Showing papers on "GABAergic published in 1977"
TL;DR: Intracerebral injection of nanomolar quantities of kainic acid appears to cause degeneration of neurons with cell bodies near the injection site while sparing axons terminating in or passing through the region.
459 citations
TL;DR: While GABA synthesis is likely to occur in non-evenly distributed nerve cells, most GABA may be stored in surrounding cells, presumably glia cells, suggesting that GABA turnover might be rapid.
195 citations
TL;DR: The studies demonstrate that the sodium independent binding sites for GABA in striatum are localized on axons of extrinsic neurons, and the affinity of these receptors for GABA increases in response to GABAergic denervation.
57 citations
TL;DR: The present work will focus on the gamma-aminobutyric acid (GABA) system in the Hb, as manifested by the activity of its synthesizing enzyme glutamic acid decarboxylase (GAD), a marker of GABAergic neurons.
53 citations
TL;DR: It is suggested that in subcortical limbic regions and in the area of the DA cell body group innervating the limbic system, there exist muscarinic acetylcholine receptors which on activation can increase activity in inhibitory GABA interneurons, which in the midbrain can directly control activity in the ascending mesolimbic DA pathways.
50 citations
TL;DR: It is concluded that the differing responses of the GABAergic system in the mouse brain and cell lines may be attributed in part to the fact that the cells do not represent an integrated system and are of tumor origin.
Abstract: The GABAergic system was investigated in C-6 astrocytoma cells and C-1300 neuroblastoma cells in culture and compared to that in mouse brain. The activities of glutamate decarboxylase, GABA-transaminase, succinic semialdehyde dehydrogenase and glutamate dehydrogenase were measured. In the cultured cells, only glutamate dehydrogenase activity was equal or greater than that of mouse cerebral cortex. Glutamate decarboxylase in both cell lines was 2%, while GABA-transaminase and succinic semialdehyde dehydrogenase activities were less than 20% of those found in brain. In spite of the disparate enzyme activities, GABA, glutamate, and α-ketoglutarate concentrations were similar in the cell lines and cerebral cortex. The anticonvulsant drugs sodium valproate and aminooxyacetic acid increased cortical GABA concentrations but either had no effect or decreased GABA in the cells in a complete medium. The convulsant isoniazid decreased GABA in mouse brain but had no effect in either cell line. In the absence of pyridoxal in the medium, some drug effects could be induced in the cultured cells. It is concluded that the differing responses of the GABAergic system in the mouse brain and cell lines may be attributed in part to the fact that the cells do not represent an integrated system and are of tumor origin.
25 citations