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28 Cards in this Set
- Front
- Back
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how do NTs flow? synthesized where? what can they initiate?
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occurs in one direction from preS to postS membrane, EPSP/IPSP
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how are NTs classified?
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excitatory (depolarization) or inhibitory (hyperpolarization) based on effect on postS membrane
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what are specific and non specific pathways of NTs?
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specific: NTs made and released in specific areas (SHENDA). Non specific: widespread (GAGG)
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what are the responsibilities of glutamate and GABA?
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glutamate: 75% of excitatory in brain; GABA: 20% of CNS synpases (inhibitory NT)
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Glutamate (aspartate) location, channels opened, membrane potential and major fxs
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CNS, Ca+/Na+, depolarization, memory/learning/stim sk muscle
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GABA location, channels opened, membrane potential and major fxs
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CNS, Cl-/K+, hyperpolarization, reduce anx/inh sk muscle
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Glycine location, channels opened, membrane potential and major fxs
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spinal cord, Cl-/K+, hyperpolarization, inh sk muscle
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ionotropic receptors: NMDA receptor
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NMDA receptor (glycine co agonist, bind aspartate, Na+/Ca2+/K+ IN)
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ionotropic receptors: AMPA receptor/Kainate receptor (seaweed)
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increase in Na+. K+
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Are ionotropic/metabotropic receptors excitatory or inhibitory?
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both stimulate EPSPs
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describe interaction between NMDA and AMPA receptors
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sustained stimulation of AMPA receptors leads to depolarization, change in MP act. NMDA (Mg2+ block NMDA rec. from being permeable but depo allows Mg2+ to leave)
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why is it important for NMDA and AMPA receptors to interact?
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synaptic plasticity (alter strength of synapse in 2nd messenger pathways) AND long term potentiation (memory/learning)
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glutamate: stored? how is released initiated?
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stored in synaptic vesicles; release initiated via Ca2+ influx
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How does reuptake of glutamate happen?
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by neurons and astrocytes: astrocytes covert glutamate to glutamine (transported by neuron - neuron converts glutamine to glutamate)
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what happens when neuronal cell death occurs
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glutamate doesn't undergo reuptake: leads to excess glutamate and excitotoxicity
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glutamate receptors drugs: NMDA channels blockers
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Mg2+ (endogenous), ketamine (anesthetic), PCP (euphoria, memory loss), methadone, meantine (slow Alz)
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glutamate receptors drugs: GABAa and GABAb
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GABAa receptors (ionotropic,Cl- channel, fast response, IPSPs); GABAb (metabotropic, K efflux Ca influx, IPSP)
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GABA synthesis
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glutamate decarboxylase converts glutamate to GABA, glutamate decarboxylase only present in GABA-synthesizing neurons in CNS
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GABAa potentiation
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increase Cl- influx/inhibitory effects of GABA in CNS, benzo, barbiturates
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GABAa: benzos
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increase RATE of channel opening, bipolar/anx/panic, anticonvulsant, antiplasticity
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GABAa: barbiturates
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increase DURATION of channel opening. phenobarbital (anticonvulsant/sedative/hypnotic)
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Rx for anxiety
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anxiolytics: benzo, antiD, Beta adrenergic, buspirone (serotonin receptor agonist)
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Insomnia
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sleep promotion via GABA potentiation: benzo, non benzo (eszopiclone-lunesta - little tolarence)
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GHB
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gamma hydroxybutyrate: endogenous source - CNS, own rec, bind GABAb - sedation, addictive, wakefullness
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GHB as synthetic drug
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GHB can cross BBB, odorless, colorless liqui/powder/salty, fermentation
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GHB as recreational drug
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"liquid ecstasy" (reduce anx/euphoria), stupor/memory, prolonged sleep = increased GH release
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Glycine receptor
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ionotropic, Cl- channel, IPSP, spinal cord
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glycine inhibition
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block glycine rec (strychnine (from plant) - rat poison, loss neg control, convulsions/rigid AND inh glycine rel (tetanus toxin - spasticity)
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