China
Africa
Explore chapters and articles related to this topic
Synapses
Published in Nassir H. Sabah, Neuromuscular Fundamentals, 2020
Synaptic receptors, as well as synapses, and even neurons, are sometimes characterized by the neurotransmitter associated with them. Thus, receptors activated by glutamic acid, for example, are referred to as glutamatergic receptors, and those activated by γ-aminobutyric acid (GABA) are referred to as GABAergic receptors. Some receptors may be activated by more than one neurotransmitter, and some neurons may release more than one neurotransmitter from the same site or from different sites, as mentioned in the next section.
Role of central GABA in the regulation of blood pressure and the development of hypertension in the SHR
Published in H. Saito, Y. Yamori, M. Minami, S.H. Parvez, New Advances in SHR Research –, 2020
Maarten Van Den Buuse, Geoffrey A. Head
The dorsomedial nucleus of the hypothalamus appeared to be the site of action of bicuculline and muscimol in the posterior hypothalamus (Anderson and DiMicco, 1990; Soltis and DiMicco, 1991a). Furthermore, an interaction of GABAergic mechanisms and glutamate receptor-mediated mechanisms was found. In the dorsomedial nucleus, the effect of micro-injection of bicuculline could be blocked by pretreatment with the non-selective glutamate antagonist kynurenic acid (Soltis and DiMicco, 1991b). Treatment with APS, an antagonist of N-methyl-D-aspartate (NMDA) receptors or with CNQX, an antagonist of non-NMDA receptors, produced partial inhibition of the effect of bicuculline and these effects were additive, indicating that NMDA- as well as non-NMDA type glutamate receptors were involved in the action of bicuculline (Soltis and DiMicco, 1991b). Also the tachycardia induced by air-jet stress could be blocked by kynurenic acid and inhibited by AP5 or CNQX micro-injected into the dorsomedial hypothalamus (Soltis and DiMicco, 1992), again indicating the similarity between the cardiovascular effects induced by blockade of GABA receptors in the posterior hypothalamus and those induced by emotional stress.
Antianxiety Drugs
Published in Sahab Uddin, Rashid Mamunur, Advances in Neuropharmacology, 2020
Gamma amino butyric acid (GABA) is the main neurotransmitter that is known to regulate the anxiety-related behavior and the potentiation of GABAergic neurotransmission in the brain mediated anxiolytic effect (Mohler, 2011). However, the GABAergic modulators often imposed the risk of abuse tolerance and potentially fatal withdrawal symptoms (Roy-Byrne et al., 1993).
Pharmacological Treatment of Generalised Anxiety Disorder: Current Practice and Future Directions
Published in Expert Review of Neurotherapeutics, 2023
Harry A. Fagan, David S. Baldwin
RCTs of benzodiazepines in GAD demonstrate efficacy vs. placebo, however the dropout rates are higher in the benzodiazepine groups on average [18]. Benzodiazepines with a relatively long half-life are preferred in treatment of GAD, to prevent the need for multiple daily dosing. Common adverse effects of benzodiazepine treatment include cognitive effects (sedation, drowsiness, and mental slowing) and psychomotor impairment (including when driving), both related to increased GABAergic stimulation, and the development of tolerance and dependence [49]. Tolerance to benzodiazepines can occur for the anticonvulsant and sedative effects; however, it is less clear to what extent this occurs for the anxiolytic effects [49]. Dependence on benzodiazepines can also occur with an associated withdrawal syndrome, usually characterized by anxiety-related physical and psychological symptoms alongside perceptual disturbances [50]. Treatment of benzodiazepine dependence, usually entails the conversion of benzodiazepine polypharmacy to monotherapy and the gradual tapering of the total dose, combined with psychological support [51].
A double-blind, placebo-controlled, randomised-designed GABA tea study in children diagnosed with autism spectrum conditions: a feasibility study clinical trial registration: ISRCTN 72571312
Published in Nutritional Neuroscience, 2021
Penelope Hannant, Sarah Cassidy, Derek Renshaw, Anna Joyce
There are specific areas of the brain associated with sensorimotor integration. These include: the cerebellum, which is considered to be intrinsic to predicting movement outcomes [60] and is thought to contain pathways that are responsible for linking sensory input to motor output [5–6,61]; and the basal ganglia, also thought to be involved in multisensory integration in addition to automaticity and motor habit [7–8,62–64]. Both brain regions are involved in GABAergic activity. The cerebellum contains Purkinje cells, which are considered the sole output of all motor coordination in the cerebellar cortex [65], whilst the striatum in the basal ganglia contains medium spiny neurons (MSN), also a GABAergic cell [66]. Yet, 95% of autistic cerebella examined at autopsy had a significantly decreased number of Purkinje cells, [12–14]. In addition, a decreased volume in the basal ganglia [11], and excess functional connectivity in the striatum, one of the largest components of the basal ganglia and consisting of 95% MSN [66], have been reported in ASC [67].
High-yield synthesis and purification of recombinant human GABA transaminase for high-throughput screening assays
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2021
Mingu Gordon Park, Ah-reum Han, Su Yeon Kim, Tai Young Kim, Ho Min Kim, C. Justin Lee
γ-aminobutyric acid (GABA) is the major inhibitory neurotransmitter synthesised and released from GABAergic neurons and astrocytes in the mammalian central nervous system (CNS)1–4. GABA is synthesised by glutamate decarboxylase (GAD; EC 4.1.1.15) in GABAergic neurons and by monoamine oxidase (MAO-B; EC 1.4.3.4) or diamine oxidase (DAO; EC 1.4.3.22) in astrocytes4–6. However, the only GABA-catabolizing enzyme in the mammalian CNS is GABA transaminase (GABA-T; EC 2.6.1.19) encoded by the ABAT gene7. GABA-T catalyses the conversion of GABA to succinic semialdehyde (SSA) concomitantly with the conversion of α-ketoglutarate (α-KG) to glutamate. Subsequently, SSA is oxidised to succinic acid (SA) by the enzyme SSA dehydrogenase (SSADH; EC 1.2.1.24). GABA-T and SSADH are mitochondrial enzymes and exist both in GABAergic neurons and astrocytes8–10. Because the transaminase reaction cannot be directly monitored, we can utilise dehydrogenation of SSA from GABA-T reaction to indirectly monitor GABA-T activity by detecting a conversion of NADP+ to NADPH11.