psych 202: final exam
Chapter 2: Cells and Structures of the Nervous System
Cells of the Nervous System
Neurons: Basic unit of the nervous system
Receive, integrate, and transmit information
Glial cells: Support and protect neurons
Astrocytes, microglia, oligodendrocytes (CNS), Schwann cells (PNS)
Anatomy of a Neuron
Dendrites: Receive information
Cell body (soma): Integrates information
Axon: Conducts information
Axon terminals: Release neurotransmitters
Synapse
Junction between neurons
Includes presynaptic membrane, synaptic cleft, postsynaptic membrane
Neural Communication
Electrical: Within neuron
Chemical: Between neurons (neurotransmitters)
Nervous System Organization
Central Nervous System (CNS): Brain and spinal cord
Peripheral Nervous System (PNS): Cranial and spinal nerves
Somatic (voluntary)
Autonomic (involuntary): Sympathetic (fight or flight), Parasympathetic (rest and digest)
Chapter 3: Neurophysiology
Resting Membrane Potential
Difference in electrical charge across the membrane
Inside is negative relative to outside
Maintained by sodium-potassium pump (3 Na+ out, 2 K+ in)
Action Potential
Rapid reversal of membrane potential
All-or-none response
Threshold of excitation (~-40mV)
Phases: Depolarization, Repolarization, Hyperpolarization
Synaptic Transmission
Arrival of action potential at axon terminal causes release of neurotransmitter
Neurotransmitter binds to receptors on postsynaptic membrane
Types: Ionotropic (fast), Metabotropic (slow)
Neurotransmitters
Examples: Acetylcholine, Dopamine, Serotonin, GABA, Glutamate
Chapter 4: The Chemical Bases of Behavior
Neurotransmitter Systems
Cholinergic (Acetylcholine): Learning, memory
Dopaminergic: Motor control, reward
Noradrenergic: Alertness
Serotonergic: Mood, sleep
Drugs and Behavior
Agonists: Enhance neurotransmitter action
Antagonists: Block neurotransmitter action
Chapter 5: Hormones and the Brain
Hormone Types
Peptide, Amine, Steroid
Endocrine Glands
Pituitary (master gland), adrenal, thyroid, gonads
Stress Response
HPA axis: Hypothalamus → Pituitary → Adrenal cortex → Cortisol
Chapter 7: Life-Span Development of the Brain and Behavior
Neurodevelopmental Stages
Neurogenesis, Cell migration, Differentiation, Synaptogenesis, Neuronal cell death, Synapse rearrangement
Influences on Development
Genetics, Environment, Experience
Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Sensory Processing
Labeled lines, Receptor cells, Sensory transduction
Somatosensory System
Touch: Merkel’s discs, Meissner’s corpuscles, Pacinian corpuscles, Ruffini’s endings
Pain: Nociceptors, A-delta fibers (fast), C fibers (slow)
Pain modulation: Endogenous opioids
Chapter 9: Hearing, Vestibular Perception, Taste, and Smell
Auditory System
Outer, middle, inner ear
Cochlea: Hair cells, basilar membrane
Auditory pathways: Cochlear nuclei, superior olivary nuclei, inferior colliculus, medial geniculate nucleus, auditory cortex
Vestibular System
Semicircular canals, otolith organs
Taste
Papillae, taste buds
Five basic tastes: Sweet, sour, salty, bitter, umami
Smell (Olfaction)
Olfactory epithelium, olfactory bulb
Chapter 10: Biological Rhythms and Sleep **
Circadian Rhythms
Suprachiasmatic nucleus (SCN): Circadian clock, receives direct light information (from ganglion cells)
Lesions eliminate circadian rhythms
Transplant experiment: when adult hampsters received a transplant of SCN tissue from a donor hamster, the recipients adopted the donor's circadian rhythm, demonstrating the SCN's critical role in regulating these biological cycles.
Retinohypothalamic pathway: Specialized retinal ganglion cells → send light information → SCN
Melatonin: Secreted by pineal gland at night
Sleep Stages (EEG) ***
Alert, awake: Desynchronized EEG
Non-REM sleep
Stage 1: Vertex spikes
note: reticular formation
Stage 2: Sleep spindles
Stage 3 (SWS): Delta waves
note: basal forebrain
REM sleep: Paradoxical sleep
note: pons
Sleep Disorders
Orexin: A lack of orexin, which helps keep us awake, causes narcolepsy with extreme sleepiness and sudden sleep attacks
Sleep apnea: when breathing stops and starts during sleep, causing poor rest. It can be caused by a blocked airway or brain issues
REM behavior disorder (RBD): people act out their dreams during sleep, sometimes with violent movements
Sleep Physiology
Basal forebrain: Promotes slow-wave sleep (SWS) and helps initiate deep sleep by releasing acetylcholine
Hypothalamus (VLPO): Sends GABA to arousal centers; regulates the sleep-wake cycle and circadian rhythms
Reticular formation: Regulates wakefulness and helps control the transition between sleep and wake states, maintaining alertness
Pons: key role in REM sleep and controls muscle paralysis during REM to prevent acting out dreams
Molecular clock steps
Clock/Bmal1 dimers promote the transcription of Per and Cry genes.
Per and Cry proteins interact with tau proteins to form Per/Cry/tau complexes.
These complexes inhibit the Clock/Bmal1 dimers, halting the transcription of new Per and Cry proteins.
Per, Cry, and tau proteins degrade over 24 hours, resetting the cycle.
The process is influenced by melanopsin in the retina, which sends light information to the SCN, helping synchronize the cycle with the environment.
Glutamate activation in the SCN helps maintain and regulate the cycle
Chapter 11: Emotions and Stress
Neural Mechanisms
Brain-self stimulation: Electrical stimulation (septum)
Fear conditioning: Neutral stimulus + unpleasant stimulus → fear response
Polygraph test: Measures heart rate, blood pressure
Relaxation training: Mindfulness-based stress reduction (MBSR)
Conditions & Disorders
Capgras delusion: Believe loved ones are impostors (low-road connection damage)
Maternal aggression: Mother defending offspring
Decorticate (sham) rage: Sudden rage without clear direction
Klüver-Bucy syndrome: Reduced fear/anxiety (bilateral amygdala damage)
Stress Response
Adrenal medulla: Releases epinephrine (E) & norepinephrine (NE)
HPA axis: Hypothalamus → anterior pituitary → adrenal cortex
ACTH → adrenal corticosteroids (e.g., cortisol)
Glucocorticoid receptors: Respond to cortisol, form stress/fear memories
Stress Pathways
FAST: Hypothalamus → adrenal medulla → E & NE
SLOW: Hypothalamus → CRH → anterior pituitary → ACTH → adrenal cortex → cortisol
Effects of Stress
Amygdala activity increases
PFC activity decreases
Theories of Emotion
Folk psychology: Emotion → autonomic arousal
James-Lange: Autonomic arousal → emotion
Facial feedback hypothesis: Sensory feedback from facial expressions affects mood (James-Lange theory)
Cannon-Bard: Simultaneous emotion & arousal
Schachter-Singer Theory (Two-Factor Theory of Emotion): Perception + arousal → emotion
Experiment (1962):
Epinephrine (uninformed): Increased emotional response
Epinephrine (informed): No increase in emotional response
Participants' emotions matched the context (happy or angry), showing that interpretation of arousal influenced emotion.
Constructing Emotions
Low Road (Fast): Thalamus → Amygdala (Lateral Nucleus). Quick, unconscious emotional reactions.
High Road (Slow): Thalamus → Sensory Cortex → Amygdala. Slower, conscious evaluation.
Lateral Nucleus: Main input region of the amygdala, receives sensory info.
Central Nucleus: Main output region, triggers emotional responses (via hypothalamus and brainstem).
Key cortical areas modulating emotion:
Insula: Bodily awareness and emotional feelings.
Cingulate Cortex: Emotional regulation and attention.
Prefrontal Cortex (PFC): Interprets and regulates emotional responses
Chapter 12: Psychopathology
Defining Psychopathology
Psychopathology: The study of mental disorders, including their symptoms, etiology (origins), and treatment.
Criteria for diagnosis often include distress, dysfunction, and deviance.
Major Categories of Psychiatric Disorders
Schizophrenia Spectrum Disorders
Characterized by psychosis, hallucinations, delusions, disorganized thinking.
Mood Disorders
Includes depression and bipolar disorder.
Anxiety Disorders
Includes generalized anxiety, panic disorder, phobias.
Obsessive-Compulsive and Related Disorders
Includes OCD, body dysmorphic disorder.
Trauma- and Stressor-Related Disorders
Includes PTSD and acute stress disorder.
Biological Basis of Schizophrenia
Dopamine Hypothesis: Overactivity of dopamine pathways (particularly D2 receptors) contributes to positive symptoms.
Glutamate Hypothesis: NMDA receptor hypofunction may contribute to cognitive symptoms.
Structural Abnormalities:
Enlarged ventricles
Reduced hippocampus, amygdala, and thalamus volumes
Hypofrontality: Reduced activity in the frontal lobes.
Depression and Bipolar Disorder
Monoamine Hypothesis: Depression results from deficits in serotonin, norepinephrine, and/or dopamine.
HPA Axis Dysregulation: Elevated cortisol levels linked to depression.
Brain Changes:
Reduced hippocampal volume
Increased amygdala activity
Bipolar Disorder: Alternating periods of mania and depression; may involve dysregulated dopamine signaling.
Anxiety Disorders
Amygdala Hyperactivity: Increased fear responses.
GABAergic Dysfunction: Reduced inhibitory neurotransmission may underlie anxiety.
Treatment:
Benzodiazepines enhance GABA activity.
SSRIs increase serotonin availability.
PTSD (Post-Traumatic Stress Disorder)
Amygdala: Hyperresponsive to trauma cues.
PFC: Hypoactivity may fail to inhibit fear responses.
Hippocampus: Reduced volume may impair context processing.
Treatment: CBT, exposure therapy, SSRIs.
Obsessive-Compulsive Disorder (OCD)
Cortico-striato-thalamo-cortical (CSTC) circuit dysfunction
Serotonin Hypothesis: SSRIs are effective treatments.
Treatments for Psychopathology
Pharmacotherapy:
Antipsychotics (e.g., D2 antagonists)
Antidepressants (SSRIs, MAOIs, tricyclics)
Mood stabilizers (e.g., lithium)
Anxiolytics (e.g., benzodiazepines)
Psychotherapy:
Cognitive Behavioral Therapy (CBT)
Exposure therapy
Neuromodulation:
Electroconvulsive Therapy (ECT)
Transcranial Magnetic Stimulation (TMS)
Chapter 13: Learning and Memory
Types of Memory
Declarative (Explicit) Memory: Facts and events; consciously recalled
Episodic memory: Personal experiences (e.g., first day of school)
Semantic memory: Factual knowledge (e.g., capital cities)
Nondeclarative (Implicit) Memory: Skills and habits; does not require conscious thought
Procedural memory: Motor skills (e.g., riding a bike)
Priming: Exposure to one stimulus influences response to another
Conditioning: Classical and operant learning associations
Brain Regions Involved in Memory
Hippocampus: Critical for consolidation of declarative memories; spatial memory (place cells)
Amygdala: Emotional memory; fear conditioning
Cerebellum: Procedural learning, motor memory, classical conditioning
Prefrontal Cortex (PFC): Working memory, decision making
Mammillary bodies and Thalamus: Memory relay; implicated in Korsakoff’s syndrome
Memory Processes
Encoding: Converting sensory input into a form that can be stored
Consolidation: Stabilization of memory traces (sleep plays a key role)
Storage: Retention of information over time
Retrieval: Accessing stored information when needed
Reconsolidation: Memories become unstable when retrieved and need to be restabilized
Long-Term Potentiation (LTP)
Persistent strengthening of synapses based on recent activity
Found primarily in the hippocampus
Involves NMDA and AMPA receptors
Basis for synaptic plasticity and memory formation
Memory Disorders
Amnesia
Retrograde amnesia: Loss of pre-existing memories
Anterograde amnesia: Inability to form new memories (e.g., H.M.)
Korsakoff’s Syndrome: Thiamine deficiency; damages mammillary bodies; severe anterograde amnesia and confabulation
Alzheimer’s Disease: Progressive loss of memory; neurofibrillary tangles and amyloid plaques
Chapter 15: Schizophrenia, Affective Disorders, and Anxiety Disorders
Schizophrenia
Symptoms:
Positive: Hallucinations, delusions
Negative: Flat affect, social withdrawal
Dopamine Hypothesis: Overactivity of dopamine, especially at D2 receptors.
Treatments: Antipsychotics (D2 antagonists)
Depression (Affective Disorders)
Monoamine Hypothesis: Low levels of serotonin, norepinephrine, or dopamine.
HPA Axis Dysfunction: Elevated cortisol linked to depressive symptoms.
Treatments:
Antidepressants: SSRIs, MAOIs, tricyclics
Electroconvulsive Therapy (ECT)
Cognitive Behavioral Therapy (CBT)
Anxiety Disorders
Types: Generalized anxiety, panic disorder, phobias
Mechanisms:
Amygdala hyperactivity
GABAergic dysfunction
Treatments:
Benzodiazepines (enhance GABA)
SSRIs
CBT
Chapter 16: Autism Spectrum Disorder, ADHD, and Stress-Related Disorders
Autism Spectrum Disorder (ASD)
Core features: Social communication deficits, restricted/repetitive behaviors.
Associated with: Theory of mind deficits, sensory sensitivities.
Attention-Deficit/Hyperactivity Disorder (ADHD)
Symptoms: Inattention, hyperactivity, impulsivity.
Neurobiology: Dopamine dysregulation in frontal-striatal circuits.
Treatments: Stimulants (e.g., methylphenidate), behavioral interventions.
Post-Traumatic Stress Disorder (PTSD)
Symptoms: Re-experiencing trauma, avoidance, hyperarousal.
Neural basis: Amygdala hyperactivity, reduced PFC regulation, hippocampal atrophy.
Treatments: CBT (exposure therapy), SSRIs
Chapter 16: Autism Spectrum Disorder, ADHD, and Stress-Related Disorders
Autism Spectrum Disorder (ASD)
Social communication deficits, restricted interests
Theory of mind deficits
ADHD
Inattention, hyperactivity, impulsivity
Treatments: Stimulants (methylphenidate)
PTSD
Re-experiencing trauma
Hyperarousal
Treatments: Cognitive-behavioral therapy (CBT), SSRIs