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Circadian System and Diurnal Activity
Published in Anthony N. Nicholson, The Neurosciences and the Practice of Aviation Medicine, 2017
Sleep pressure acts upon a mutually inhibitory interaction between sleep-promoting and arousal-promoting systems. Sleep-promoting neurons localized in the ventrolateral preoptic area and median preoptic nucleus exert gabaergic and galaninergic inhibitory control over arousal-promoting cell groups localized in multiple arousal centres in the upper brainstem and diencephalon (Fuller et al., 2006). Nonrapid eye movement sleep occurs as a consequence of the activation of neurons within the ventrolateral preoptic area and the progressive decrease in the firing rate of aminergic and cholinergic arousal-promoting neurons resulting from increased release of γ-aminobutyric acid (GABA). Both the activation of the neurons and the GABA release increase proportionally with growing sleep depth. After an adequate amount of sleep, wakefulness occurs at a circadian time during the transition from night to day (Fuller et al., 2006). It is the circadian system that determines the timing of sleep propensity and wakefulness and is often defined as the wake-promoting system (Borbély 1982; Borbély and Achermann, 1999). In the absence of the circadian component, after an SCN lesion, sleep will still occur, but it becomes highly fragmented and is expressed as a continuous series of relatively short sleep episodes promoted by the homeostatic drive alone (Cohen and Albers, 1991).
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.
Oleanolic acid suppresses pentylenetetrazole-induced seizure in vivo
Published in International Journal of Environmental Health Research, 2023
Canan Akünal Türel, Oruç Yunusoğlu
GABA is an amino acid that functions as the main inhibitory neurotransmitter for the brain (Ergul et al. 2022; Sarlo et al. 2021; Yunusoğlu et al. 2022). It functions to decrease neuronal excitability by inhibiting nerve transmission (Sarlo et al. 2021). Pre-clinical and clinical study evidence suggests that GABA has a critical role in the mechanism and treatment of epilepsy. Benzodiazepines (diazepam, lorazepam, clonazepam, and clobazam) are examples of drugs that act by activating the GABAergic system (Sarlo et al. 2021). However, their use for long-term treatment is limited because of the development of tolerance (Sarlo et al. 2021). PTZ causes a decrease in GABAergic functions in acute and repeated dose administration (Ergul et al. 2022; Ilhan and Gurel et al. 2005; Samokhina et al. 2018; Yuskaitis et al. 2021). In previous studies, oleanolic acid has been shown to have a positive effect on the GABAergic system (Ha, Lee, et al. 2002; Ibarra et al. 2010; Khan et al. 2016). This mechanism may have contributed to the anti-seizure effect of oleanolic acid.
Physiological and pathophysiological implications of hydrogen sulfide: a persuasion to change the fate of the dangerous molecule
Published in Journal of the Chinese Advanced Materials Society, 2018
Jan Mohammad Mir, Ram Charitra Maurya
Another example of H2S effect on neurotransmitter receptors is gamma-aminobutyric acid (GABA). GABA is a major inhibitory neurotransmitter, serving 20%–30% of all synapses in CNS.[127] Deficiency in GABAergic inhibition leads to febrile seizures and neuronal hyperexcitability.[30, 128] H2S has been shown to decrease hippocampal damage induced by recurrent febrile seizures by enhancing GABAergic inhibition. Rather than increasing GABA level, H2S in fact upregulates GABAB receptors at both mRNA and protein levels located at pre- and postsynaptic sites. This upregulation of receptor expression is likely associated with an increases in [Ca2+]i, which would stimulate Ca2+-dependent transcription.[129, 130] The increased GABAergic inhibition by H2S may find its application in other situations where the excitation/inhibition balance is disturbed in CNS, such as seizures and epilepsy, stimuli leading to pain,[131] and cerebral ischemia.[132]