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The data suggest that GABA, by activating specific receptors, causes inhibition of firing of dopaminergic neurones and the opposite effect on the noradrenergic neurones.
Moreover, both selective GABA(B) receptor antagonist CGP35348 and selective GABA(A) receptor antagonist bicuculline were capable of partially blocking the inhibitory response of IN neurons to GABA (n = 14 and 11), suggesting that the GABA-induced inhibition may contain two components, a GABA(B) receptors-mediated component and a GABA(A) receptors-mediated one.
Here, we report that the brief GABA exposure induces a decrease in the percentage of α3-containing receptors, a receptor subtype that exhibits a high degree of coupling between GABA and benzodiazepine binding sites.
These results suggest that GABA affects the cholinergic transmitter release through bicuculline- and picrotoxin-sensitive receptors, showing low affinity toward the agonist.
The presence of GABA(C) receptors in many GABAergic neurons suggests that this receptor type may be involved in the regulation of local inhibition.
This study shows that the cyclopentane and cyclopentene analogues of GABA affect GABA(C) receptors in a unique manner, defining a preferred stereochemical orientation of the amine and carboxylic acid groups when binding to GABA(C) receptors.
Thus, by the criterion of being insensitive to both bicuculline and baclofen, both GABA receptors qualify as potential GABAC receptors.
It is then suggested that this effect might depend on an indirect activation of GABAB receptors through release of GABA.
These functional and pharmacological differences between the two effects of GABA suggest that two separate receptors are involved.
We can speculate that different subsets of GABA-B receptors are influenced by the two agonists but further studies are necessary.

Related Questions

What are the effects of using codeine?4 answersCodeine has various effects on the body. It is commonly used as an analgesic and antitussive agent in pediatric patients. However, there is genetic variability in the activity of the hepatic enzyme responsible for metabolizing codeine, leading to individual patient responses ranging from no effect to high sensitivity. Adverse effects of codeine, such as respiratory depression and death, have been documented in children, particularly in those with obstructive sleep apnea and rapid metabolism. Mast cell degranulation and the systemic release of histamine are common side effects of codeine and morphine. Codeine can also induce secretion of inflammatory mediators in human mast cells. Additionally, codeine and tramadol, both opiates, can cause serious side effects such as sleepiness and respiratory depression, and there is a risk of dependence with repeated use. Codeine is often associated with paracetamol in pharmaceutical specialties and has been linked to an elevated risk of driving accidents. In severely depressed patients, codeine has shown limited effectiveness and can cause constipation and sedation.
How does GABA affect sleep?5 answersGABA, a neurotransmitter, plays a key role in sleep regulation. It is involved in memory consolidation during sleep, as well as in controlling sleep amount, latency, and consolidation. GABAergic activity is implicated in memory reactivation processes during sleep, possibly through its effects on slow oscillations, spindles, and theta. Astrocytic GABA transporters (GAT) also contribute to sleep regulation by decreasing GABAergic tone and promoting proper sleep amount and quality. GABA administration has been shown to shorten sleep latency and increase total non-REM sleep time. Additionally, a GABA/l-theanine mixture has been found to decrease sleep latency and increase sleep duration. Overall, GABA plays a crucial role in sleep control and its modulation can have significant effects on sleep quality and memory consolidation.
Does taurine supplementation increase GABA levels in the brain?5 answersTaurine supplementation has been shown to increase GABA levels in the brain. Studies have found that taurine-fed mice have reduced GABAA receptor expression and increased GAD and somatostatin expression in the brain, indicating changes in the GABAergic system. Additionally, taurine-fed mice showed hyperexcitability, which is associated with increased neuronal excitability. These findings suggest that taurine supplementation can lead to an increase in GABA levels in the brain, potentially contributing to its neuroprotective effects.
How do psychostimulates affect the gabaergic system?5 answersPsychostimulants affect the GABAergic system by involving transmitters other than dopamine and brain areas other than the nucleus accumbens and the striatum. The effects of psychostimulants are mediated by the activation of circuits, and different pharmacological properties of these stimulants involve different circuits, although they share some neuroeffector systems. GABAergic inputs have been demonstrated in the central nucleus of the amygdala (ACe), but the contribution of these inhibitory inputs to the cardiovascular responses elicited from the ACe is not clear. Stimulation of GABA receptors has been reported to modify the activity of various cerebral neurotransmitter systems, suggesting that GABA receptor agonists represent a potential class of new drugs with a wide therapeutic spectrum.
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