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GABAergic
About: GABAergic is a research topic. Over the lifetime, 9595 publications have been published within this topic receiving 473568 citations.
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TL;DR: Findings demonstrate selective abnormalities of sub-populations of GABAergic interneurons in the hippocampus of isolation reared rats, which resemble the neuronal deficits seen in this region in schizophrenia.
Abstract: Post-mortem studies have provided evidence for abnormalities of the γ-aminobutyric acid (GABA)-ergic system in schizophrenia. The calcium-binding proteins (CBPs), parvalbumin (PV), calbindin (CB) and calretinin (CR) can be used as markers for specific subpopulations of GABAergic neurons in the brain.
140 citations
TL;DR: It is demonstrated that spinal TRpV1 plays a critical role as a synaptic regulator and the utility of central nervous system-specific TRPV1 antagonists for treating neuropathic pain is suggested.
139 citations
TL;DR: It is demonstrated that in the septum NMDA receptors tonically activate GABAergic neurons which in turn inhibit the cholinergic septohippocampal neurons.
Abstract: The modulation of the septohippocampal cholinergic pathway by glutamatergic or GABAergic inputs was studied by monitoring the outflow of ACh collected via a transversal microdialysis probe implanted into the hippocampus and other brain areas of freely moving rats In one set of experiments a transversal microdialysis membrane was inserted in the dorsal hippocampus, drugs were administered intracerebroventricularly through a cannula implanted in the lateral ventricle, and ACh outflow in the dialysate was measured by an HPLC method with an electrochemical detector The dialysis membrane was usually perfused with Ringer's solution containing 7 microM physostigmine sulfate Intracerebroventricular injections of the NMDA antagonists 3-((RS)-2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (CPP; 1-50 nmol), MK801 (05-20 nmol), and D(-)-2-amino-7-phosphonoheptanoic acid (100 nmol) brought about an increase in hippocampal ACh outflow while the non-NMDA antagonist 6,7-dinitroquinoxaline-2,3-dione (025-20 nmol) was without effect The increase in ACh outflow following CPP administration was dose dependent and reached a maximum of about 500% It was abolished by TTX (05 microM) delivered locally to the hippocampus via the dialysis membrane and prevented by intracerebroventricular injection of the GABA agonist muscimol (5 nmol) In a second set of experiments, one microdialysis membrane was inserted in the dorsal hippocampus to detect ACh outflow and another in the septum to administer drugs locally and at the same time detect septal GABA outflow The septal dialysis membrane was perfused with Ringer's solution without physostigmine, and GABA levels in the dialysate were measured by an HPLC method with a fluorescence detector CPP (100 microM) perfused through the septum resulted in a decrease in septal GABA outflow and a concomitant increase in hippocampal ACh outflow Muscimol (100 microM) administration into the septum abolished the effect of CPP on hippocampal ACh outflow but did not affect septal GABA outflow These results demonstrate that in the septum NMDA receptors tonically activate GABAergic neurons which in turn inhibit the cholinergic septohippocampal neurons
139 citations
TL;DR: Results show that cortical GABAergic cells can be differentiated on basis of their calcium binding protein and neuropeptide immunoreactivity.
Abstract: In the cat visual cortex, almost all parvalbumin-positive cells are GABAergic, and about 80% of the calbindin D-28K-positive neurons are also GABA-immunoreactive. About 37% of the GABAergic neurons contain parvalbumin and a smaller fraction (about 18%) contains calbindin. Furthermore, parvalbumin and calbindin are localized in two separate neuronal populations in the cat visual cortex, suggesting that two GABAergic populations can be distinguished, one containing parvalbumin and one containing calbindin. Double staining for parvalbumin and neuropeptides (CCK, SRIF and NPY), revealed no double-labeled cells, with the exception of a few SRIF- and parvalbumin-positive neurons. These results show that cortical GABAergic cells can be differentiated on basis of their calcium binding protein and neuropeptide immunoreactivity.
139 citations
TL;DR: Findings suggest that in hepatic encephalopathy due to fulminant hepatic failure (a) there is increased GABAergic tone, (b) an amelioration ofEncephalopathy can be induced by blockade of GABA or benzodiazepine receptors, (c) benzodiazine receptor antagonists may be of clinical value in the management of hepatic Encephalopathy, and (d) an endogenous substance with GABA potentiating properties may be present in liver disease.
139 citations