Psychobiology Exam Notes PDF

#### An action potential is a rapid and temporary electrical signal that travels along the axon of a neuron, allowing it to communicate with other neurons, muscles, or glands. #### 1. Definition #### An action potential is an electrical impulse that occurs when a neuron sends information down it...

#### An action potential is a rapid and temporary electrical signal that travels along the axon of a neuron, allowing it to communicate with other neurons, muscles, or glands. #### 1. Definition #### An action potential is an electrical impulse that occurs when a neuron sends information down its axon. #### It involves a transient change in the electrical charge across the neuronal membrane, shifting from a resting negative state (inside the neuron) to a positive state and back to negative. #### 2. Resting Membrane Potential #### At rest, the inside of the neuron has a negative charge relative to the outside, typically around -70 millivolts (mV). This state is maintained by: #### Sodium-potassium pump: Actively transports 3 Na⁺ ions out of the cell and 2 K⁺ ions into the cell, creating a net negative charge inside. #### Ion channels: Allow selective movement of ions like potassium (K⁺) and sodium (Na⁺). At rest, K⁺ can leak out, but Na⁺ is largely kept outside. #### Negatively charged proteins: These large molecules remain inside the cell, contributing to the negative charge. #### 3. Triggering an Action Potential #### Action potentials are initiated when the membrane potential reaches a certain threshold, typically around -55 mV. This occurs due to stimuli such as: #### Signals from other neurons (via synaptic inputs). #### Sensory stimuli (e.g., pressure, light). #### If the stimulus is strong enough to depolarize the membrane to the threshold, an action potential begins. #### 4. Phases of an Action Potential #### a. Depolarization #### Voltage-gated sodium channels open, allowing Na⁺ ions to flood into the cell. #### This influx makes the inside of the cell more positive, causing the membrane potential to rise sharply (up to about +30 mV). #### b. Peak #### At the peak of the action potential, Na⁺ channels inactivate (close), stopping the influx of sodium. #### At the same time, voltage-gated potassium channels begin to open. #### c. Repolarization #### K⁺ ions flow out of the neuron through the open potassium channels. #### This outflow restores the negative charge inside the cell, returning the membrane potential toward its resting state. #### d. Hyperpolarization #### Potassium channels close slowly, causing an overshoot where the membrane potential briefly becomes more negative than the resting potential (e.g., -80 mV). #### The sodium-potassium pump then restores the resting potential. #### 5. Refractory Periods #### After an action potential, the neuron cannot fire again immediately due to the refractory period: #### Absolute refractory period: No action potential can occur because Na⁺ channels are inactivated. #### Relative refractory period: A stronger-than-usual stimulus is needed to trigger another action potential because the membrane is hyperpolarized. #### 6. Propagation of the Action Potential #### The action potential travels along the axon without losing strength. #### Unmyelinated axons: The impulse moves in a wave-like fashion. #### Myelinated axons: The impulse jumps between nodes of Ranvier (gaps in the myelin sheath) in a process called saltatory conduction, which speeds up signal transmission. #### 7. Importance of Action Potentials #### Communication: They allow neurons to send signals over long distances. #### Triggering release of neurotransmitters: At the axon terminal, the action potential causes the release of neurotransmitters into the synaptic cleft, enabling communication with other cells. #### Muscle contraction: In motor neurons, action potentials lead to muscle activation. #### **Migraines and Blindsight** - - - - - - - #### **Sensation and Perception** - - - - #### **Sensory Receptors** - - - - - - - - #### **Neural Relays** - - #### **Coding and Topographic Mapping** - - - - - - #### **Visual System's Anatomy** - - - - - - - - #### **Photoreceptors** - - - - - - #### **Visual Pathways** - - - - - - - - #### **Occipital Cortex and Streams** - - - - - #### **Processing Shape** - - - - - - #### **Color Vision** - - - - - #### **Visual Disorders** - - - - - - - #### **Plasticity** - - #### **Evolution of Music and Language** - - - - - - - - #### **Physical Dimensions of Sound Waves** 1. - - - - 2. - 3. - - #### **Tinnitus** - - - - - - #### **Perception of Sound** - - - #### **Functional Anatomy of the Auditory System** - - - - - - - - - - #### **Transducing Sound to Neural Impulses** - - - - - - - - - #### **Pathways to the Auditory Cortex** 1. 2. - 3. - 4. - - #### **Echolocation** - - - #### **Hearing Pitch** - - - - - #### **Detecting Loudness and Location** 1. - 2. - - #### **Language and Music in the Brain** 1. - - 2. - - - - 3. - #### **Nonhuman Auditory Communication** 1. - - - - 2. - - #### **Hierarchical and Parallel Movement Control** - - - - - - - #### **Neuroprosthetics** - - - - - #### **Somatosensory and Motor Systems** - - - - - - #### **Movement Initiation** - - - - - - - #### **Motor Cortex and Skilled Movement** - - - - - #### **Brainstem and Movement** - - - - - #### **Spinal Cord and Reflexes** - - - - - - #### **Basal Ganglia and Force Control** - - - - - - #### **Cerebellum and Movement Accuracy** - - - - - - - #### **Somatosensory System** - - - - - - - - - - #### **Pain Perception and Treatment** - - - - - - #### **Vestibular System** - - - - - - #### **Somatosensory Cortex** - - - - - - - - #### **Integration with Visual System** - - - - - - - - - - - - - - - - 1. - 2. - 3. - 4. - 5. - - - 1. - 2. - 3. - 4. - 5. - ### **Circadian Rhythms and Biological Clocks** #### **Biological Rhythms** - - - - - - #### **Circadian Rhythms** - - - - #### **Suprachiasmatic Nucleus (SCN)** - - - - ### **Sleep Stages and Patterns** #### **Sleep Stages** - - - - #### **NREM Sleep (N-sleep)** - - - #### **REM Sleep (R-sleep)** - - - #### **Typical Sleep Patterns** - - - - - ### **Disorders of Sleep** #### **Insomnia** - - #### **Hypersomnias** - - #### **Breathing Disorders** - - - #### **Parasomnias** - - - - ### **Dreaming** - - - - - - #### **Lucid Dreams** - - ### **Learning and Memory** #### **Types of Memory** - - - - #### **Neural Circuits for Memory** - - - #### **Plasticity and Memory** - - - #### **Memory Disorders** - - ### **Brain Plasticity** - - - ### **The Nature of Thought** - - - - - - ### **Characteristics of Human Thought** - - - - - - ### **Neural Units of Thought** - - - - - ### **Cognition and the Association Cortex** - - - - - - - ### **Streaming Visual Information** - - ### **Multisensory Integration** - - - ### **Spatial Cognition** - - - - - - - - - ### **Attention** - - - - - - ### **Planning and Executive Function** - - - ### **Imitation and Understanding** - - - - ### **Cognitive Neuroscience** - - - ### **Cognition and the Cerebellum** - - ### **Social Neuroscience** - - - - - ### **Neuroeconomics** - - - - ### **Cerebral Asymmetry in Thinking** - - - - - ### **Synesthesia** - - ### **Intelligence** - ### **Consciousness** - - - - **Seasonal Affective Disorder (SAD)** - - - - - - - - - #### **Reticular Activating System (RAS) and Sleep Regulation** - - - - - - - - #### **Emotional Memory Circuits** - - - - - - - - - #### **Detailed Mechanisms of Sleep Disorders** 1. - - - 2. - - 3. - - - - - ### **From Week 12 - Thinking** #### **Bálint Syndrome** - - - - - - - #### **Dissociation Between Motor Behavior and Conscious Awareness** - - - - - - - - #### **Lucid Dreaming Mechanisms** - - - - - - - Here is a comprehensive breakdown of all topics covered in the document, sorted by category for clarity: 1\. Clinical Neuroscience Definition: A specialty in neuroscience focusing on the diagnosis and treatment of diseases and disorders affecting the brain and central nervous system. Behavioral Disorders: Traditionally classified as social, psychological, psychiatric, or neurological. Causes: Genetic errors, epigenetic mechanisms, cell death, neural dysfunction, and life stress. Examples of causes and disorders: Genetic error: Tay-Sachs disease. Infection: Encephalitis. Injury: Traumatic brain injury. Stress: Anxiety disorders, PTSD. Brain function involves interaction between genes, chemicals, glia, and neurons. 2\. Psychiatric Disorders Assumed to result from brain malfunction. Focus on psychoses, mood disorders, and anxiety disorders. Schizophrenia Symptoms (DSM): Delusions, hallucinations, disorganized speech, disorganized or catatonic behavior, negative symptoms. Genetics: Concordance rate: 80% in identical twins. Linked to \~300 mutations on 10 genes. Developmental Factors: Evidence suggests prenatal origins. Brain Correlates: Enlarged ventricles, thinner medial temporal and frontal cortices. Child-onset linked to excessive pruning of cortical connections. Neurochemical Correlates: Dopamine abnormalities, GABA changes, glutamate receptor dysregulation. Mood Disorders Major Depression: Symptoms: Worthlessness, disrupted eating/sleep, slowed behavior, suicidal ideation. Bipolar Disorder: Alternating depression and mania. Mania: Excessive excitement, sometimes harmful. Treatment: SSRIs, cognitive-behavioral therapy (CBT), and neurogenesis-focused interventions. Anxiety Disorders Includes phobias, panic disorders, OCD, PTSD, etc. Acute and chronic types affect 15-35% of the population. Treatment: SSRIs and GABA-enhancing benzodiazepines. CBT with fear exposure techniques. 3\. Neurological Disorders Traumatic Brain Injury (TBI) Common in people under 40. Causes: Blows to the head, accidents, falls (common in elderly and children). Symptoms: Amnesia, confusion, fatigue, dizziness, slurred speech. Outcome: Long-term effects: Cognitive impairments, personality changes, and potential for neurodegenerative diseases. Stroke Types: Ischemic (blockage), Hemorrhagic (bleeding). Consequences: Glutamate release, calcium toxicity, brain swelling, neural shock. Treatment: Clot-busting drugs (t-PA), neuroprotectants, physical therapy, transcranial magnetic stimulation (TMS). Epilepsy Classification: Focal: Localized seizures. Generalized: Rapidly spread across both hemispheres. Treatment: Fast-acting GABA agonists, surgical resection, deep brain stimulation (DBS). Disorders of Myelin Multiple Sclerosis (MS): Autoimmune disease leading to myelin loss in motor and sensory nerves. Causes: Vitamin D deficiency, environmental factors, misfolded proteins. Symptoms fluctuate with relapses and remissions. 4\. Neurodegenerative Disorders Alzheimer's Disease (AD): Major cause of cognitive decline. Key changes: Amyloid plaques, neurofibrillary tangles, cortical degeneration. Predisposing factors: Age, genetics, environmental toxins. Age-Related Cognitive Loss: Declines in sensory perception, motor, and executive function. Can be slowed by cognitively stimulating activities. 5\. Treatments for Neurological Disorders Neurosurgical Treatments Deep Brain Stimulation (DBS): Electrodes implanted in the brain to treat Parkinson's, TBI, depression, and OCD. Stem Cell Therapy: Induces neurogenesis. Electrophysiological Treatments Electroconvulsive Therapy (ECT): Used for severe depression; risks include memory loss. Transcranial Magnetic Stimulation (TMS): Targets brain regions to treat depression, schizophrenia, and anxiety. Pharmacological Treatments Types: Neuroleptics (schizophrenia), SSRIs (depression/anxiety), L-Dopa (Parkinson's). Challenges: Side effects (e.g., tardive dyskinesia), lack of behavioral tools for coping. Behavioral Treatments Examples: CBT, rehabilitation post-stroke or brain injury, and constraint-induced therapy.