Neuron
ArticleSubstance P and somatostatin inhibit calcium channels in rat sympathetic neurons via different G protein pathwavs
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2015, Biochemical and Biophysical Research CommunicationsCitation Excerpt :Here we investigated additional ways by which peripheral GABAB receptors might influence nociceptive transmission. GABAB, similar to other Gi/o-coupled receptors, inhibit HVA currents using a ‘fast’ pathway that involves direct interaction of G protein with the channels [34–38] resulting in a conformational change of the channel complex that makes it harder to open by voltage [39,40]. There are also number of other pathways by which GPCR can inhibit VGCC, including phosphatidylinositol 4,5-bisphosphate (PIP2) depletion [41,42], arachidonic acid [43] and Src kinase [15].
NK<inf>1</inf> receptors antagonism of dorsal hippocampus counteract the anxiogenic-like effects induced by pilocarpine in non-convulsive Wistar rats
2014, Behavioural Brain ResearchCitation Excerpt :At this point, it would be important to know the circumstances (aversive and/or convulsive) in which NK1-SP transmission is actually altered in these brain structures. SP excites neurons by suppressing an inwardly rectifying potassium current and by suppressing the M- and N-type calcium currents [83–86] leading to a reduction of Ca2+-activated potassium currents and resulting in after-hyperpolarization [87]. SP also enhances glutamate currents mediated by NMDA receptors [88] as well as glutamate release from hippocampal slices [32].
Modulation of N-type Ca<sup>2+</sup> currents by moxonidine via imidazoline I1 receptor activation in rat superior cervical ganglion neurons
2011, Biochemical and Biophysical Research CommunicationsCitation Excerpt :This moxonidine-induced inhibition was totally prevented by pretreatment with 10 μM efaroxan, and nearly completely occluded by ω-CgTx GVIA (Fig. 1B, C), suggesting that moxonidine inhibited mainly ICa–N via IR1 activation in rat SCG neurons. In peripheral sympathetic neurons, PTX-sensitive G protein is activated by various neurotransmitters such as NE, somatostatin and adenosine and is involved in inhibition of ICa–N [16,35]. As shown in Supplementary Fig. 2, this inhibition displays the hallmarks of voltage-dependent inhibition, namely kinetic slowing and prepulse facilitation or relief of current inhibition by conditioning depolarizing pulses and the absence of diffusible messenger (membrane-delimited manner) [16,36,37].
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