Study Guide for PSY 364- Behavioral Neuroscience Final Exam Fall 2023
PSY 364 Study Guide – Fall 2024
behavioral neuroscience :
How are proteins measured?
Techniques: Proteins are quantified using methods like Western blotting, ELISA, mass spectrometry, and immunohistochemistry.
Western Blotting: Separates proteins by size, then uses antibodies for detection.
ELISA: Detects and quantifies specific proteins using enzyme-linked antibodies.
Mass Spectrometry: Identifies proteins and their post-translational modifications with high precision.
How are neurotransmitter concentrations measured?
Techniques:
High-Performance Liquid Chromatography (HPLC) coupled with electrochemical detection.
Microdialysis for real-time measurement in the brain.
Immunoassays and radioligand binding assays for sensitivity and specificity.
Describe the main anatomical features of a neuron.
Soma (Cell Body): Contains the nucleus and organelles.
Dendrites: Branched extensions receiving synaptic inputs.
Axon: Long projection transmitting action potentials.
Axon Hillock: Site of action potential initiation.
Synaptic Terminals: Release neurotransmitters.
Describe the distribution of Na+ and K+ ion concentrations in a neuron at rest.
Na+: Higher outside the cell (~145 mM extracellular; ~15 mM intracellular).
K+: Higher inside the cell (~140 mM intracellular; ~4 mM extracellular).
Maintained by the Na+/K+ pump, which exchanges 3 Na+ out for 2 K+ in.
Electrochemical forces on ions at various potentials:
At -70 mV (resting potential):
Na+: Strong inward driving force due to both concentration and electrical gradients.
K+: Weak outward driving force due to a concentration gradient opposing the electrical gradient.
At +45 mV (peak of action potential):
Na+: Minimal driving force; equilibrium potential (~+60 mV).
K+: Strong outward driving force due to concentration and electrical gradients aligning.
Action Potential and Synaptic Transmission
Describe saltatory conduction.
Occurs in myelinated axons where action potentials "jump" between nodes of Ranvier.
Myelin insulates the axon, increasing conduction speed.
Voltage-gated Na+ channels at the nodes regenerate the action potential.
Composition and features of the neuron’s cell membrane:
Phospholipid Bilayer: Semi-permeable barrier.
Membrane Proteins: Ion channels, receptors, and pumps.
Cholesterol: Adds rigidity.
Glycoproteins: Cell signaling and adhesion.
What is the role of ATP?
Provides energy for the Na+/K+ pump, maintaining ion gradients critical for action potential generation.
Fuels synaptic vesicle recycling and neurotransmitter synthesis.
Ionotropic vs. Metabotropic receptors:
Ionotropic: Fast-acting; ligand-gated ion channels (e.g., AMPA, NMDA for glutamate).
Metabotropic: Slow; G-protein-coupled receptors (e.g., dopamine D1/D2 receptors).
Metabotropic signaling through second messengers:
Neurotransmitter binding activates G-proteins.
G-proteins stimulate effectors (e.g., adenylyl cyclase).
Second messengers (e.g., cAMP) mediate downstream effects like protein phosphorylation.
Synaptic Dynamics
Elements in the presynaptic terminal:
Synaptic vesicles, docking proteins (e.g., SNAREs), mitochondria, and voltage-gated Ca²⁺ channels.
Neurotransmitter removal mechanisms:
Reuptake: Transport back into the presynaptic cell (e.g., via SERT for serotonin).
Enzymatic degradation: Breakdown by enzymes (e.g., acetylcholinesterase for acetylcholine).
Diffusion: Passive dispersal from the synaptic cleft.
Neurotransmitter regulation via negative feedback:
Autoreceptors: Located on the presynaptic neuron; inhibit further release or synthesis (e.g., dopamine D2 autoreceptors).
Neurotransmitters
Neurotransmitter-to-Brain Region, Function, and Drug:
Dopamine: Basal ganglia; motor control, reward; targeted by antipsychotics, stimulants.
Serotonin: Raphe nuclei; mood regulation; SSRIs.
Glutamate: Cortex; excitatory signaling; NMDA receptor antagonists (e.g., ketamine).
GABA: Basal ganglia, cerebellum; inhibitory signaling; benzodiazepines.
Brain and Behavior
Basal ganglia and information processing (Direct Pathway):
Excitation from the cortex activates the striatum.
Striatum inhibits the globus pallidus internus.
Reduced GPi activity disinhibits the thalamus, facilitating movement.
Limbic system elements:
Amygdala, hippocampus, cingulate cortex, hypothalamus, and nucleus accumbens.
Research and Validity
Animal models of disease:
Predictive Validity: Models predict treatment responses.
Face Validity: Models mimic symptoms.
Construct Validity: Models replicate disease mechanisms.
Pharmacodynamics vs. Pharmacokinetics:
Pharmacodynamics: Drug effects on the body.
Pharmacokinetics: Drug absorption, distribution, metabolism, excretion.
Agonists vs. Antagonists:
Agonists: Activate receptors (e.g., morphine).
Antagonists: Block receptor activity (e.g., naloxone).
APA Ethical Principles:
Beneficence: Prioritize participant well-being.
Justice: Ensure fairness in research practices.
Respect: Maintain confidentiality and informed consent.
Key Disorders Overview
Schizophrenia (SZ):
Positive Symptoms: Delusions, hallucinations.
Negative Symptoms: Flat affect, catatonia.
Cognitive Symptoms: Disorganized thought.
Alzheimer's Disease (AD):
Hallmarks: ß-amyloid plaques, Tau tangles.
Regions: Hippocampus.
Treatments: Memantine, cholinesterase inhibitors.
ADHD:
Dopamine Dysfunction: Default Mode vs. Task-On Network imbalance.
Treatments: Stimulants (e.g., Adderall).
Addiction:
Key Mechanism: Nucleus accumbens DA elevation.
Treatments: Replacement strategies, sensitization.
Major Depressive Disorder:
HPA Dysregulation: Elevated cortisol.
Treatments: SSRIs, ECT, BDNF enhancement.
Anxiety Disorders:
Amygdala Hyperactivity.
Treatments: Benzodiazepines, CBT.