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psych 119 m1
| Question | Answer |
|---|---|
| What are the two main divisions of the nervous system? | CNS (brain + spinal cord) and PNS (everything outside the CNS). The PNS further divides into somatic (voluntary) and autonomic (involuntary — sympathetic & parasympathetic). |
| What is the VTA and why does it matter for pharmacology? | Ventral Tegmental Area — one of two main dopamine-producing areas (with substantia nigra). Source of the mesocorticolimbic (MCL) pathway. Critical for reward and addiction. |
| What is the role of the nucleus accumbens (ventral striatum)? | Reward processing and addiction. Primary site where all addictive drugs elevate dopamine (DiChiara & Imperato, 1988). Part of the mesocorticolimbic pathway |
| What is the nigrostriatal pathway and what disease results from its damage? | Dopamine pathway from Substantia Nigra → Striatum. Critical for movement control. Death of these neurons = Parkinson's disease. |
| What are the 3 types of synapses and what does each connect? | Axodendritic (axon → dendrite, most common), Axosomatic (axon → cell body), Axoaxonic (axon → another axon; modulates NT release) |
| What is the role of astrocytes in pharmacology? | Part of the Blood-Brain Barrier (their feet wrap around blood vessels). Also recycle choline for ACh synthesis. Drugs must pass through astrocyte sheaths to enter the brain. |
| What are the 3 requirements for a drug to cross the Blood-Brain Barrier? | Must be (1) small in size, (2) lipid soluble, and (3) not flagged by brain efflux pumps for removal. |
| What are convergence and divergence in neural signaling? | Convergence: many neurons synapse onto one (allows summation). Divergence: one neuron synapses onto many (broadcasts a signal widely). |
| What are the ion concentrations at rest? (K+, Na+, Ca2+) | K+ is HIGH INSIDE, low outside. Na+ is LOW inside, HIGH outside. Ca2+ is LOW inside, HIGH outside. Resting membrane potential is ~-65 to -70 mV (inside negative). |
| What are the 2 electrochemical forces acting on ions? | (1) Concentration gradient: pushes ions toward equal distribution (from high to low concentration). (2) Electrostatic pressure: opposites attract. Concentration gradient is STRONGER. |
| What does the Na+/K+ pump do and what does it cost? | Pumps 3 Na+ OUT and 2 K+ IN. Works AGAINST concentration gradients to maintain resting potential. Consumes ATP (very energy expensive). |
| List the steps of an action potential in order. | 1)Resting -70mV(2)EPSP→ligand-gated Na+ opens(3)Threshold -55mV: voltage-gated Na+ opens → rapid depolarization(4)+40mV: Na+ channels inactivate(5)Voltage-gated K+ opens → repolarization(6)Undershoot/hyperpolarization(7)Pump restores resting potential. |
| What is the refractory period and what causes it? | Period when another AP cannot be triggered. Caused by inactivation (not just closure) of voltage-gated Na+ channels. They only unblock when the membrane returns to resting potential. This enforces ONE-DIRECTIONAL propagation |
| What is saltatory conduction and why is it faster? | AP jumps between Nodes of Ranvier along myelinated axons instead of triggering at every point. Faster and more energy-efficient. Unmyelinated axons must retrigger AP continuously |
| What is an EPSP vs. IPSP? | EPSP (excitatory): Na+ enters → inside more positive → depolarization → closer to threshold. IPSP (inhibitory): Cl- enters → inside more negative → hyperpolarization → further from threshold |
| How does Ca2+ trigger NT release? | When an AP arrives at the axon terminal, depolarization opens voltage-gated Ca2+ channels. Ca2+ enters the terminal and triggers EXOCYTOSIS: vesicles fuse with the membrane and dump NT into the synaptic cleft |
| What is the difference between ionotropic and metabotropic receptors? | Ionotropic: NT binds and directly opens an ion channel (fast). Metabotropic: NT binds and activates a G-protein, which indirectly affects ion channels or second messengers (slower but amplified). |
| What are the 3 ways NT can be cleared from the synapse? | (1) Reuptake: transporters bring NT back into presynaptic neuron. (2) Enzymatic degradation: enzymes break NT into inactive metabolites. (3) Diffusion: NT drifts away. |
| What are autoreceptors? | Receptors on the PRESYNAPTIC neuron that detect the NT the neuron itself releases. They send feedback to reduce further NT release — like a thermostat. Effect is receptordependent. |
| What are the 3 conditions required for the NMDA receptor to open? | (1) Two glutamate molecules must bind. (2) A co-agonist (glycine or D-serine) must bind. (3) The membrane must ALREADY BE DEPOLARIZED to remove the Mg2+ block. When open: Na+, K+, and Ca2+ all flow through. |
| Why is glutamate excitatory and GABA inhibitory? | Glutamate opens ion channels that let in Na+ → depolarization (EPSP). GABA opens Clchannels → more negative inside → hyperpolarization (IPSP). The ions they let in determine the effect. |
| What is the dopamine synthesis pathway? | Tyrosine → L-DOPA (rate-limiting step, requires tyrosine hydroxylase) → Dopamine. LDOPA is used as a treatment for Parkinson's because dopamine itself cannot cross the BBB but L-DOPA can. |
| What does AChE do and what happens when it's blocked? | AChE (acetylcholinesterase) rapidly breaks down ACh at the synapse. Blocking it (nerve gases, pesticides) → ACh accumulates → uncontrolled muscle contractions, potential diaphragm paralysis and death |
| What is the dopamine prediction error signal? | DA neurons fire strongly to unexpected rewards; shift to fire to the CUE predicting a reward once learned; go SILENT when an expected reward doesn't arrive. Explains how cues control craving and behavior. |
| What does RADME stand for? | Route of administration, Absorption, Distribution, Metabolism, Elimination. The five processes by which the body handles a drug. |
| Rank the routes of administration from fastest to slowest | Inhalation ≈ IV injection (fastest) > Mucous membranes/skin > Oral (slowest). IV is the fastest injection; inhalation is fastest overall (lungs surface area ≈ half tennis court). |
| Why can't cocaine be taken orally? | Cocaine cannot survive the acidic environment and enzymes of the stomach. It is enzymatically degraded before absorption. (Similarly, insulin cannot be taken orally.) |
| What is depot binding and give an example | When a drug binds to fat or plasma proteins and is slowly released over time. THC is lipid-soluble and binds to fat tissue → slow, prolonged release, explaining long detection time in drug tests. |
| What are active metabolites? Give an example | Metabolites that retain pharmacological activity after the parent drug breaks down. Caffeine → paraxanthine + theobromine + theophylline (all active, longer half-lives). Effects continue even after caffeine is cleared. |
| What is enzymatic induction (metabolic tolerance) and how does smoking cause it? | Chronic drug exposure increases production of metabolizing CYP enzymes → drug is broken down faster → lower blood levels → need more drug. Smoking induces CYP1A2 → smokers metabolize caffeine FASTER than non-smokers. |
| What is half-life? | The time required to reduce the blood concentration of a drug by 50%. Follows exponential decay. Alcohol is an exception (linear decay). A longer half-life means the drug stays active in the body longer. |
| What is 'first pass metabolism'? | When a drug taken orally is absorbed from the gut and passes through the LIVER before reaching systemic circulation. The liver may metabolize a large fraction of the drug before it reaches the brain. |
| What is the difference between affinity and efficacy? | Affinity = how tightly a ligand BINDS to a receptor (strength of binding). Efficacy = whether binding ACTIVATES the receptor. An antagonist can have HIGH affinity but ZERO efficacy (binds strongly, does nothing) |
| What distinguishes a full agonist, partial agonist, and antagonist? | Full agonist: produces maximum response (like the endogenous NT). Partial agonist: binds and activates but produces submaximal response. Antagonist: binds but does NOT activate (zero efficacy). Only agonists can be full or partial. |
| What is the difference between competitive and non-competitive antagonists? | Competitive: binds at the SAME site as the NT; can be displaced by high NT concentrations. Non-competitive: binds at a DIFFERENT site; alters receptor function; CANNOT be displaced by the NT. Example: ketamine = non-competitive NMDA antagonist. |
| What is a selective vs. non-selective drug? | Selective: only binds specific receptor subtypes (e.g., nicotine → nicotinic ACh only, not muscarinic). Non-selective: binds multiple receptor types (e.g., caffeine blocks all adenosine receptors A1 and A2A). |
| What is the ED50 and how is it used? | Effective Dose 50% — the dose that produces 50% of the maximum response. Used to compare POTENCY between drugs. Lower ED50 = more potent (smaller dose needed for the same effect). |
| How do you calculate therapeutic index and what does it tell you? | Therapeutic Index (or margin of safety) = TD50/ED50 (toxic dose / effective dose). A LARGER ratio = safer drug (there's more room between effective and toxic doses). |
| What is the placebo effect and how is it controlled experimentally? | The placebo effect is a change not attributable to the drug's chemistry but to EXPECTATIONS. Controlled with a DOUBLE-BLIND experiment: neither participant nor researcher knows who received drug vs. placebo. |
| What secondary effect do ALL addictive drugs share? | All addictive drugs increase dopamine release in the MESOCORTICOLIMBIC pathway (specifically the nucleus accumbens / ventral striatum), regardless of their different primary mechanisms. (DiChiara & Imperato, 1988) |
| What is receptor desensitization? | After repeated agonist exposure, the receptor becomes LESS responsive despite the drug still being present. In full desensitization, the drug may be bound but the channel no longer opens. This contributes to tolerance. |
| What is receptor downregulation and when does it occur? | Reduction in the TOTAL NUMBER of receptors on the cell membrane, usually after prolonged agonist exposure. The cell removes receptors as a homeostatic response to excessive activation. Leads to tolerance. |
| Give an example of receptor upregulation from caffeine use. | Caffeine chronically blocks adenosine receptors → body compensates by making MORE adenosine receptors → when caffeine is stopped, all that extra adenosine now has more receptors to bind → extra sleepiness and withdrawal. |
| What is pharmacodynamic vs. metabolic tolerance? | Pharmacodynamic: tolerance due to changes IN THE BRAIN (fewer receptors, desensitization). Metabolic: tolerance due to increased liver enzyme production → drug is broken down faster. Both can occur simultaneously. |
| What is cross-tolerance? Give an example. | Tolerance to one drug reduces sensitivity to another that uses the SAME receptor system. Example: chronic cocaine use → fewer D2 receptors in striatum → reduced dopamine response to natural rewards like chocolate. |
| Can tolerance and sensitization occur for the same drug? | YES — for DIFFERENT effects. The desired effect typically shows tolerance (need more for the euphoria). Side effects can sensitize (get worse over time). Example: meth tolerance to euphoria but sensitization to motor agitation. |
| What is Long-Term Potentiation (LTP)? | Lasting strengthening of a synapse after repeated strong stimulation. The primary cellular mechanism of LEARNING AND MEMORY. After LTP, the same weak stimulus produces a LARGER EPSP. |
| Why is the NMDA receptor critical for LTP? | Bc lets in Ca2+, which acts as the second messenger triggering LTP. AMPA receptors dont let in Ca2+. The Mg2+ block in NMDA that lifts with depolarization makes NMDA a 'coincidence detector' (fires only when both pre and post are active simultaneously). |
| What is the molecular sequence of LTP induction? | Strong stimulation → AMPA opens → depolarization removes Mg2+ from NMDA → NMDA opens → Ca2+ enters → Ca2+ activates kinases → AMPA receptors inserted at synapse (early LTP) or new AMPA synthesized (late LTP) |
| What is the difference between early and late LTP? | Early LTP: INSERTION of existing AMPA receptors (moving them to the synapse); faster, shorter-term; no gene transcription. Late LTP: UPREGULATION (new AMPA receptors synthesized via gene transcription); longer-lasting, permanent structural change. |
| What is the A/N ratio and what does it measure? | AMPA-to-NMDA receptor ratio at a synapse. After LTP, more AMPA receptors are inserted → higher A/N ratio = stronger synapse. One release of glutamate activates more AMPA receptors → bigger EPSP. |
| What is drug-induced LTP and which synapse is key? | Addictive drugs preferentially induce LTP at the VTA DA synapse. The PFC sends glutamate to VTA DA neurons. Drug + PFC glutamate simultaneously → LTP conditions met → pathway strengthens → cues alone can trigger DA release and craving. |
| How does cue-induced craving relate to LTP? | Through LTP at the VTA synapse, environmental cues become associated with drug reward. The cue now directly triggers DA release (just like the drug did). This is why seeing a person or place associated with drug use causes craving and relapse. |
| What is the DSM-5 definition of Substance Use Disorder? | 'A problematic pattern of substance use leading to clinically significant impairment or distress.' NOT all drug use = SUD. Must meet specific criteria. Develops in stages and is a chronic, relapsing condition. |
| What is the diathesis-stress model of addiction? | Addiction results from a predisposition (diathesis = biological/genetic vulnerability) combined with environmental trigger (stress/exposure). You need BOTH. You can become addicted even without a predisposition given enough exposure. |
| How does route of administration affect addiction potential? | Faster onset = higher addiction potential (positive correlation). Longer duration of action = lower addictiveness. IV/inhalation are most addictive; oral/patch are least. Same drug, different route = different addiction risk (crack vs. powder cocaine). |
| What is caffeine's primary mechanism of action? | Non-selective COMPETITIVE ANTAGONIST of adenosine A1 and A2A receptors. Caffeine blocks adenosine from binding at its own site. The brain thinks it has LESS adenosine. Caffeine DOES NOT directly excite; it DISINHIBITS (removes inhibitory brake). |
| What does adenosine A1 receptor activation normally do? | A1 receptors are presynaptic. Activation INHIBITS voltage-gated Ca2+ channels → less Ca2+ entry → less vesicle exocytosis → less NT release → general sedation/decrease in neural activity. When tired, adenosine suppresses neuronal firing. |
| What does adenosine A2A receptor activation normally do, and how does it affect dopamine? | A2A receptors on GABA neurons in striatum are EXCITATORY -> increase GABA release. More GABA → less DA (inhibition). A2A also forms heteromers with D2 receptors → adenosine binding decreases D2 responsiveness. Caffeine blocks A2A → INDIRECT DA increase. |
| Why is caffeine considered a stimulant if it doesn't directly excite neurons? | Because blocking adenosine REMOVES INHIBITION on glutamate, ACh, DA, and NE systems. This disinhibition = net stimulation. Caffeine is an INDIRECT agonist of stimulatory NT systems, working through disinhibition. |
| What enzyme metabolizes caffeine, and what factors speed/slow it? | CYP1A2 (Cytochrome P450 1A2). Smoking INDUCES CYP1A2 → faster caffeine breakdown in smokers. Estrogen SLOW caffeine metabolism. Infants metabolize caffeine slowly. All metabolites (paraxanthine, theobromine, theophylline) remain pharmacologically active. |
| What are the effects of high-dose caffeine? | At very high doses: GABAA blockade, intracellular Ca2+ release, tachycardia, arrhythmia, seizure risk. Lethal dose ~10g (~100 cups of coffee). Not typically from coffee; energy drinks and concentrated caffeine pose higher risk. |
| Why does caffeine withdrawal cause headaches? | Chronic caffeine use causes adenosine receptor UPREGULATION (more receptors). When caffeine is removed, all that extra adenosine now floods the extra receptors → intense adenosine activity → vasodilation, fatigue, headache. |
| What is nicotine's primary mechanism of action? | Full, SELECTIVE, COMPETITIVE agonist at NICOTINIC ACh receptors (nAChRs). Does NOT bind muscarinic receptors. Binds at the same site as ACh and activates the receptor directly. |
| What is nicotine's two-phase (biphasic) effect? | Phase 1: Agonist/Excitatory — nicotine binds nAChRs → Na+/Ca2+ in → NT release (DA, Glu, serotonin, NE). Phase 2: Rapid desensitization within one cigarette → receptors close and can't open → nicotine acts as FUNCTIONAL ANTAGONIST. |
| Which nAChR subunit is critical for nicotine's reinforcing effects? | α4β2 nAChR. Knockout mice lacking the β2 subunit will NOT self-administer nicotine — proving this receptor is required for nicotine's reinforcing (addictive) properties |
| What enzyme metabolizes nicotine and what are the genetic implications? | CYP2A6. People with low CYP2A6 activity metabolize nicotine slowly → possible protective effect against heavy smoking/dependence. Estrogen increases CYP2A6 activity. Metabolite tested in drug tests: COTININE. |
| How does nicotine indirectly increase dopamine? | nAChRs are located on VTA dopamine neurons AND on axon terminals projecting to nucleus accumbens. Nicotine activates these nAChRs → DA neurons fire more → more DA released in the ventral striatum. This is the reinforcement pathway |
| Why are e-cigarettes considered more addictive than traditional cigarettes? | E-cigs deliver HIGHER concentrations of nicotine (more controllable, no combustion byproducts). Higher nicotine levels → greater receptor activation & DA surge → stronger reinforcement. Mint flavoring may further increase addictive potential. |
| What does it mean that nicotine is a 'functional antagonist'? | Nicotine is chemically an agonist (activates nAChRs). But bc it's effective at causing receptor desensitization, the net functional outcome is antagonism (receptors are closed and unresponsive). This is its secondary/functional mechanism, not primary. |
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minalogy