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| Gq protein coupled muscarinic receptors |
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| Gi/o coupled muscarinic receptors |
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increase PLCB
increase Ca++
increase MAP kinases
decrease M current |
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decrease adenylate cyclase
increase MAP kinases
increase GIRK channels
decrease voltage-gated Ca channels |
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liver enzyme that metabolizes nicotine
-individual variation in this enzyme, people with reduced metabolism are less likely to become smokers (if it stays in you longer you get more unpleasant side effects) |
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| inhibits P450 2A6, so people experience unpleasant side effects of too much nicotine |
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amino acid (found in phenylalanine in diet) converted to Dopa by TH, then DA by AADC, then NE by DBH |
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| rate limiting step in DA synthesis (converts tyrosine into DOPA) |
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| converts DOPA into dopamine |
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DNAB (dorsal noradrenergic bundle) |
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originates in locus coeruleus, broad forebrain innervation |
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VNAB (ventral noradrenergic bundle) |
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| innervates bed nucleus of stria terminals |
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| nigrostriatal pathway, mesocorticolimbic pathway |
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blocks DA transmission, interferes with normal behavioral activity interferes with VMAT function, behavior is shut down (restored by L-DOPA) |
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neurotoxin that is taken up into catecholamine terminals by DAT and NERT and then kills them Rats with these lesions are severely akinetic |
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| low-grade, very cheap cocaine that can be smoked (often with tobacco) |
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| inactive metabolite of cocaine, detectable in urine for several days |
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| what the leaves of KHAT have in them (very potent stimulant) |
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| synthetic stimulant (very similar to other illicit stimulants) with roots in Ann arbor |
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| what the FDA is trying to substitute for ephedrine and pseudoephedrine in sudafed, not very effective |
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| dopamine receptors that are coupled with Gs |
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| Dopamine receptors that are coupled to inhibitory G protein (Gi/o) |
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| target of D1 action in the striatum (excititory) |
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| target of D2 action in striatum |
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| block the inhibition of the stop action in DA cells (major trainquilizers) |
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| drug enhanced DA release in dorsal/lateral (sensorimotor) parts of the brain cause... |
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| Drug-enhanced DA release in ventral/medial (cognitive emotional) parts |
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| increased locomotion, motivation |
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| endogenous opioid that acts at kappa receptors on DA terminals (reduces release when upregulated in response to prolonged elevations of DA levels) |
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Da actins as reinforcement learning signal "reward prediction error" |
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Definition
| It has been shown in studies that midbrain DA cells repond to unexpected reward-related stimuli. omitting a reward causes a pause in cell firing, while giving unexpected causes a burst. Therefore, DA responds when you are wrong about your expectation of a reward, which is good for behavioral learning because it teaches you to do the behavior again for the reward. |
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produce LTP (heterosynaptic plasticity) |
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| heterosynaptic plasticity |
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Definition
Occurs when two transmitters work together to produce an LTP. For example, DA acts on glutamate synapse to control the influenec of glutamate on the receptor cells. Can affect strength of synapse. (DA and Glu work cooperatively to alter gene expression, consolidate synaptic change) |
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| rate limiting step in serotonin synthesis |
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Definition
| converstion of tryptophan to 5-HTP by TH (tryptophan hydroxylase [TPH]) |
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| - Gi coupled, inhibits AC, hyperpolarizes the cell by opening K+ channels -SOMATODENRIDIC AUTORECEPTOR IN RAPHE: feedback inhibition, decreases the firing rate of 5-HT neurons -In forebrain: postsynaptic -high density in frontal cortex, amygdale, hippocampus, raphe NONE IN STRIATUM, CEREBELLM |
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| 2 forms of tryptophan hydroxylase |
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TPH 1 - periphery TPH 2 - brain-specific |
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PCPA (irreversibly inhibits TPH) |
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ATD (acute tryptophan depletion) cocktail of large, neural amino acids that compete with tryptophan for entry into the brain, blocks entry transient and reversible |
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| -Gi coupled, inhibits AC, opens K+ channels -TERMINAL AUTORECEPTOR (decreases release) -presynaptic heteroreceptors, inhibits release of different NTs *agonists used as anti-migrane drugs, controversial whether effects are due to vasoconstriction or to inhibition of pain info |
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atypical antipsychotic 5HT2a antagonist |
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| -Gq coupled, stimulates phosphilipase C (PLC) -postsynaptic receptors (highest expression on glutamatergic neurons, but t here are more GLU than GAB anyway) |
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| -ionotropic, Na+ Ca++ channels – depolarizations -high density in area postrema (antagonists used to treat nausea) -expressed by both GLU and GAB neurons, CNS and periphery, frontal corex, cingulated, motor areas |
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| Why do SSRIS take weeks to work? |
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Definition
| delayed down-regulation of 5-HT1 receptors |
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5-HT1A antagonist (enhances and speeds up SSRI action) |
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tingling in extremities cuased by constriction of blood vessesls (can cuase gangrene) delirium, hallucinations caused by Ergot fungus |
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