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Neuroscience Ch6
| Question | Answer |
|---|---|
| three criteria for molecule to be considered neurtrans | 1) must be synthesized and stored in presynaptic neuron 2) must be released from presyn terminal on stimulation (not as secondary effect) 3) must be injectable to mimic effects |
| immunocytochemistry | inject neurotransmitter candidate into bloodstream, wait for antibodies to bind to it, extract them, tag them, wait to see where they go [(why not just tag candidate?)] |
| in situ hybridization | mRNAs are unique for the proteins they encode. we can build unique compliments to them called "probes," which stick to them in "hybridization." wash off the remainder, and the tagged probes can be used (via autoradiography) to localize specific mRNAs |
| microionophoresis | inject neurotransmitter candidate, charged, next to neuron (w/tiiiiiny pipette). does it fire? |
| ligand | a ligand for a receptor is a chem compound that binds to a specific site on that receptor (the neurotrasmitter itself, an agonist, an antagonist, etc) |
| acetylcholine | only NT not an amino acid or a peptide derived from amino acids. ACh synthesis requires ChAT, only contained by cholinergic neurons (so good marker). ChAt needs choline, so the transport of choline into the neuron is called the "rate-limiting step" |
| catecholaminergic | NTs: dopamine (DA), norephinepherine (NE), and epinephrine/adrenaline. all these neurons contain the enzyme "tyrosine hydroxylase" (TH). no chemical breakdown cleanup--all reuptake |
| norephinephrine | comes about by the enzyme "dopamine B-hydroxylase" (DBH) converting dopamine into it. no DBH in cystol, only synaptic vesicles, so DA from cystol needs to be sent there. |
| epinephrine | adrenaline. phentolamine N-methyltransferase (PNMT) converts NE to this. oddly, PNMT is in the cystol, so NE must be taken out of its vesicles, turned into adrenaline, then put back in. |
| MAO | monoamine oxidase. enzymatic destroyer of extra catecholamines after reuptake (if not reused) |
| serotonergic | neurons (few in number but important for mood) releasing serotonin (5-HT), synthesized in two steps. tryptophan is converted into 5HTP by TH. 5HTP is then converted into 5-HT by the enzyme 5-HTP decarboxylase. |
| dopamine | "tyrosine hydroxylase" (TH) forms dopa, which combines w/"dopa decarboxylase" to make dopamine. |
| glutamatergic | since glutamate is just another amino acid, its going to be abundant in lots of neurons; but it'll be two to three times more abundant in glutamatergic ones. qualitatively unique, however, is that there is a different transporter loading synaptic vesicles |
| GABAergic | these neurons must synthesize GABA from glutamate w/enzyme "glutamic acid decarboxylase" (GAD). GAD is a good marker of GABAergic. after uptake, GABA metabolized by GABA transaminase |
| AMPA | a glutamate-gated channel which bears the name of its agonist. permeable to Na+ and K+, and mostly not permeable to Ca2+. net effect is Na+ and depolarization on postsynapse |
| NMDA | a glutamate-gated channel which also bears the name of its agonist. lets in Na+ causing excitation, but are permeable to Ca2+, and because Mg2+ ions block these at neg resting potential, are voltage gated |
| Ca2+ | trigger NT release at presynapse (mech unknown). postsynaptically: can affect enzymes, regulate opening of channels, affect gene expression, overdose leads to cell death. connected to long term memory? |
| benzodiazepine and barbiturate | sedatives that work by opening the gates (either more frequently or for longer) of inhibitory channels like GABA or glycine. |
| g protein process | 1) g protein broken into alpha beta gamma 2) resting, it binds GDP 3) when actvated by coupled recept, swaps GDP for GTP 4) splits into alpha and beta-gamma, which both activ e-proteins 4) removes phosphate from GTP, convrting it to GDP to restart process |
| g protein shortcut pathway | when g-proteins exert their effects by binding to ion channels. this is quicker than other g-protein effect (30-100 msec). localized: apparently g-protein can't diffuse very far |
| g protein secondary messenger cascades | the slower, convoluted chain of enzymatic reactions that follow a gprotein. though slower, can be amplified at any of its steps. |
| protein kinases | PKA, PKC, or CaMK. in a process called "phosphorylation", this protein takes phosphate from loose ATP and gives it to other proteins (such as channels). this changes these proteins conformation slightly, which can have diff net fx depending on the neuron |
| protein phosphatases | act rapidly to remove phosphate groups, so that kinases doesn't phosphorylate proteins unchecked. |
| cAMP secondary messenger cascade | NE Beta receptor stimulates G protein, "Gs", which stim membrane bound "adenylyl cyclase", which converts ATP into cAMP. cAMP simulates protein kinases A (PKA), which phosphorylates channels |
Created by:
jwdink
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