GABAergic Deficits Research Articles

Hippocampal benzodiazepine receptors in schizophrenia.

Benzodiazepine receptor sites were determined by saturable [3H]flunitrazepam binding in hippocampal tissue from schizophrenic and control subjects. No difference in receptor density or affinity between the two groups was observed, indicating that the previously identified GABAergic deficit in the hippocampus in schizophrenia does not apparently lead to up-regulation of these receptor sites. The implications of this finding are discussed.

The GABAergic striatonigral neurons of the cat: demonstration by double peroxidase labeling

GABAergic striatonigral neurons were demonstrated in the adult cat by the specific double peroxidase labeling of a transmitter marker with an agranular appearance (GAD, the synthetic enzyme of GABA) anda connectivity marker with a granular appearance (WGA-HRP). Each marker was associated with different organelles confined to the perikaryal cytoplasm of neurons. GABAergic striatonigral neurons were of medium size, high frequency and wide location in the rostral caudate nucleus and putamen based on correlative light and electron microscopic identification. These cells had somatic and/or proximal dendritic spines and folded nuclear envelopes in some cases. They received GABAergic axosomatic and axodendritic inputs with symmetric synaptic specializations. They were also contacted by axosomatic, axodendritic and axospinous terminals with asymmetric synaptic specializations. These results indicate that the GABAergic striatonigral neurons are, for the most part, medium spiny cells that also emit intrastriatal axonal collaterals. Their intra- and extrastriatal axons mediate inhibitory postsynaptic influences on their targets. Their degeneration might contribute to the GABAergic deficits found in the basal ganglia in Huntington's disease.

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