Glutamate synaptic localization

Obata, K, Fukuda, T, Konishi, S, Ji, FY, Mitoma, H and Kosaka, T (1999) Synaptic localization of the 67,000 mol. wt isoform of glutamate decarboxylase and transmitter function of GABA in the mouse cerebellum lacking the 65,000 mol. wt isoform. Neuroscience 93 1475-1482. 

Luruta, A., Martin, L. J., Lin, C. L Dykes-Hoberg, M., and Rothstein, J. D. (1997) Cellular and synaptic localization of the neuronal glutamate transporters excitatory amino acid transporter 3 and 4. Neuroscience 81,1031-1042. 

Giustetto M, Bovolin P, Fasolo A, Bonino M, Cantino D, et al. 1997. Glutamate receptors in the olfactory bulb synaptic circuitry Heterogeneity and synaptic localization of N-methyl-D-aspartate receptor subunit 1 and AMPA receptor subunit 1. Neuroscience 76 787-798. 

SYNAPTIC LOCALIZATION OF GLUTAMATE AND RELATED AMINO ACIDS... 

When the creation of long-term memories— repeated stimulations interrupted by rest periods—was simulated in this preparation by repeated pulses of serotonin, anatomical changes occurred. Specifically, new synaptic connections were created. It is likely that there are two underlying components to formation of new synaptic connections. One is local protein synthesis in the nerve terminal and the other is CREB (cAMP response element binding) dependent transcription in the neuronal nucleus. Of course, serotoiun pulses also stimulated the release of glutamate. So now the question is how repeated pulses of serotonin are related to protein synthesis and formation of new synapses. 

Physiological studies have identified both post- and presynaptic roles for ionotropic kainate receptors. Kainate receptors contribute to excitatory post-synaptic currents in many regions of the CNS including hippocampus, cortex, spinal cord and retina. In some cases, postsynaptic kainate receptors are codistributed with AMPA and NMDA receptors, but there are also synapses where transmission is mediated exclusively by postsynaptic kainate receptors for example, in the retina at connections made by cones onto off bipolar cells. Extrasynaptically located postsynaptic kainate receptors are most likely activated by spill-over glutamate (Eder et al. 2003). Modulation of transmitter release by presynaptic kainate receptors can occur at both excitatory and inhibitory synapses. The depolarization of nerve terminals by current flow through ionotropic kainate receptors appears sufficient to account for most examples of presynaptic regulation however, a number of studies have provided evidence for metabotropic effects on transmitter release that can be initiated by activation of kainate receptors. The hyperexcitability evoked by locally applied kainate, which is quite effectively reduced by endocannabinoids, is probably mediated preferentially via an activation of postsynaptic kainate receptors (Marsicano et al. 2003). 

Schematic diagram of a primary afferent neuron mediating pain, its synapse with a secondary afferent in the spinal cord, and the targets for local pain control. The primary afferent neuron cell body is not shown. At least three nociceptors are recognized acid, injury, and heat receptors. The nerve ending also bears opioid receptors, which can inhibit action potential generation. The axon bears sodium channels and potassium channels (not shown), which are essential for action potential propagation. Synaptic transmission involves release of substance P, a neuropeptide (NP) and glutamate and activation of their receptors on the secondary neuron. Alpha2 adrenoceptors and opioid receptors modulate the transmission process.

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