Glutamate, opiates, neuropeptides, anandimide, and neuromodulators Flashcards Preview

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Flashcards in Glutamate, opiates, neuropeptides, anandimide, and neuromodulators Deck (7)
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Glutamate and aspartate

-Glu is major excitatory NT, both are implicated in excitotoxicity and have high-affinity reuptake systems
-Reuptake can be to glial cells, and uses Na/K gradients to facilitate reuptake
-Glutamate receptors: both gated ion channels (fast, ionotropic) and GPCR (slow, second messengers)
-All are excitatory: AMPA, Kainate, NMDA
-Selective agonists of metabotropic glu receptors (GPCRs) may be useful in Rx anxiety and schizophrenia


AMPA and Kainate receptors

-AMPA: various forms of 16 different subunits, activation cause depolarization via outward flow of K and inward flow of Na (also permeable to Ca)
-AMPA found largely in striatum, hippocampus and cerebellum
-Influx of Ca can trigger apoptosis
-Kainate receptors: binds kainic acid better than glutamate, excessive excitation can lead to seizures and kill neurons
-Neuro-active steroids can protect against the seizures/toxicity


NMDA receptors

-NMDA receptors: voltage sensitive (regulated by Mg) ad requires glycine as co-agonist along w/ Glu binding
-PCP (phencyclidine) compete w/ Mg for NMDA channel binding but are not removed w/ depolarization
-PCP produces delusions, hallucinations, and cognitive defects (high doses of etoh can produce similar effects)
-MSG also binds to these receptors



-Opiates are exogenous (morphine and codeine) and endogenous (endorphins, enkephalins, dynorphins) that bind to opioid receptors to produce analgesic effects
-Most potent compound is morphine and its antagonist is naloxone
-Morphine and endogenous opiates bind to the same receptors
-All endogenous opiates are made from a pro-peptide (POMC, pro-opiomelanocortin, makes beta-endorphin) by proteases to make pro-opioids (neuron specific)


Opioid receptors

-3 classes: mu, kappa, and delta
-Most significant is mu, since it binds most to morphine-like derivatives (naloxone, endorphins)
-Mu is a GPCR that activates cAMP in presynaptic cells to decrease NT release
-Also increases K efflux in postsynaptic cell to hyperpolarize neurons, which decreases the firing of pain neurons in the SC
-They inhibit pain pathways including presynaptic release of substance P (pain-causing neuro-peptide) which is released onto efferent neurons of STT tract to convey pain to the brain
-Capsaicin produces rapid release of substance P
-Other neuropeptides: nociceptin and nocistatin (regulate pain perception)



-Derivative of arachidonic acid, actives cannabioid receptors (CB), same receptors THC activates
-CB1 found in CNS, CB2 has peripheral distribution (in leukocytes and testicles)
-CB1 acts via GPCR to reduce the presynaptic cell's ability to conduct Ca and thus lowers NT release from presynaptic cell
-Most complicated effects of long term THC use are cognitive



-In general are not release via synaptic vessels
-May not change the membrane potential of postsynaptic cell but changes the membrane's capacity to respond to further signals
-Ex: protaglandins act on NE neurons to reduce NE release
-NO is also a neuromodulator that influences the levels of cGMP (released from postsynaptic cell to act on presynaptic cell like anandamide)

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