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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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Journal ArticleDOI
TL;DR: It is suggested that KCC2 is responsible for maintaining the low intracellular Cl- concentration in nigral GABAergic neurons, whereas a sodium-dependent anion (Cl--HCO3-) exchanger and ClC-2 are likely to serve this role in dopaminergic neurons.
Abstract: The regulation of intracellular chloride has important roles in neuronal function, especially by setting the magnitude and direction of the Cl - flux gated by GABA A receptors. Previous studies have shown that GABA A -mediated inhibition is less effective in dopaminergic than in GABAergic neurons in substantia nigra. We studied whether this phenomenon may be related to a difference in Cl-regulatory mechanisms. Light-microscopic immunocytochemistry revealed that the potassium-chloride cotransporter 2 (KCC2) was localized only in the dendrites of nondopaminergic (primarily GABAergic) neurons in the substantia nigra, whereas the voltage-sensitive chloride channel 2 (ClC-2) was observed only in the dopaminergic neurons of the pars compacta. Electron-microscopic immunogold labeling confirmed that KCC2 is localized in the dendritic plasma membrane of GABAergic neurons close to inhibitory synapses. Confocal microscopy showed that ClC-2 was selectively expressed in the somatic and dendritic cell membranes of the dopaminergic neurons. Gramicidin-perforated-patch recordings revealed that the GABA A IPSP reversal potential was significantly less negative and had a much smaller hyperpolarizing driving force in dopaminergic than in GABAergic neurons. The GABA A reversal potential was significantly less negative in bicarbonate-free buffer in dopaminergic but not in GABAergic neurons. The present study suggests that KCC2 is responsible for maintaining the low intracellular Cl - concentration in nigral GABAergic neurons, whereas a sodium-dependent anion (Cl - -HCO 3 - ) exchanger and ClC-2 are likely to serve this role in dopaminergic neurons. The relatively low efficacy of GABA A -mediated inhibition in nigral dopaminergic neurons compared with nigral GABAergic neurons may be related to their lack of KCC2.

134 citations

Journal ArticleDOI
TL;DR: Findings indicate that the acquisition of fear induced a downregulation of mRNA markers related to a decrease in amygdala GABAergic function, whereas the acquisition and extinction of Pavlovian fear produced an upregulation of neurons related to enhanced GABAergic transmission.
Abstract: Previous work suggests the γ-aminobutyric acid (GABA)ergic system may be dynamically regulated during emotional learning. In the current study we examined training-induced changes in the expression of GABAA-related genes and the binding of GABA receptor radioligands in the amygdala after the acquisition and extinction of Pavlovian fear. Using in situ hybridization, we examined the expression pattern changes of mRNAs for GABAergic markers in the lateral, basolateral and central subdivisions of the amygdala in C57Bl/6J mice. These markers included GABA-synthesizing enzymes (GAD67 and GAD65), major GABAA receptor subunits (α1, α2, α3, α5, β2 and γ2) and the expression of mRNAs that are involved in a variety of GABA-related intracellular processes, including GABA transporter-1 (GAT1), GABAA receptor-associated protein and the GABAA clustering protein, gephyrin. With fear conditioning, we found decreased mRNA levels of α1, α5 and GAD67, as well as deceased benzodiazepine binding in the amygdala. Fear extinction induced an increase in mRNA levels of α2, β2, GAD67 and gephyrin, as well as a decrease in GAT1. Together, these findings indicate that the acquisition of fear induced a downregulation of mRNA markers related to a decrease in amygdala GABAergic function, whereas the acquisition of fear extinction produced an upregulation of GABAergic markers related to enhanced GABAergic transmission.

134 citations

Journal ArticleDOI
TL;DR: Combined light and electron microscopic investigations show that the thalamic reticular nucleus of the rat contains a homogeneous population of GABA-immunoreactive neurons receiving extensive GABAergic connections suggestive of self-inhibitory inputs.

134 citations

Journal ArticleDOI
TL;DR: This study shows for the first time how GABAergic mechanisms develop in the human visual cortex across the lifespan, and provides key information for translating therapies developed in animal models into effective treatments for amblyopia in humans.
Abstract: Functional maturation of visual cortex is linked with dynamic changes in synaptic expression of GABAergic mechanisms. These include setting the excitation-inhibition balance required for experience-dependent plasticity, as well as, intracortical inhibition underlying development and aging of receptive field properties. Animal studies have shown developmental regulation of GABAergic mechanisms in visual cortex. In this study, we show for the first time how these mechanisms develop in the human visual cortex across the lifespan. We used Western blot analysis of postmortem tissue from human primary visual cortex (n=30, range: 20 days to 80 years) to quantify expression of 8 pre- and post-synaptic GABAergic markers. We quantified the inhibitory modulating cannabinoid receptor (CB1), GABA vesicular transporter (VGAT), GABA synthesizing enzymes (GAD65/GAD67), GABAA receptor anchoring protein (Gephyrin), and GABAA receptor subunits (GABAA∝1, GABAA∝2, GABAA∝3). We found a complex pattern of changes, many of which were prolonged and continued well into into the teen, young adult, and even older adult years. These included a monotonic increase or decrease (GABAA∝1, GABAA∝2), a biphasic increase then decrease (GAD65, Gephyrin), or multiple increases and decreases (VGAT, CB1) across the lifespan. Comparing the balances between the pre- and post-synaptic markers we found 3 main transitions (early childhood, early teen years, aging) when there were rapid switches in the composition of the GABAergic signaling system, indicating that functioning of the GABAergic system must change as the visual cortex develops and ages. Furthermore, these results provide key information for translating therapies developed in animal models into effective treatments for amblyopia in humans.

134 citations

Journal ArticleDOI
TL;DR: Findings provide evidence for a selective role for GABA-sensitive neurons in the medial accumbens shell in the regulation of ingestive behavior and suggest that GABA A receptors in this region do not modulate palatability, macronutrient selection, or rewarding properties of food.
Abstract: This study investigated the areas of the nucleus accumbens shell involved in the modulation of feeding behavior by GABAergic stimulation and characterized this response using macronutrient diets as well as saline, sucrose, and saccharin solutions. The GABA agonist muscimol induced a pronounced feeding response when infused in the medial nucleus accumbens shell but not in the ventral or lateral accumbens shell. In the macronutrient preference study, muscimol increased the intake of both high fat and high carbohydrate diets when presented separately. When both diets were available simultaneously, muscimol stimulated feeding of both diets to the same degree. Muscimol elicited a robust increase in the consumption of sucrose solution. However, no effect of muscimol was demonstrated for water, saline, or saccharin intake. These findings provide evidence for a selective role for GABA-sensitive neurons in the medial accumbens shell in the regulation of ingestive behavior and further suggest that GABA A receptors in this region do not modulate palatability, macronutrient selection, or rewarding properties of food.

134 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
2023371
2022749
2021341
2020320
2019301
2018297