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26 Cards in this Set
- Front
- Back
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Voltage gated channels
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open with voltage changes
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Ligand-gated (ionotropic nt receptors)
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needs a ligand or NT to bind to it's receptor in order to open and increase premeability.
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G-protein coupled receptors (GPCR)(metabotropic nt receptors)
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receptor that couples with G protein to modulate cellular physiology by either acting on io channels and/or second messengers.
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Amino Acid NTs: Glutamate
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EXCITATORY.//
Synth. from Gln by glutaminase.// Cleared via Glu transporter back into nerve or into a glial cell, where it is converted to Gln with Glu sythetase. // |
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Glutamate: ionotropic R mediated
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AMPA-R: pereable to Na and K.//
Kainate-R: Na and K.// NMDA-R: Na, Ca in and K out. |
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Glutamate's NMDA-R activation
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requires Glu and Gly to be bound. Once the AP arrives, the depolarization causes Mg release, to unblock and open the channel, resulting in Na and Ca rushing in, and K moving out.
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Glutamate: Metabotropic receptors (GPCR): mGluR
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Type I: mGluR1 and mGluR5: increase IP3 via PLC.//
Type II: mGluR2 and mGluR3: decrease cAMP via AC.// Type III: mGluR4, 6-8: decrease cAMP via AC.// |
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Amino Acid NTs: GABA
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INHIBITORY.
Synth. from Glu by glutamic acid decarboxylase (GAD).// Cleared by GABA transporters (GAT-1).// Catobolized by GABA transaminase (GABA-T) in mintochondria of both presnyap. neuron and glial cells.// |
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GABA receptors: Ionotropic
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GABAa-R: post-synap. only, permeable to Cl-, hyperpolarizing the cell.//
GABAb-R: both pre-and post-syanp. |
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Presynap. GABAb-R
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In the presynapse, blocks Ca influx into the nerve ending >> causing decrease NT release
Also, it increase K conductance out of the cell, making it hyperpolar and decrease ca influx and NT release that way. |
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POSTsynap. GABAb-R
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done via increasing K conduction >> hypopolarization
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ACh R
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Ionotropic: nAChRn.//
Metabotropic-R: M1, M3: excitatory, incrase IP3/Ca.// M2, M4: inhibitory, decrase cAMP.// |
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Dopamine
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Sythesized from Tyrosine > Dopa> DA. Especially in Substantia Nigra.//
Loaded into vesicle by Vesic. Monoamine Transp (VMAT).// Catabolized by MAO and inactivated by COMT.// Cleared from synapse by DAT.// DA system implicated in Parkinson's Dz, schizophrenia, depression and anxiety.// All DA receptors metabotropic (GPCR). |
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DA Receptors: all metabotropic via G proteins.
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EXCITATORY: D1, D5. activate AC.//
INHIBITORY: D2-D4: inhibit AC and Ca currents; activate K currents |
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NE
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Synth. from DA
Catabolized by MAO and inact. COMT.// Cleared via transporters.// Implicated in Sleep-wake cycle. Prevelant in HT, amygdala, and dentate gyrus (esp in Locus Coeruleus).// All NE-R are metabotropic.// |
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NE-R
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alpha 1: stim. PLC
alpha 2: inhibit AC, increase K, decrase Ca. Presynaptic autoreceptor.// Beta: stimulate AC.// |
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Serotonin: (5HT, 5 Hydroxytryptamine)
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Synthesis: Tryptophan > 5hydroxytrptophan with trp hydroxylase > Serotonin with L-amino acid decarboxylase.//
Catobolized by MAO.// Cleared by SERT from synapse.// Most originate from Raphe' Nuclei (midline regions of Pons and upper brainstem).// Prevelant input in Ctx, limbic and diencephalon.// Implicated in depression, anxioty, stress, schizophrenia, substance abuse, migrane and sleep.// |
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Serotonin Receptors
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Ionotropic-Rs:
5HT3-R: mediate EPSPs, activation, causing emesis and anti-nociception (pain blocking).// Metabotropic Rs (GPCR): all remaining (14) receptors. Some excitatory, others inhibitory.// |
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Neuropeptides: enkephalin, endorphin, somatostatin, substance P etc.
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Synthesized in RER, can be released from any stie in the neuron, slow modulators, co-localized with other NTs. //
Need high rate of stim. for its release.// All receptors are metabotropic (GPCR). |
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ENDOCANNABIOIDS: anandamide, 2-arachidonylglycerol.
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e.g. Marijuana.//
endogenous brain lipids, on the spot synthesis after depolarization and Ca influx.// Can act as RETROGRADE transmitter.// Receptors: Metabotropic: CB1, CB2: inhibits AC and Ca conductance.// Implicated in memory, congnition and pain.// |
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Purines: ATP, Adenosine
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release from both glia and neurons.//
Adenosine R: P1 (subtype A1-3) are metabotropic. ATP R: P2 subtype P2X (ionotropic) and P2Y (metabotropic). // co-released with catecholamines from adrenergic vesicles.// |
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Nitric Oxide (NO)
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RETROGRADE TRANSMITTER.//
Synth: Arginine with NO Synthase (NOS) to NO plus citrulline. // NOS activated by Ca-Calmodulin and /or Ca influx through NMDA-R activation.// NO activates guanylyl cyclase.// |
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Blood Brain Barrier (BBB)
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less prominent in Hypothalamus, and less effective in median eminence, area postrema, pineal gland. //
compromised following trauma, infection, ischemia etc. // |
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Effects of chrnoic drug admin. on CNS.
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may elicit tolerance, dependance, and /or homeostatic plasticity.
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Drug Tolerance
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diminishing effect with repeated exposure.//
pharmacodynamic tolerance (cellular): due to desensitization of receptors due to its phosphorylation and internalization, and down regulation of receptor synthesis.// Pharmcokinetic tolerance (metabolic): induce own degradation/ metabolism.// |
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Drug Dependance
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withdrawal effects following abrupt cessation. Due to receptor or downstream effector UPREGULATION or changes in neuronal circuitry (homestatic plasticity).
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