a(CHEBI:"gamma-aminobutyric acid")
Third, nAChR-mediated GABA release can cause neuronal hyperpolarization, which in turn affects neuronal function via several mechanisms, including removal of inactivation of inward currents (89). PubMed:19126755
Activation of alpha7 nAChRs in somatodendritic and preterminal/ terminal areas of interneurons in various strata of the CA1 region and in the dentate gyrus facilitates spontaneous quantal release of GABA (14, 25). Glutamate release from mossy fibers onto CA3 pyramidal neurons is also modulated by alpha7 nAChRs present in the mossy fiber terminals (190). PubMed:19126755
Exogenously applied nicotinic agonists enhance and nicotinic antagonists often diminish the release of ACh, dopamine (DA), norepinephrine, and serotonin, as well as glutamate and GABA. PubMed:17009926
Exogenously applied nicotinic agonists enhance and nicotinic antagonists often diminish the release of ACh, dopamine (DA), norepinephrine, and serotonin, as well as glutamate and GABA. PubMed:17009926
Presynaptic and preterminal nAChRs increase the release of neurotransmitters in the hippocampus, particularly the main neurotransmitters, GABA and glutamate (41, 78, 81, 97). PubMed:17009926
Stimulation of nicotinic receptors present at the CNS presynaptic neuronal membrane leads to an increase in presynaptic Ca2+ concentration, which may facilitate the release of a number of neurotransmitters, such as glutamate, GABA, dopamine, serotonin, norepinephrine, as well as ACh PubMed:26813123
The neurons release additional GABA, activating presynaptic GABAB receptors on the excitatory inputs to pyramidal neurons, which diminish the release of glutamate onto the pyramidal neurons (Figure 2) PubMed:21482353
This transporter lowers the internal Cl- concentration of the neuron and changes GABA from a depolarizing to a hyperpolarizing or inhibitory neurotransmitter PubMed:21482353
Typically, activation of brain nAChRs results in enhanced release of various key neurotransmitters, including dopamine, serotonin, glutamate and GABA (gamma-aminobutyric acid). PubMed:19721446
Also, Endo et al. [141] found naturally-expressed a3b2- and a6b2-nAChRs on superior colli- culus neurons, and these receptors are likely located on pre- synaptic terminals of GABAergic neurons where they modulate GABA release. PubMed:21787755
Recently, we reported a novel discovery that functional a6*-nAChRs are located on GABAergic presynaptic boutons associated with VTA DAergic neurons, where these a6*- nAChRs mediate nicotinic modulation of GABA release onto those DAergic neurons [122]. PubMed:21787755
Also, Endo et al. [141] found naturally-expressed a3b2- and a6b2-nAChRs on superior colli- culus neurons, and these receptors are likely located on pre- synaptic terminals of GABAergic neurons where they modulate GABA release. PubMed:21787755
Third, nAChR-mediated GABA release can cause neuronal hyperpolarization, which in turn affects neuronal function via several mechanisms, including removal of inactivation of inward currents (89). PubMed:19126755
The neurons release additional GABA, activating presynaptic GABAB receptors on the excitatory inputs to pyramidal neurons, which diminish the release of glutamate onto the pyramidal neurons (Figure 2) PubMed:21482353
The neurons release additional GABA, activating presynaptic GABAB receptors on the excitatory inputs to pyramidal neurons, which diminish the release of glutamate onto the pyramidal neurons (Figure 2) PubMed:21482353
The neurons release additional GABA, activating presynaptic GABAB receptors on the excitatory inputs to pyramidal neurons, which diminish the release of glutamate onto the pyramidal neurons (Figure 2) PubMed:21482353
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If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.