Topic
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: It is confirmed that valerian extracts have effects on GABAA receptors, but can also interact at other presynaptic components of GABAergic neurons, as well as at at least two different biological activities interacting with [3H]flunitrazepam binding sites.
Abstract: Extracts of Valeriana officinalis have been used in folkloric medicine for its sedative, hypnotic, tranquilizer and anticonvulsant effects, and may interact with gamma-aminobutyric acid (GABA) and/or benzodiazepine sites. At low concentrations, valerian extracts enhance [3H]flunitrazepam binding (EC50 4.13 x 10(-10) mg/ml). However, this increased [3H]flunitrazepam binding is replaced by an inhibition at higher concentrations (IC50 of 4.82 x 10(-1) mg/ml). These results are consistent with the presence of at least two different biological activities interacting with [3H]flunitrazepam binding sites. Valerian extracts also potentiate K+ or veratridine-stimulated release of radioactivity from hippocampal slices preloaded with [3H]GABA. Finally, inhibition of synaptosomal [3H]GABA uptake by valerian extracts also displays a biphasic interaction with guvacine. The results confirm that valerian extracts have effects on GABA(A) receptors, but can also interact at other presynaptic components of GABAergic neurons.
125 citations
TL;DR: A more complete understanding of the intrinsic excitatory/inhibitory circuit balance of the amygdala and how imbalances in inhibitory control contribute to excessive BLA excitability will guide the development of novel therapeutic approaches in neuropsychiatric diseases.
Abstract: The brain comprises an excitatory/inhibitory neuronal network that maintains a finely tuned balance of activity critical for normal functioning. Excitatory activity in the basolateral amygdala (BLA), a brain region that plays a central role in emotion and motivational processing, is tightly regulated by a relatively small population of γ-aminobutyric acid (GABA) inhibitory neurons. Disruption in GABAergic inhibition in the BLA can occur when there is a loss of local GABAergic interneurons, an alteration in GABAA receptor activation, or a dysregulation of mechanisms that modulate BLA GABAergic inhibition. Disruptions in GABAergic control of the BLA emerge during development, in aging populations, or after trauma, ultimately resulting in hyperexcitability. BLA hyperexcitability manifests behaviorally as an increase in anxiety, emotional dysregulation, or development of seizure activity. This Review discusses the anatomy, development, and physiology of the GABAergic system in the BLA and circuits that modulate GABAergic inhibition, including the dopaminergic, serotonergic, noradrenergic, and cholinergic systems. We highlight how alterations in various neurotransmitter receptors, including the acid-sensing ion channel 1a, cannabinoid receptor 1, and glutamate receptor subtypes, expressed on BLA interneurons, modulate GABAergic transmission and how defects of these systems affect inhibitory tonus within the BLA. Finally, we discuss alterations in the BLA GABAergic system in neurodevelopmental (autism/fragile X syndrome) and neurodegenerative (Alzheimer's disease) diseases and after the development of epilepsy, anxiety, and traumatic brain injury. A more complete understanding of the intrinsic excitatory/inhibitory circuit balance of the amygdala and how imbalances in inhibitory control contribute to excessive BLA excitability will guide the development of novel therapeutic approaches in neuropsychiatric diseases.
125 citations
TL;DR: Results indicate that GABA is a transmitter of a large portion of the SCN neuronal population and GAD protein and GABA were identified by immunocytochemistry using specific antisera.
124 citations
TL;DR: The current literature does not reveal consistent alterations in in vivo GABA neuroimaging measures in schizophrenia, as might be hypothesized from animal models and postmortem data, and highlights the need for further GABA neuroIMaging studies with improved methodology and addressing potential sources of heterogeneity.
Abstract: Data from animal models and from postmortem studies suggest that schizophrenia is associated with brain GABAergic dysfunction. The extent to which this is reflected in data from in vivo studies of GABA function in schizophrenia is unclear. The Medline database was searched to identify articles published until 21 October 2016. The search terms included GABA, proton magnetic resonance spectroscopy (1H-MRS), positron emission tomography (PET), single photon emission computed tomography (SPECT), schizophrenia and psychosis. Sixteen GABA 1H-MRS studies (538 controls, 526 patients) and seven PET/SPECT studies of GABAA/benzodiazepine receptor (GABAA/BZR) availability (118 controls, 113 patients) were identified. Meta-analyses of 1H-MRS GABA in the medial prefrontal cortex (mPFC), parietal/occipital cortex (POC) and striatum did not show significant group differences (mFC: g=-0.3, 409 patients, 495 controls, 95% confidence interval (CI): -0.6 to 0.1; POC: g=-0.3, 139 patients, 111 controls, 95% CI: -0.9 to 0.3; striatum: g=-0.004, 123 patients, 95 controls, 95% CI: -0.7 to 0.7). Heterogeneity across studies was high (I2>50%), and this was not explained by subsequent moderator or meta-regression analyses. There were insufficient PET/SPECT receptor availability studies for meta-analyses, but a systematic review did not suggest replicable group differences in regional GABAA/BZR availability. The current literature does not reveal consistent alterations in in vivo GABA neuroimaging measures in schizophrenia, as might be hypothesized from animal models and postmortem data. The analysis highlights the need for further GABA neuroimaging studies with improved methodology and addressing potential sources of heterogeneity.
124 citations
TL;DR: It is reported that numerous small neurons in the peri-LC region become retrogradely labeled after focal injections of wheat germ agglutinin-apo (inactivated) horseradish peroxidase conjugated to colloidal gold, or pseudorabies virus (PRV), into the nuclear core of the rat LC.
Abstract: Most nuclei in the CNS are composed of principal neurons that project to other areas and interneurons that serve to integrate information among afferents. The noradrenergic brain nucleus locus ceruleus (LC) has appeared to be an exception to this general rule, because the LC is composed almost entirely of noradrenergic principal neurons. Here, we report that numerous small neurons in the peri-LC region become retrogradely labeled after focal injections of wheat germ agglutinin-apo (inactivated) horseradish peroxidase conjugated to colloidal gold, or pseudorabies virus (PRV), into the nuclear core of the rat LC. A substantial number of these neurons were routinely found within the dendritic field of the LC, in the area surrounding the compact cell-dense region classically defined as LC. Double labeling revealed that a large percentage of these cells stained for GABA. Ultrastructural analyses revealed axodendritic and axosomatic contacts between PRV-labeled afferents and LC neurons labeled with tyrosine hydroxylase immunohistochemistry. In addition, PRV-labeled neurons or axons were immunopositive for GABA in ultrastructural localizations. Analysis of the synaptology of immunopositive profiles demonstrated that these LC afferents in the peri-LC region receive several non-LC synaptic inputs. These results indicate that a population of small GABAergic neurons in the peri-LC dendritic zone may provide interneuronal integration for LC noradrenergic neurons.
124 citations