GABAergic

About: GABAergic is a research topic. Over the lifetime, 9595 publications have been published within this topic receiving 473568 citations.

The intrinsic organization of the central extended amygdala.

Abstract: The central component of the extended amygdala (CEA) comprises the central amygdaloid nucleus (Ce), the dorsal substantia innominata (SI), and the bed nucleus of the stria terminalis (BNST). Anatomical studies have suggested the presence of an intrinsic system of GABAergic neurons that not only connects homologous subareas of the Ce, SI, and BNST but that also acts as an interface between sensory afferents and brain stem-projecting neurons. CEA outputs, with a few exceptions, arise from separate populations of neurons, but all, including GABAergic neurons themselves, are heavily innervated by GABAergic terminals. GABAergic neurons may serve to integrate output activity of the CEA, though GABAergic neurons form a heterogeneous population whose differential intrinsic connections appear related to their peptide content. Afferents from the dysgranular insular cortex and lateral parabrachial complex preferentially innervate GABAergic neurons, suggesting these neurons may also integrate afferent activity. Afferents from the basolateral amygdala (BL) appear to innervate both output neurons and intrinsic GABAergic neurons. Evidence will be presented to show that BL afferents form synaptic complexes with cortical, GABAergic, and TH-immunoreactive terminal boutons on GABAergic dendritic spines. These complexes may be a key element in control of CEA output activity.

Long-Range–Projecting GABAergic Neurons Modulate Inhibition in Hippocampus and Entorhinal Cortex

Abstract: The hippocampus and entorhinal cortex play a pivotal role in spatial learning and memory. The two forebrain regions are highly interconnected via excitatory pathways. Using optogenetic tools, we identified and characterized long-range γ-aminobutyric acid-releasing (GABAergic) neurons that provide a bidirectional hippocampal-entorhinal inhibitory connectivity and preferentially target GABAergic interneurons. Activation of long-range GABAergic axons enhances sub- and suprathreshold rhythmic theta activity of postsynaptic neurons in the target areas.

DNA-methyltransferase 1 mRNA is selectively overexpressed in telencephalic GABAergic interneurons of schizophrenia brains.

Abstract: A down-regulation of reelin and glutamic acid decarboxylase (GAD) 67 mRNAs was detected in γ-aminobutyric acid (GABA)ergic cortical interneurons of schizophrenia (SZ) postmortem brains (10), suggesting that the availability of GABA and reelin may be decreased in SZ cortex. In situ hybridization of the mRNA encoding for DNA-methyltransferase 1, which catalyzes the methylation of promoter CpG islands, shows that the expression of this mRNA is increased in cortical GABAergic interneurons but not in pyramidal neurons of SZ brains. Counts of reelin mRNA-positive neurons in Brodmann's area 10 of either nonpsychiatric subjects or SZ patients show that the expression of reelin mRNA is decreased in layer-I, -II, and -IV GABAergic interneurons of SZ patients. These findings are consistent with the hypothesis that the increase of DNA-methyltransferase 1 expression in telencephalic GABAergic interneurons of SZ patients causes a promoter hypermethylation of reelin and GAD67 and perhaps of other genes expressed in these interneurons. It is difficult to decide whether this dysfunction of GABAergic neurons detected in SZ is responsible for this disease or is a consequence of this disorder. Although at present we cannot differentiate between these two alternatives, it is important to consider that so far a molecular pathology of cortical GABAergic neurons appears to be the most consistent finding associated with SZ morbidity.

The neurotrophins BDNF, NT-3 and NT-4/5 promote survival and morphological and biochemical differentiation of striatal neurons in vitro.

Abstract: The neurotrophins, brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), neurotrophin 4/5 (NT-4/5) and nerve growth factor (NGF), were compared for their effects on the survival and differentiation of embryonic rat striatal neurons grown in low-density cultures. Treatment with BDNF for 8 days resulted in a 40% increase in overall neuronal survival, a 3- to 5-fold increase in the number of calbindin-immunoreactive neurons, and an 80% increase in GABA-positive neurons. Treatment with NT-3 or NT-4/5 produced a 2- to 3-fold increase in the number of calbindin-positive neurons and an increase in GABA-positive cell number similar to that induced by BDNF. BDNF treatment produced a striking morphological differentiation of striatal GABAergic neurons, which was characterized by a doubling of the number of neurite branch points, the total area of arborization and the perikaryal area compared to control cultures. All three of these factors increased high-affinity GABA uptake 2-fold. NGF had no effect on any of the parameters examined. Our results show that BDNF, NT-3 and NT-4/5 promote the survival and/or differentiation of calbindin-immunopositive and GABAergic striatal neurons.

Parvalbumin-containing gabaergic interneurons in the rat neostriatum

Abstract: Antibodies to the intracellular calcium binding protein parvalbumin were shown to label specifically a distinct group of neostriatal GABAergic neurons. These neurons corresponded to the intensely staining subclass of neostriatal GABAergic neurons that have previously been shown to be a class of aspiny interneurons in the neostriatum. The parvalbumin neurons were aspiny neurons with varicose dendrites distributed throughout the neostriatum in a pattern identical to the intensely stained GABA neurons, and both populations of neurons showed increased numbers in the lateral part of the neostriatum. Double labeling of single neurons with both the GABA and parvalbumin antisera showed that all parvalbumin neurons were positive for GABA, but some GABA labelled neurons were not immunoreactive for parvalbumin. These parvalbumin-negative GABAergic neurons were morphologically similar to the spiny projection neurons, which are GABAergic but usually are not so heavily stained. The relationship of the GABA-containing parvalbumin neurons to the striatal mosaic organization was determined by using immunocytochemistry for another calcium binding protein, calbindin D28K, to label the matrix compartment of the striatum. The distribution of parvalbumin-positive neurons relative to the calbindin-positive matrix and calbindin-poor patches was determined by using pairs of adjacent sections stained with the calbindin and parvalbumin antisera. This analysis showed that the somata of the parvalbumin neurons were present in both patch and matrix compartments, and their axons and dendrites crossed the boundaries between compartments. A quantitative analysis of the number of neurons in each compartment revealed that the neurons showed no preferential distribution in either compartment, but instead were present according to the area occupied by that compartment. Approximately 10% of parvalbumin neurons were in the patch compartment, and in these same sections, the patch compartment occupied approximately 10% of the area of those sections. Staining with parvalbumin antibodies can therefore be used to identify a single class of GABAergic aspiny interneurons that is present in both patch and matrix compartments, and whose processes cross the borders between these compartments.