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26 Cards in this Set

  • Front
  • Back
Voltage gated channels
open with voltage changes
Ligand-gated (ionotropic nt receptors)
needs a ligand or NT to bind to it's receptor in order to open and increase premeability.
G-protein coupled receptors (GPCR)(metabotropic nt receptors)
receptor that couples with G protein to modulate cellular physiology by either acting on io channels and/or second messengers.
Amino Acid NTs: Glutamate
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. //
Glutamate: ionotropic R mediated
AMPA-R: pereable to Na and K.//

Kainate-R: Na and K.//

NMDA-R: Na, Ca in and K out.
Glutamate's NMDA-R activation
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.
Glutamate: Metabotropic receptors (GPCR): mGluR
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.//
Amino Acid NTs: GABA
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.//
GABA receptors: Ionotropic
GABAa-R: post-synap. only, permeable to Cl-, hyperpolarizing the cell.//

GABAb-R: both pre-and post-syanp.
Presynap. GABAb-R
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.
POSTsynap. GABAb-R
done via increasing K conduction >> hypopolarization
Ionotropic: nAChRn.//

Metabotropic-R: M1, M3: excitatory, incrase IP3/Ca.// M2, M4: inhibitory, decrase cAMP.//
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).
DA Receptors: all metabotropic via G proteins.
EXCITATORY: D1, D5. activate AC.//

INHIBITORY: D2-D4: inhibit AC and Ca currents; activate K currents
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.//
alpha 1: stim. PLC
alpha 2: inhibit AC, increase K, decrase Ca. Presynaptic autoreceptor.//
Beta: stimulate AC.//
Serotonin: (5HT, 5 Hydroxytryptamine)
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.//
Serotonin Receptors

5HT3-R: mediate EPSPs, activation, causing emesis and anti-nociception (pain blocking).//

Metabotropic Rs (GPCR): all remaining (14) receptors. Some excitatory, others inhibitory.//
Neuropeptides: enkephalin, endorphin, somatostatin, substance P etc.
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).
ENDOCANNABIOIDS: anandamide, 2-arachidonylglycerol.
e.g. Marijuana.//

endogenous brain lipids, on the spot synthesis after depolarization and Ca influx.//

Can act as RETROGRADE transmitter.//


Metabotropic: CB1, CB2: inhibits AC and Ca conductance.//

Implicated in memory, congnition and pain.//
Purines: ATP, Adenosine
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.//
Nitric Oxide (NO)

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.//
Blood Brain Barrier (BBB)
less prominent in Hypothalamus, and less effective in median eminence, area postrema, pineal gland. //

compromised following trauma, infection, ischemia etc. //
Effects of chrnoic drug admin. on CNS.
may elicit tolerance, dependance, and /or homeostatic plasticity.
Drug Tolerance
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.//
Drug Dependance
withdrawal effects following abrupt cessation. Due to receptor or downstream effector UPREGULATION or changes in neuronal circuitry (homestatic plasticity).