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Glutamate In Action
Glutamate is an
that is major mediator of excitatory signals in the central nervous system.
Most common sites of action, and action exerted at those sites (excitatory/inhibitory/modulatory?)
Mostly acts on the receptors of neurons like the
NMDA glutamate receptor
and is always excitatory and leads to the activation of the cell and/or neuron. The release of glutamate typically happens throughout the brain but is more effective on the glutamageric synapses in the
hippocampus and neocortex
due to its long-term potentiation.
Receptors (type, differences in signaling depending on receptor?)
Acts on the
AMPA receptors, NMDA receptors, kainate receptors, and metabotropic receptors.
When acting on NMDA it excites this receptor and helps with creating memory. When acting on the kainate, post synapse, it regulates excitatory neurotransmission and when acting pre synapse, glutamate regulates inhibitory neurotransmission. When acting on metabotropic receptors they are excitatory and have to do with the creation of memory, perception of pain, learning, and anxiety.
Mechanism to stop signaling
Reuptake via the glutamate transporter - located in the presynaptic neuron and the glial cells
Behavioral outcomes of release
Generally activation of a system. The release of glutamate in to the synapse triggers Long Term Potentiation, learning, and the creation of memory. Disruption of glutamate can cause depression.
Drugs that act on this system (where? what do they do? what is the behavioral outcome?)
PCP and Ketamine act on this system by being non-competitive antagonists at the NMDA glutamate receptors, which blocks binding of glutamate. Ketamine reduces depression in patients. In PCP can invoke schizophrenia-like symptoms as in strong auditory hallucinations, depersonalization, and delusions.
-Tyler Moore, Bryana Roberts, Kwasi Ayisi
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