Drugs and Behavior, Week 4
Drugs and Behavior, Week 4 333
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This 6 page Class Notes was uploaded by Sarah Kincaid on Tuesday September 27, 2016. The Class Notes belongs to 333 at 1 MDSS-SGSLM-Langley AFB Advanced Education in General Dentistry 12 Months taught by Caine in Fall 2016. Since its upload, it has received 82 views. For similar materials see Drugs and Behavior in Psychology at 1 MDSS-SGSLM-Langley AFB Advanced Education in General Dentistry 12 Months.
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Date Created: 09/27/16
Introduction to Neuroscience & Synaptic Pharmacology For quiz on 9.28.16, Study info from Outline 2, especially the 6 pathways (synaptic mechanisms) that are drawn below. Cell soma (body): contains nucleus Dendrites: receive information (neurotransmitters bind to receptors on the dendrites) Axons: transport materials and conduct impulse to nerve terminal where transmitter is released Presynaptic neuron: releases neurotransmitter Synaptic vesicles: store neurotransmitter Postsynaptic neuron: receives neurotransmitter signal Receptors: what neurotransmitter binds to in order to produce its effect Synapse: space in between the presynaptic membrane and postsynaptic membrane Reuptake channels: recycle neurotransmitter back into presynaptic cell Neurotransmitter depletion: occurs when reuptake is blocked and cell cannot produce enough neurotransmitter to keep up with signals *Naming of neurons: based on the principle neurotransmitter that the presynaptic membrane releases across the synapse. Naming is not based on the signals dendrites in the postsynaptic membrane receive – most neurons receive many neurotransmitters. Introduction to Neuroscience & Synaptic Pharmacology The resting potential is considered -65 mV or -70 mV. Depolarization occurs when potassium channels open and K+ comes into cell making it more positive When the cell’s electrical membrane potential reaches the threshold, -55mV, most sodium ion channels open and positive sodium ions flood in causing the depolarization of the cell’s membrane potential. Repolarization occurs when the potential reaches +40 mV and the potassium ions rush out of the cell causing the cell’s potential to become very negative very fast dropping from -40 mV to about -90 mV in one ms. Refractory Period is the time the cell’s membrane potential is below the resting potential (-65 or -70 mV) The membrane potential returns to its resting potential by letting a few more positive ions in Postsynaptic potentials (IPSPs, EPSPs) result from incoming signals received by the dendrites IPSPs: inhibitory postsynaptic potential – makes the cell potential a little more negative EPSPs: excitatory postsynaptic potential – makes the cell potential a little more positive - Often both EPSPs and IPSPs are in play – an action potential occurs if the potential reaches -55 mV Introduction to Neuroscience & Synaptic Pharmacology Neuropharmacology: synaptic mechanisms of drug actions 6 Pictures of neuropharmacology 1. Direct Agonists mimic effects of transmitter by stimulating receptor (hydrocodone) - not same shape, but similar enough to bind o important because sometimes people do not have the presynaptic parts in their neurons and do not have the neurotransmitter but can get synthesized agonists to mimic the effects of the transmitter o problem: late Alzheimer’s, only have 20% of acetylcholine neurons (why drugs don’t work because you cannot produce more only preserve what you have) - this neuron is not having an action potential (the vesicle has not fused to the membrane and released neurotransmitter into the synapse) because endorphins only release neurotransmitter when you are in pain o in contrast, serotonin and dopamine have action potentials often 2. Indirect Agonists block transmitter reabsorption into nerve terminal - Act on presynaptic membrane, in family of direct agonists - blocks reuptake and increases serotonin concentration in synapse - SSRI: selective serotonin reuptake inhibitor Introduction to Neuroscience & Synaptic Pharmacology 3. Releasers cause release of neurotransmitter from nerve terminal (3 mechanisms) - First, Adderall binds to vesicles causing them to dump neurotransmitter into the presynaptic membrane - Second, reverse transport causes the neurotransmitter to exit presynaptic membrane via “transporter” (aka reuptake site) - Third, MAOI (mono amino oxidase inhibitor) ties up MAO, an enzyme that breaks down neurotransmitters that escaped reuptake (see 4. Enzyme Inhibitors to see step 3: MAOI) 4. Enzyme Inhibitors or “MAOI” - MAO is going to break down the neurotransmitter escaping reuptake, but the “x’s” on it mean that it is being tied up by an enzyme inhibitor and cannot break down the neurotransmitter, increasing [neurotransmitter] 5. Precursors increase endogenous transmitter in synapse Introduction to Neuroscience & Synaptic Pharmacology 6. Antagonists block transmitter from binding to receptors; aka “receptor blockers” (Narcan in OD) - Can be surmounted with enough agonist Neurotransmitters Opioids Endogenous endorphins – provide pain relief; ice age, naturally suppress pain so you can run from homo habilis (handyman with club) to a safe place Meds – exogenous opioids, aka pain killers GABA Most common neurotransmitter in brain Inhibits brain cells (IPSPs) – chance of action potential ( membrane potential) Alcohol (bud lite) < ANXIOLYTICS (XANAX) < SEDATIVES (Ambien, “good morning”) < General Anesthetics (remain unconscious under the knife) Glutamate nd 2 most common neurotransmitter Excites brain cells (EPSPs) - chance of action potential ( membrane potential) cannot be enhanced like GABA – seizures (excitotoxicity) antagonist: ketamine o aka dissociative anesthetics o blocks glutamate receptors Dopamine Adderall, “all ppl with ADD,” does three main things: 1. Wakefulness 2. Attention (to new stuff, specifically) 3. Recall of memories associated with rewards (aka “yes!” I got the right answer) Movement: motor strip, control body In Parkinson’s disease (PD), dopamine is replaced by dopamine precursors (direct agonists) Examples of Psychostimulants aka releasers aka RIs (reuptake inhibitors) o Cocaine, crystal meth, bath salts Introduction to Neuroscience & Synaptic Pharmacology Antipsychotics = dopamine agonists Addiction theory has involvement of brain dopamine systems The Triad = where cortex, midbrain, & basal ganglia meet Serotonin Impulse control (mood disorders, depression, obesity, anxiety*) SSRI antidepressants o 15% of depressed patients commit suicide (SSRIs control this impulse) o Most common impulse: stay in bed Depression is #2 cause of in productivity globally Part of “reticular core” Norepinephrine (synonym of noradrenaline) Fight or flight (stress) – under direct threat adrenal gland adrenaline & noradrenaline dumped into blood Beta-blockers for singular events (e.g. anxious for presentation) NSRI antidepressants: norepinephrine Attention (signal: noise) Acetylcholine Memory & cognition (puzzles: where is your car?) Alzheimer’s meds are supposed to acetylcholine: problem – doesn’t work well o Degenerates in hippocampus in AD (GPS), then cortex (complex thinking) o AD meds are AChE inhibitors (enzymes breaking down acetylcholine) End of Outline 2: the quiz material. Notes from Outline 3 will be in the next week’s notes. *Even though GABAergics are better anxiolytics than SSRIs, Prozac (SSRI) encouraged over XANAX (GABAergic) bc it has less abuse potential: therapeutic vs side effects
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