single ganglion cell that Humans perceive wavelengths between chromosome Important for visually guided has an axon to the brain 400 and 700 nanometers (nm) Caused by either the lack of a type of movements The ganglions cells in the fovea are Depends on specific receptors within the cone or a cone that has abnormal called midget ganglion cells because eye properties Normal behavior makes use of both each is small and responses to just a Two major interpretations of color vision Most common form is difficulty pathways in collaboration single cone distinguishing between red and green Damaging either stream will produce Trichromatic theory/Young- different deficits Periphery of Retina Helmholtz theory Results from the long- and Ventral stream damage: can see More receptors converge onto bipolar Opponent-process theory medium-wavelength cones having where objects are but cannot identify and ganglion cells Trichromatic theory (Young Helmholtz theory) the same photopigment them Brain cannot detect the exact location or Color perception occurs through the Processing Visual Information Dorsal stream damage: can identify shape of a peripheral light source relative rates of response by three kinds Rods and cones of the retina make objects but not know where they are Summation enables perception of fainter of cones synaptic contact with horizontal cells lights Short-wavelength and bipolar cells Has better sensitivity to dim light Medium-wavelength Horizontal cells are cells in the eye that Ability to detect detail is limited by Long-wavelength make inhibitory contact onto bipolar interference from other nearby objects. Each cone responds to a broad range of cells wavelengths, but some more than others Bipolar cells make synapses onto The ratio of activity across the three amacrine cells and ganglion cells types of cones determines the color Different cells are specialized for More intense light increases the different visual functions brightness of the color but does not Ganglion cell axons form the optic nerve change the ratio The optic chiasm is the place where the Three kinds of cones are unevenly two optic nerves leaving the eye meet distributed Ventral and Dorsal Paths L9 - Motor System Muscle control by Proprioceptors Brain Mechanisms of Movement Proprioceptors: receptors that detect Cerebral Cortex Early lack of stimulation of one eye: Control of Movement the position or movement of a part of leads to synapses in the visual cortex Muscles and their movement the body becoming gradually unresponsive to input from that eye All animal movement depends on muscle Muscle spindles are proprioceptors Early lack of stimulation of both eyes: contractions parallel to the muscle that respond to cortical responses become sluggish but Smooth muscles: control the digestive a stretch: cause a contraction of the do not cause blindness system and other organs muscle CRITICAL PERIODS IN DEVELOPMENT Skeletal/striated muscles: control movement of the body in relation to the A stretch reflex occurs when Sensitive/critical periods are periods of muscle proprioceptors detect the time during the lifespan when environment Cardiac muscles: heart muscles that stretch and tension of a muscle experiences have a particularly and send messages to the spinal strong/enduring effect have properties of skeletal and smooth muscles cord to contract it Ends with the onset of chemicals that The Golgi tendon organ is another Primary Motor Cortex inhibit axonal sprouting Muscle Fibers type of proprioceptor that responds Specific areas of the primary motor Changes that occur during critical Muscles are composed of many to increases in muscle tension cortex are responsible for control of period require both excitation and individual fibers Located in the tendons at the specific areas of the opposite side of the inhibition of some neurons Each muscle fiber receives opposite ends of the muscle body Cortical plasticity is greatest in early life, information from only one axon but a Acts as a “brake” against Some overlap does exist but never ends single axon may innervate many excessively vigorous contraction by sending an impulse to the The primary motor cortex is active when Long-term consequences of impaired infant muscle fibers people intend a movement A neuromuscular junction is a synapse spinal cord where motor neurons vision are inhibited The primary motor cortex “orders” an Study of people born with cataracts but between a motor neuron axon and a outcome had them removed indicate that vision muscle fiber Units of Movement Release of acetylcholine causes the Voluntary & Involuntary Movements Planning a Movement can be restored gradually, but problems muscle to contract Reflexes are involuntary, consistent, and Posterior Parietal Cortex persist Monitors position of the body relative to Difficulty in recognizing objects Antagonistic Muscle automatic responses to stimuli the world Unable to tell that components are Movement requires the alternating Most movements are a combination of voluntary and involuntary; reflexive and Damage to this area causes: part of a whole contraction of opposing sets of muscles Difficulty in coordinating visual stimuli Best prognosis is for children whose called antagonistic muscles nonreflexive Movements vary with respect to with movement vision problems are corrected early in Acetylcholine always excites skeletal Trouble finding objects in space life muscles to contract feedback Some are ballistic and cannot be When walking they frequently bump A flexor muscle is one that flexes or Others raises an appendage changed once initiated into obstacles Visual Agnosia: The inability to recognize Others are guided by feedback Important for planning movement An extensor muscle is one that extends objects despite satisfactory vision Stimulation: results in intention to Prosopagnosia: The impaired ability to an appendage or straightens it Sequences of Behaviors move. recognize faces Fast & Slow Muscles Many behaviors consist of rapid Intense stimulation: results in Motion Blindness: The inability to Skeletal muscle types range from: sequences of individual movements. believing that they made the move determine the direction, speed & Fast-twitch: fibers produce fast Central pattern generators are neural Supplementary Motor Cortex whether objects are moving contractions but fatigue rapidly mechanisms in the spinal cord or elsewhere that generate rhythmic Plan and organize rapid sequence of Saccades: Several mechanisms prevent Slow-twitch: fibers produce less movements in a specific order; inhibitory confusion or blurring of images during vigorous contraction without fatigue patterns of motor output if necessary. eye movements People have varying percentages of Example: wing flapping in birds or Active seconds before the movement. fast-twitch and slow-twitch muscles “wet dog shake” Active following an error in movement so Slow-twitch fibers are aerobic and A motor program refers to a fixed you can inhibit the incorrect movement require oxygen during movement and sequence of movements that is either the next time. therefore do not fatigue learned or built into the nervous system Inhibit incorrect (possibly habitual) Nonstrenuous activities utilize slow- Once begun, the sequence is fixed movement. twitch and intermediate fibers from beginning to end Premotor Cortex Fast-twitch fibers are anaerobic and use Automatic in the sense that thinking Active immediately before a movement. reactions that do not require oxygen, or talking about it interferes with the Receives information about a target resulting in fatigue action Integrates information about position Behaviors requiring quick movements Examples: mouse grooming itself; and posture of the body. utilize fast-twitch fibers yawning Receives information necessary to direct a movement toward a target. Prefrontal Cortex Active during a delay before movement Stores sensory information relevant to the movement Necessary to consider the probable outcomes of a movement Inhibition of Movement Often associated with balance & Substantia nigra usually sends L10 - Learning & Memory How do we stop from following our coordination dopamine-releasing axons to the impulse? More neurons in the cerebellum than caudate nucleus and putamen Learning Two brain areas are sending competing in all other brain areas combined Behaviors: Damage to the cerebellum causes Loss of dopamine leads to less messages; the outcome depends on stimulation of the motor cortex and Reflexes whether the stop message arrives in trouble with rapid movements requiring aim/timing slower onset of movements Instincts time to cancel the action message. Examples: clapping hands, pointing at Genetic factors: especially with early- Learned behavior Ability to inhibit improves as prefrontal moving object, speaking, writing, onset Parkinson’s Non-associative learning: cortex matures; peak levels in young typing, playing musical instrument, Exposure to toxins; Insecticides, Habituation adulthood. sports activity. herbicides, and fungicides Sensitization Performance deteriorates in old age, the Functions other than movement: Traumatic head injury prefrontal cortex is highly vulnerable to Associative learning: Treatment to increase dopamine level damage. Responds to sensory stimuli even in since dopamine cant’s cross BBB but L- Classical Conditioning absence of movement. Instrumental/Operant Conditioning Mirror Neurons Responds to violations of sensory Dopa can (increase dopamine levels in Mirror neurons, active during expectations. basal ganglia - to improve movement Non-associative learning preparation for a movement and while can cause mvmt-related prob) Habituation: Organism reduces its Behaviors that depends on precise watching someone else perform the timing of short intervals; ex. tapping a Huntington’s Diease response to unchanging, harmless same or similar movement. rhythm with a finger. Begin with arm jerks and facial twitches. stimuli Active when people smile or see Also important for certain aspects of Tremors spread to other parts of the Sensitization: when repeated exposure someone else smile. attention, such as the ability to shift body to a strong stimulus increases responses to other environmental stimuli Connection from the brain to the spinal cord attention and attend to visual stimuli Genetic cause: autosomal dominant Mechanism of Synaptic Plasticity Messages from the brain must reach the Basal Ganglia gene. A group of large Symptom emerge during middle age: Plasticity: to modifiability of synapses medulla and spinal cord to control the Strength of connections bet neurons muscles subcortical Chorea (involuntary, spasmodic mvmt) structures in the Impaired coordination & balance can increase or decrease as a Corticospinal tracts are paths from the function of xperience cerebral cortex to the spinal cord forebrain Muscle rigidity Two tracts: Caudate Difficulty speaking n/or swallowing Habituation: Lateral corticospinal tract nucleus Cognitive symptoms (dementia) Repeated stimulation reduce the size Medial corticospinal tract Putamen Psychiatric symptoms (depression) of excitatory postsynaptic potential. Globus pallidus Associated with neurodegeneration, or Smaller amount of input from sensory Lateral Corticospinal Tract the deterioration n death of neurons neurons to the motor neurons. A set of axons from the primary motor Mutation in a single gene - huntingtin Repeated stimulation depletes the cortex, surrounding areas, and red Caudate nucleus and putamen receive Dominant mutation - 3 three nucleotides amount of available neurotransmitter nucleus to the spinal cord input from the cerebral cortex and send (cytosine, adenine, guanine) in repetition in the presynaptic sensory neuron. Controls movement in peripheral output to the globus pallidus kwn as Trinucleotide repeat. Diminished activity between motor areas (hands and feet) Globus pallidus connects to the Huntingtin protein gp together n not neurons and muscles. Red nucleus: a midbrain area with thalamus, which relays information to easily removed by brain enzymes Sensitization: output mainly to the arm muscles the motor areas and the prefrontal Additional stimulus + single stimulus Axons extend from one side of the brain cortex Stimulus gains the ability to influence to the opposite side of the spinal cord, Responsible for spontaneous, self- more than one neural pathway and control opposite side of the body initiated behaviors. Additional stimulus sensory Not for stimulus-elicited actions neurons interneurons Medial Corticospinal Tract Changing lanes when driving, raising A set of axons from many parts of the hand for question Learning: Synaptic Plasticity cortex Synaptic plasticity: Control The medial tract controls the muscles of Movement Disorders Single stimulus Sensory neurons release the neck, shoulders, and trunk Parkinson’s Disorder neurodegenerative normal amounts of NT Responsible for bilateral movements Characteristics: muscle tremors, like walking, turning, bending, rigidity, slow movements, and difficulty Motor neuron releases Normal response normal amounts of NT standing up, and sitting down initiating physical and mental activity Axons of the medial tract go to both Impairment in initiating spontaneous sides of the spinal cord. movement in the absence of stimuli Synaptic plasticity: Habituation Cerebellum to guide the action Repeated stimulus Sensory neurons release less NT Difficulty activating a movement and difficulty inhibiting inappropriate movements. Weaken response Motor neurons release less NT Lack of motivation and pleasure, depression. Cognitive deficits: attention, language, memory. Caused by gradual and progressive death of neurons, especially inthe substantia nigra Synaptic plasticity: Sensitization Memory Nondeclarative Memory Implicit / unconscious 4. Severe impairment of episodic memory Additional stimulus Learning & Memory: as a continuum Procedural Motors skills & procedures He could describe facts (semantic that includes: Classical Conditioning Association memory) that he learned before the Stimulus Attention operation. Sensory neuron release NT Sensation Priming He could describe clear memories for Perception Exposure to one stimulus changes only two personal experiences. Sensory neuron subsequent responding to another Interneurons release NT releases increased NT Steps along pathway of memory Other case of scattered damage in the processing: Working Memory hippocampus: complete loss of episodic Memory encoding Working memory (short-term memory) memory. Motor neuron releases * Brain treats episodic memories Interneurons increased NT Transformation of input into a (Baddeley & Hitch, 1994). form the brain can process The way we store information while differently from other memories. further we are working with it Episodic memories allows for imagining Stronger than normal the future. response Memory consolidation The case of H.M 5. Better implicit than explicit memory Organization of memory The Hippocampus: H.M Explicit memory @ declarative memory information into more long-term The case of H.M. (Henry Molaison) Deliberate recall of information that storage Surgeon: William Scoville one recognizes as memory H.M. suffered epileptic seizures (10 Associative Learning Memory Retrieval minor seizures/day, 1 major i.e. state it in words, draw a picture, Classical Conditioning Recovery of the stored demonstrate that you remember it. seizure/week) information. Removal of the hippocampus and Implicit memory Once retrieved, they become strucutres ner the medial temporal Influence of experience on behavior, vulnerable to modification cortex. even if you do not recognize that Needs stabilization through the Reduced epilepsy to no more than 2 influence. process of reconsolidation. major seizure/year. H.M. became comfortable and familiar with certain people. Information Processing Models But resulted with severe memory 6. Intact procedural memory Sensory Memory impairment. Leading to discovery of hippocampus Procedural memory role during formation of memories and Implicit memory: development of Short-term memory motor skills and habit. later recall. H.M.’s memory function Summary Long-term memory 1. Anterograde & retrograde amnesia Intact working memory, unless Anterograde amnesia distracted. Declarative Nondeclerative Inability to form memories for events Severe anterograde amnesia for that happened after brain damage declarative memory. Retrograde amnesia Severe loss of episodic memories. Semantic Procedural Loss of memory for events that Better implicit than explicit memory occurred before the brain damage Intact procedural memory. Episodic Classical conditioning H.M. is representative of other people The hippocampus Priming who suffered amnesia after damage to Theories of Function of the Hippocampus the hippocampus and surround 1. Critical for declarative memory, structures of the medial temporal lobe. especially episodic memory (Larry Sensory Memory Information sensed enters the sensory 2. Intact working memory Squire, 1992). Short-term or working memory 2. Hippocampus as a coordination center; memory brings together representations from Holds large amounts of data for a brief remained intact, unless he was distracted various locations of the brain, in the period of time correct order; allows for recall (episodic Short-Term Memory 3. Impaired storage of Long-Term Memory Severely impaired in forming new long- memories include: sights, sounds, Selected information is further location, series of events). processed. term memories. Underestimated his age. 3. Memories with much contextual detail Operant Conditioning Contains data that we are currently depend on the hippocampus, but older, Results with an organisms’ naturally thinking. Read the same magazine repeatedly or work the same jigsaw puzzle less detailed memories depend on occurring behavior becomes more or Has limited capacity and is temporary. cerebral cortex with less contribution repeatedly, without losing interest. less frequency in response to its Long-Term Memory Couldn’t remember his favorite uncle from the hippocampus consequence. Final destination for information. had died. Hippocampus & Navigation Reinforcements increase the Few limitations on capacity or duration. Hippocampus is important for spatial likelihood of the behavior to occur Told his childhood incident and then retell the story to the same person orientation again. Declarative memory Explicit / conscious again. Place cells: respond when in particular Positive & negative reinforcement Semantic Memory Moved to a nursing home in 1980, 4 place, looking in a particular direction Punishments decrease the likelihood Basic knowledge of facts & language years later, couldn’t not say where he Time cells: respond at a particular point of the behavior to occur again lived or who cared for him. in a sequence of time Episodic Memory Failed to learn meanings of new words. Relates to episodic memory Positive & negative punishment Relates to your own personal Formed few weak semantic memories. experience. Episodes of your life. The Striatum L11 - Motivation & Emotion Maslow’s Hierarchy of Needs Distention of duodenum hormone Depends on parts of the basal ganglia; Motivation cholecystokinin (CCK) : limits meal size Biological the striatum (caudate nucleus and the Google dictionary: motivation: 1. CCK constricts the sphincter putamen) a reason or reasons for acting or hunger, thirst, muscle between stomach and Involved in mechanisms for gradually behaving in a particular way. temperature duodenum; stomach hold its learning habits or learning what Desire or willingness to do maintenance, contents. probably will or will not happen under something; enthusiasm sex, seek of 2. CCK stimulates vagus nerve to certain circumstance. “an internal process that modifies the pleasure, avoid send signals to hypothalamus Long-Term Potentiation (LTP) way an organism responds to a certain pain, etc. produce shorter version of CCK LTP: one or more axons connected to a class of external stimuli” (Numan & Short -term regulation: limits size of the dendrite bombard it with a rapid series Woodside, 2010) meal. of stimuli Burst of intense stimulation leaves some Activates and directs behavior toward a 4. Gluucose goal. Pancreatic hormones: Insulin dan of the synapses potentiated; making Motivating factors can be: them more responsive to new input of glucagon the same time for minutes/days/weeks. Intrinsic Insulin : before, during, after meal, Properties of LTP Extrinsic enable glucose enter the cells (except: Both brain cells; enter w/o insulin. Specificity Theories on Motivation Hunger Excess glucose, enters liver, converts to If some of the synapses onto a cell Instinct theory of motivation (William glycogen for storage. have been highly active and others James): Behavior: eating Digestion and food selection Glucagon : convert glycogen to have not, only the actives ones A mother’s protection of her baby. glucose. become strengthened. Urge to lick sugar Function of digestive system? Cooperative Mouth esophagus stomach 5. Leptin Hunting prey Nearly simultaneous stimulation by Role of associative learning? small intestine large intestine Long-term mechanisms to compensate two or more axons produces LTP Select food that can be digested. day -today mistakes. Drive theory of motivation Food selection and behavior Leptin; signals brain about fat reserves. more strongly than does repeated Deviations from homeostasis create stimulation by just one axon. Belief that eating sugar makes Fat reserves leptin levels physiological needs. children hyperactive? T/F Decline leptin eat more, less active Associativity Results in psychological drive that Eating turkey causes sleepiness? Brain Mechanism Pairing weak input with a strong direct behavior to meet the need T/F Arcuate Nucleus input enhance later response to the Fish is brain food? T/F Part of the hypothalamus weak input. hunger seek out and consume food Regulation of Feeding There are two sets of neurons Improving memory Habits: pattern of behavior in brain gets messages from mouth, Sensitive to hunger signals Drugs to improve memory through LTP? which we regularly engage stomach, intestines, fat cells, etc. to Sensitive to satiety signals Drugs study in animals: but with Optimal level of arousal (Berlyne, 1960) regulate eating behavior. Input: hormones, insulin, leptin, cells in unacceptable side effects when applied to humans. Underaroused: bored and seek out 1. Oral Factor amygdala, basal forebrain, thalamus, stimulation People taste and chew even when they Hunger signals: Ghrelin Use of stimulant drugs. Input to hunger sensitive cells. Overaroused: engage in behaviors to are not hungry. Increased energy slightly improves reduce arousal Feeding without tasting can lead to Stomach releases ghrelin during memory and cognition for average or Optimal level of arousal depends on satiety; but with desire to taste or chew food deprivation stomach below average students, but complexity and difficulty of task something. contractions. provides little or no benefit and Yerkes-Dodson law Sham -feeding experiment: animals eat Ghrelin signal hypothalamus to maybe even harm for best students. and swallow almost continually without increase appetite. Simple task is performed best High production of ghrelin Supplements: Gingko biloba, Bacopa when arousal levels are relatively becoming satiated monnieri 2. Stomach response strongly to sight of food, high. twice likely to become obese Limited study to support Complex tasks are best performed Signal to end a meal: distension of the Satiety signals from various input Best recommendations: behavioral when arousal levels are lower stomach Distention of the intestines methods Self-efficacy Why sham feeding does not satisfy cholecystokinin (CCK) Study it now, rehearse, periodically Individual’s belief in own capability hunger Blood glucose insulin test yourself. to complete a task. Why eating satisfies your hunger Body fat leptin Physical exercise Impacted by previous successful before nutrition reaches any of the Nicotine – decrease appetite Good nutrition completion of the exact task or a cells Adequate sleep similar task. Vagus nerve: sends signal to the brain Paraventricular Hypothalamus Stress managament about distension of stomach Output from arcuate nucleus Social motives paraventricular hypothalamus (PVN) Achievement: drives accomplishment 3. Duodenum Certain cells in PVN inhibit lateral and performance Major site for absorbing nutrients hypothalamus Affiliation: positive interactions Nerves from duodenum signals about (hunger signals) Arcuate nucleus Intimacy: seek deep, meaningful distension and type/amount of nutrition (inhibit) PVN (inhibit) lateral relationships (taste receptors) hypothalamus Taste receptors: do not provide Inhibition of inhibitor excitation: conscious experience, but alter brain hunger stimuli increased eating activity to influence sense of satiety. and arousal  (satiety signals) Arcuate nucleus Weight Loss Technique Schachter-Singer Two-Factor Theory What is emotion? (excitation) PVN melanocortins & Obesity considered a disease? Physiological arousal? glutamate Pros and cons “cognition, feeling, action & Melanocortin receptors in PVN limit Diet plan? physiological changes” food intake Consider: Damages to receptors lead to How long they kept the weight off overeating How many other people tried the Nervous feel but you don’t know why Additional pathway: orexin increases plan and failed (no cognition), do nothing about it (no Lazarus’s Cognitive-mediation Theory action). persistence in seeking food, increases Techniques: Arousal appraisal Emotional feelings correlate strongly activity and motivation. Small changes biological/physical response Promote good health: with arousal of ANS, no particular Lateral Hypothalamus Must there be physiological arousal to emotion is consistently association Output from paraventricular nutrition+exercise Reduce/eliminate soft drinks. experience emotional feelings? with distinct pattern of autonomic hypothalamus (PVN) lateral activity hypothalamus Weight-loss drugs wt S/E Based on James-Lange theory, Control insulin secretion, alters taste Gastric bypass surgery suggests: Functions of emotion responsiveness, facilitates feeding in ?!?!: microorganisms in digestive People with weak autonomic 0r Obvious functions: other ways system skeletal response feel less emotion. Fear alerts for escape from danger Damage to the area refuse food and Bulimia Nervosa Increasing one’s response enhance Anger directs us to attack an water Condition which people alternate an emotion. intruder Stimulation of the lateral hypothalamus between binges of overeating and Research findings: Disgust tells us to avoid something increases drive to eat periods of strict dieting Damaged spinal cord: no sensations that might cause illness. Input from taste pathway: alter taste Anorexia Nervosa or voluntary movement: report Less obvious functions: happiness, sensation and salivation response to Characterized by refusal to each experiencing emotions the same as sadness, embarrassment, others taste enough to maintain a healthy body before injury. Emotional expressions help us Sends signals to cortex increase weight. Pure autonomic failure: communicate our needs to others response to taste smell, sight of food. Emotion Does not react to stressful Understand other people’s needs Increase pituitary gland’s secretion Google Definition: a strong feeling experience with changes in heart and probable actions of hormones that increase insulin deriving from one’s circumstances, rate, blood pressure, or sweating. Provide useful guide when we need secretion mood, or relationship with others. They report having the same to make a quick decision. Sends signals to spinal cord control “cognitive evaluations, subjective emotions, no difficulty identifying Brain Mechanism autonomic responses for digestive changes, autonomic and neural arousal, emotion. secretions. Limbic system: considered critical for and impulses to action” (Plutchik, 1982) BOTOX: experience weaker than emotion processing. Medial Areas of the Hypothalamus Motivation? = “an internal process that usual emotional response. Cerebral cortex also reacts to emotional Output from ventromedial modifies the way an organism responds People with certain brain damage: situations. hypothalamus inhibit feeding. to a certain class of external stimuli” experience normal emotional Locations of brain activity for each Damage leads to overeating and weight (Numan & Woodside, 2010) responses emotion varies. gain Motivation ≈ Emotion ? Physiological arousal Emotions Neurons in amygdala active when Normal sized meals but more Generally includes components of According to James-Lange theory: perceiving a particular emotion in frequently: due to increased stomach cognition, feeling, action & physiological emotional feelings result from the someone’s expression. motility and secretions. changes body’s action: No brain area appears to be specific for Damage increase insulin production Emotion & Autonomic Arousal Heart racing, sweating, breathing experiencing any particular emotion. stored as fat. Autonomic nervous system rapidly fear? Do we have few basic emotions? No Gain weight not necessarily from Sympathetic: “fight-or-flight” Vigorous exercise heart racing, brain area is specific for each emotion. overeating, but because increased Parasympathetic: increases digestion sweating, breathing rapidly. Basic emotions are studied based on storage of fat. and processes that save energy and Physiological response alone not facial expression. Eating Disorders prepare for later events. sufficient for emotional feelings, but Amygdala: Genetics and Body Weight can impact the feelings. How do we process emotion? Important for enhancing the startle Syndromal obesity: reflex and for learned fears Feel & emotion that changes your Increased heart rate intensify Gene causes a medical problem that ratings for emotions, for people