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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 demonstrated that CBD provides neuroprotection against 3NP‐induced striatal damage, which may be relevant for Huntington's disease, a disorder characterized by the preferential loss of striatal projection neurons.
Abstract: The neuroprotective potential of cannabinoids has been examined in rats with striatal lesions caused by 3-nitropropionic acic (3NP), an inhibitor of mitochondrial complex II. We used the CB1 agonist arachidonyl-2-chloroethylamide (ACEA), the CB2 agonist HU-308, and cannabidiol (CBD), an antioxidant phytocannabinoid with negligible affinity for cannabinoid receptors. The administration of 3NP reduced GABA contents and also mRNA levels for several markers of striatal GABAergic projection neurons, including proenkephalin (PENK), substance P (SP) and neuronal-specific enolase (NSE). We also found reductions in mRNA levels for superoxide dismutase-1 (SOD-1) and -2 (SOD-2), which indicated that 3NP reduced the endogenous antioxidant defences. The administration of CBD, but not ACEA or HU-308, completely reversed 3NP-induced reductions in GABA contents and mRNA levels for SP, NSE and SOD-2, and partially attenuated those found in SOD-1 and PENK. This indicates that CBD is neuroprotective but acted preferentially on striatal neurons that project to the substantia nigra. The effects of CBD were not reversed by the CB1 receptor antagonist SR141716. The same happened with the TRPV1 receptor antagonist capsazepine, in concordance with the observation that capsaicin, a TRPV1 receptor agonist, failed to reproduce the CBD effects. The effects of CBD were also independent of adenosine signalling as they were not attenuated by the adenosine A2A receptor antagonist MSX-3. In summary, this study demonstrates that CBD provides neuroprotection against 3NP-induced striatal damage, which may be relevant for Huntington's disease, a disorder characterized by the preferential loss of striatal projection neurons. This capability seems to be based exclusively on the antioxidant properties of CBD.

132 citations

Journal ArticleDOI
28 May 2009-Neuron
TL;DR: The DCN to IO synapse was described, finding that GABA release was almost exclusively asynchronous, with little conventional synchronous release, and Synaptic transmission was extremely frequency dependent, with low-frequency stimulation being largely ineffective.

132 citations

Journal ArticleDOI
TL;DR: Results suggest that RB cells of mammalian retinae express at least three different types of GABA receptors at synaptic sites in the IPL: GABAC receptors, GABAAreceptors containing the α1 subunit, andGABAA receptors containing theα3 subunit.
Abstract: Rod bipolar (RB) cells of mammalian retinae receive synapses from different gamma-aminobutyric acid (GABAergic) amacrine cells in the inner plexiform layer (IPL). We addressed the question whether RB cells of the rabbit and of the rat retina express different types of GABA receptors at these synapses. RB cells were immunolabeled in vertical sections of rat retinae with an antibody against protein kinase C (PKC). The sections were double-labeled for the alpha 1, alpha 2, alpha 3, or gamma 2 subunits of the GABAA receptor. Punctate immunofluorescence, which represents synaptic localization, was found for all four subunits. Many of the alpha 1-, alpha 3-, or gamma 2-immunoreactive puncta coincided with the axon terminals of the PKC-immunolabeled RB cells. Sections and wholemounts of rabbit retinae were also double labeled for PKC and the rho subunits of the GABAC receptor. Rabbit RB cells were decorated by many rho-immunoreactive puncta, which were shown by electron microscopy to represent synaptic localization. Previous work from our laboratory has shown that the alpha 1, alpha 2, alpha 3, and rho subunits are not found within the same synapse but are expressed at different synaptic sites. Taken together, these results suggest that RB cells of mammalian retinae express at least three different types of GABA receptors at synaptic sites in the IPL: GABAC receptors, GABAA receptors containing the alpha 1 subunit, and GABAA receptors containing the alpha 3 subunit.

132 citations

Journal ArticleDOI
TL;DR: γ‐Aminobutyric acid receptor binding was increased in postmortem brain samples of chronic alcoholic patients compared to control patients and ergic mechanisms might play a role in chronic alcoholism.
Abstract: gamma-Aminobutyric acid (GABA) receptor binding was increased in postmortem brain samples of chronic alcoholic patients compared to control patients. Numbers of binding sites were augmented in alcoholic brain, with no change in affinity. Muscarinic cholinergic and benzodiazepine receptors did not differ between controls and alcoholic brains, while a modest reduction in beta-adrenergic receptors may have been related to postmortem receptor changes. The results suggest that GABAergic mechanisms might play a role in chronic alcoholism.

132 citations

Journal ArticleDOI
TL;DR: This article investigated activation of GABA(B)-Rs on excitatory terminals within the cerebellar glomerulus, a structure where glutamatergic and GABAergic inhibitory terminals are in close apposition and make axodendritic synapses onto granule cells.
Abstract: GABA type B receptors (GABA(B)-Rs) are present on excitatory terminals throughout the CNS, but surprisingly little is known about their role in modulating neurotransmission under physiological conditions. We have investigated activation of GABA(B)-Rs on excitatory terminals within the cerebellar glomerulus, a structure where glutamatergic excitatory and GABAergic inhibitory terminals are in close apposition and make axodendritic synapses onto granule cells. Application of the GABA(B)-R agonist baclofen depressed evoked mossy fiber EPSCs by 54% at 1 Hz. The amplitude of miniature EPSCs recorded in tetrodotoxin was unchanged in the presence of baclofen, but the frequency was significantly reduced, indicating a purely presynaptic action of baclofen under our recording conditions. At physiological temperature (37 degrees C) presynaptic GABA(B)-Rs were not tonically activated by spontaneous GABA release from Golgi cells, which fire at approximately 8 Hz in slices at this temperature. However, tonic activation could be induced by blocking GABA uptake or by lowering temperature. GABA(B)-Rs were activated at physiological temperature when Golgi cell firing was increased above the basal level by stimulating a single inhibitory Golgi cell input at 50 Hz, suppressing the mossy fiber-evoked EPSC by 24% at 1 Hz. Furthermore, glutamate release was selectively inhibited at low-frequency mossy fiber inputs (<10 Hz) during Golgi cell stimulation. Our findings suggest that GABA spillover in the glomerulus modulates sensory input to the cerebellar cortex.

132 citations


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