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psychopharm exam 1
| Question | Answer |
|---|---|
| resting potential | when the battle between electrostatic pressure and diffusion is balanced for K+ |
| change in voltage when depolarization occurs | -70 my to 40 mv |
| what types of effects can local potentials have | EPSP (excitatory) or IPSP (inhibitory) |
| what types of effects can action potentials have | EPSP only; excitatory |
| do neurotransmitters enter the cell? | no |
| spatial summation | relates to local potentials the idea that IPSP/EPSPs from local potentials physically come together in the axon hillock |
| how do local potentials travel | decrementally their charge decreases as they move |
| temporal summation | relates to local potentials the idea that the charges of the local potential have to add up to 20 mv in order to bring the cell from -70 mv to -50 mv |
| at what charge does the cell decide to send an action potential | -50 mv |
| where do IPSP and EPSPs have effect | along the input zone |
| saltatory conduction | the prostration of the AP down the axon; jumps between nodes of ranvier using myelin to speed it up,,,like a slip and slide… goes at a constant rate |
| how does sodium underly the action potential | once the voltage gated channel for protein is opened, sodium rushes down the axon which is what causes the hyperpolarization. once it hits each new node of ranvier, the node generates its own kind of new action potential to get o the next node |
| axodendric synapse | the most common; what we always talked about in biopsych axon terminal button synapses with a dendrite of the next neuron neurons are contiguous; dont touch |
| axosomatic synapse | between a nerve terminal (button) and a cell body axo SOMA tic function similar to axodendric synapses neurons here are contiguous, meaning there are gaps between neurons |
| axoaxonic | can alter release of NTs at the terminal button; this can inhibit or facilitate NT release;; this is because it is synapsing higher up on the neuron before NTs are released involves one axon synapsing on the axon terminal of another neuron |
| presynaptic inhibition/facilitation | when the presynaptic neuron in an axoaxonic synapse inhibits/facilitates NT release of the postsynaptic neuron |
| characteristics of neurotransmitters | 1. manufactured in the presynaptic neuron (endogenous) 2. Released from the axon terminal 3. After release from the synapse, they bind to the post synaptic receptors (which changes the postsynaptic neurons cell polarity/charge) |
| similarities between hormones and neurotransmitters | they are both endogenous ligands (bind to cell receptors) |
| differences between hormones and NTs | generally speaking, glands secrete hormones while NTs are made in the terminal button -hormones travel via bloodstream to target organs or other glands, NTs stay in brain between synapses -Hormones have slower effect and have to travel longer distance |
| synaptic transmission of NTs | depolarization (the action potential) causes calcium (Ca2+) channels to open (they are voltage gated) , this leads to calcium influx |
| what does an influx of calcium cause | exocytosis |
| exocytosis | migration of vesicles to the outer membrane and release of NT into the synapse *vesicles migrate to active zones |
| active zone | like docks on a lake; vesicles need to get to one in order to get off has proteins that support docking and release |
| SNARE protein complex | the proteins that support the docking and fusing with outer membrane at active sites |
| synaptobrevin | one of the proteins that help vesicles fuse during endocytosis |
| synaptotagmin | |
| tetanus | degrades synaprobrevin therefore prevents exocytosis of GABA at the spinal cord this prevents the vesicle full of GABA from fusing with membrane if the GABA (primary inhibitory NT) cannot bind, they cannot inhibit acetylcholine activity at spinal cord |
| which type of receptor is slower acting but longer lasting? | metabotropic |
| systemic | reach target tissue (brain) via general blood circulation (heart) both enteral and parenteral |
| enteral | gut/stomach |
| parenteral | a class of routes of administration that bypass the GI tract |
| oral route of administration | most common enteral method; the safest—because drug has to go through GI tract, it is slower acting, it must dissolve in stomach and then enter bloodstream there are internal mechanisms in the GI tract to remove toxins |
| GI tract process; digestion and absorption of enteral drugs | 1. stomach breaks down drug/food 2. absorption of drug from stomach to small intestine (which then leads to liver) 3. liver first pass metabolism (drastically reduces bioavailability) |
| factors that affect GI tract process and therefore bioavailability of a drug | exercise/activity levels, type of food (fatty food slow down) , size and fat storage of a person |
| rectal/suppository route of administration | enteral (goes through GI tract) benefit: can bypass liver *bioavailability with this method is irregular and unpredictable some of the drug will end up going through a vein to first pass metabolism (why it is so irregular) |
| superior rectal vein | (portal drainage) the vein direction you do NOT want the suppository to go; it leads to the liver and the drug ends up getting metabolized |
| inferior vena cava (rectal vein) | (systemic drainage) the vein you DO want the suppository to go to; the drug enters the bloodstream without going through liver |
| intravenous route of administration | still systemic because it is entering the general bloodstream high bioavailability because it bypasses 1st rate metabolism fastest drug action of all the routes of administration |
| inhalation | rapid absorption ^because the lungs are very vascular; lots of alveoli with capillaries on them *does not include intranasal bioavailability tends to be less because of the mucus and other fluid that lines lungs only about 10-15% of drug used |
| sublingual | putting the drug under the tongue the tongue has a mucous membrane which has a high concentration of capillaries ^causes rapid absorption into the bloodstream |
| intranasal | bypasses B.B.B. so the drug has access to the cerebrospinal fluid higher bioavailability than drugs that are inhaled |
| non systemic | routes of administration that do NOT go through the general bloodstream |
| central route of administration | |
| intracranial | helpful in animal research injected into brain |
| drug absorption in the blood depends on…? | 1. rate of administration 2. solubility of the drug |
| solubility of a drug | has to do with the general composition of the drug - is it lipid soluble? is it not? the (lipid) solubility dictates the rate of transport between the cell layers |
| high level of lipid solubility | the drug can passively diffuse through the blood and cell layers |
| low level of drug solubility | means the drug is likely ionized (when placed in water) (either fully or partially ionized) likely needs an external way of transportation because it cannot just go through cell layers |
| requirements of drugs to pass the blood brain barrier | must have high (lipid) solubility or transporters to get them through |
| cerebral flow | blood comes out of aortic arch —-> ____ —-> high vascular news of the brain veins and arteries cover the surface of the brain - they are in the subarachnoid space (the space between the pia matter and arachnoid membrane) and also penetrate the tissue |
| capillary walls | image on the slides; cover the brain |
| blood brain barrier | it is the structure of capillaries on the brain that limits the types of drugs that can be distributed into the nervous system |
| is the blood brain barrier an additional layer of/on top of the brain? | no, instead it just describes the structures around the capillaries (like tight junctions, astrocyte feet…) that surround the brain |
| what are the structures around brain capillaries that make up the blood brain barrier? | -tight junctions of endothelial cells “end feet” of astrocytes that enforce those tight junctions (these are not -present around capillaries in the rest of the body) - no fenestrations/vesicles that would typically support transport of large molecules |
| does the blood brain barrier allow for vesicles or fenestrations? what is the consequence of this? | no; these things would typically support transport of larger molecules into the blood supply (smaller allowed?) because of lack of these, reduces the diffusion of ionized drugs into the nervous system tissue ^because of this, high lipid solubility |
| depot binding | when drug molecules bind to depots in plasma, muscle or bone temporarily remains in blood circulation; sits there and isn’t used but also isn’t excreted |
| what is a depot | proteins in plasma, muscle, and bone that drugs can temporarily bind to ex: Albumin |
| what happens when a drug is attached to a depot | it cannot reach its target tissue but also isn’t metabolized by the liver it is in circulation but not active this causes delayed onset action of the drug |
| depot binding sites sensitivity | sensitivity of depot binding sites can vary from person to person (genetics) |
| is a depot binding site competitive or non competitive | competitive; if a drug is already taken and already on binding sites, that second drug may act quicker than expected because it will not sit on those binding sites before taking action |
| are depots selective? | no; they are non selective this means that multiple types of drugs can bind to these depots like a wild card this leads to a higher concentration of a drug if depot sites are occupied/bound to another drug |
| is binding to depot sites permanant? | no; it is reversible those drugs will be free when released to be used |
| some pillars of first order kinetics | exponential clearance of a drug half life |
| half life | time it takes for clearance of 50% of drug in bloodstream |
| if a drug has a longer half life how does that affect how long it is in the bloodstream? | it will be in the bloodstream longer |
| how do half lives vary | by drug; each drug has a different half life can also vary by individual (ex: ICA 2) |
| about how many half lives does it take for a drug to be largely cleared from the blood stream | about 6 |
| what is the goal of drug treatment | to maintain drug concentration in the blood at a constant and desired period of time to obtain the therapeutic effect of the drug |
| about how many half lives does it take to reach steady state plasma level? | about 5 |
| ED50 | 50% of the effective dose amount of drug required to experience 50% of the maximal effect |
| ED100 | 100% effective dose dose needed to experience full effect |
| TD50 | at this dose, 50% of people experience toxicity from the drug |
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