Please use this identifier to cite or link to this item: https://scholarbank.nus.edu.sg/handle/10635/178481
Title: DISTRIBUTION OF GLUTAMATE RECEPTOR SUBUNITS, GABA, AND CAM KINASE II IN THE CEREBRAL CORTEX AND AMYGDALA
Authors: HE YONG
Issue Date: 1996
Citation: HE YONG (1996). DISTRIBUTION OF GLUTAMATE RECEPTOR SUBUNITS, GABA, AND CAM KINASE II IN THE CEREBRAL CORTEX AND AMYGDALA. ScholarBank@NUS Repository.
Abstract: The distributions of ionotropic glutamate receptor subunit, GluR1, and the inhibitory neurotransmitter GABA were studied by immunohistochemistry in the human cerebral neocortex. Large numbers of GluRl-positive pyramidal neurons and fairly large numbers of GluRl­ positive non-pyramidal neurons were present in the cortex. The non-pyramidal neurons were more densely labelled for GluRl, than pyramidal neurons. Most of the GABAergic neurons were double labelled for GluRl. The white matter was unstained, except for a few labelled neurons. The monkey entorhinal cortex was very different from that of that of the rat neo- or entorhinal cortex, in that GluRl labelling appeared denser in its layer V pyramidal neurons than those in the rat. In the monkey, neuropil staining in layer V was less intense for GluR2/3 than for GluRl. This suggests that there were fewer GluR2 or GluRJ subunits than GluRl subunits, and that many of the GluRl subunits could exist as homomers in that layer. Since GluRl homomeric channels are permeable to calcium ions and are inwardly rectifying, the high GluRl content of the pyramidal neurons of the primate entorhinal cortex could render these cells particularly susceptible to calcium influx, and consequently, calcium-mediated neuronal injury. This could be one of the reasons why the entorhinal cortex shows some of the earliest and most severe pathological alterations in Alzheimer's disease. The distributions of GluRl, NMDARl, CaM kinase II, and GABA were also studied by immunohistochemistry in the monkey amygdala. GluRl, NMDARl, and CaM kinase II labelled neurons had morphological features of pyramidal or projection neurons, and were mostly not double labelled for GABA. CaM kinase II-positive axon terminals formed asymmetrical synapses on CaM kinase II and GluRl or CaM kinase II and NMDARl double labelled segments of dendrites, but not on GABAergic dendrites. The results of the present the present study have highlighted differences in the chemical anatomy of the asymmetrical synapses on the dendrites of projection neurons and those of GABAergic neurons in the amygdala.
URI: https://scholarbank.nus.edu.sg/handle/10635/178481
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