Depression glutamate

Cheng, G. and Kendig, J. J. Enflurane directly depresses glutamate, AMPA and NMDA currents in mouse spinal cord motor neurons independent of actions on GABAa or glycine receptors, Anesthesiology 2000, 93, 1075-1084. 

Kamiya Y, Andoh T, Furuya R, et al Comparison of the effects of convulsant and depressant barbiturate stereoisomers on AMPA-type glutamate receptors. Anesthesiology 90 1704-1713, 1999... 

Figure 15.9 Peptide modulation of striatal input to the globus pollidus. Enkephalin released from axon terminals of neurons of the indirect pathway (see Fig. 15.2 for details) is thought to inhibit GABA release from the same terminals so that feedback (auto) inhibition is reduced. This will free the neurons to inhibit the subthalamic nucleus (SThN) and its drive to GPint and SNr which in turn will have less inhibitory effect on cortico-thalamic traffic and possibly reduce akinesia. Dynorphin released from terminals of neurons of the direct pathway may also reduce glutamate release and excitation in the internal globus pallidus and further depress its inhibition of the cortico-thalamic pathway. High concentrations of these peptides may, however, result in dyskinesias. (See Henry and Brotchie 1996 and Maneuf et al. 1995)...

Gao, X. B. van den Pol, A. N. (2001). Melanin concentrating hormone depresses synaptic activity of glutamate and GABA neurons from rat lateral hypothalamus./. Physiol. 533, 237-52. 

Ammonia has deleterious effects on brain function by direct and indirect mechanisms. Concentrations of ammonia in the 1-2 mmol/1 range, equivalent to those reported in the brain in liver failure, impair postsynaptic inhibition in cerebral cortex and brainstem by a direct effect on Cl extrusion from the postsynaptic neuron. Millimolar concentrations of ammonia also inhibit excitatory neurotransmission. Synaptic transmission from Schaffer collaterals to CA1 hippocampal neurons is reversibly depressed by 1 mmol/1 ammonia, and the firing of CA1 neurons by iontophoretic application of glutamate is inhibited by 2 mmol/1 ammonia [10],... 

After 48 h, marked increase in blood glucose, depressed plasma insulin level, marked depletion of liver glycogen, significant increase in plasma creatinine phosphokinase and glutamic oxaloacetic transaminase activity (Giri etal. 1979)... 

Kainate receptors mediate a depression of evoked excitatory synaptic transmission in areas CA1 (40,88-90) and CA3 (35,37,91,92) of the hippocampus. There is strong evidence that in area CA1 the locus of this effect is presynaptic. Thus, activation of kainate receptors depresses release of L-glutamate from synaptosomes (88) and depresses both NMDA and AMPA receptor-mediated components of the evoked EPSC in parallel (88,90). Furthermore, the effects of kainate receptor activation on excitatory synaptic transmission in CA1 are associated with changes in presynaptic Ca2+ (89), an increase in paired-pulse facilitation (35,88,89), and a reduction in quantal content, as assessed using 1/CV2, but no change in mEPSC amplitude (90). 

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