Abstract
AbstractAdenosine produces depressor effects in various brain areas. However, the cellular mechanisms underlying the depressor effect of adenosine remain unclear. The presympathetic neurons in hypothalamic paraventricular nucleus (PVN) play an important role in the regulation of arterial blood pressure and sympathetic outflow through projections to spinal cord and brainstem. In this study, we performed whole‐cell patch‐clamp recordings on retrogradely labeled PVN neurons projecting to the intermediolateral cell column of the spinal cord in rats. Adenosine (10‐100 μM) dose‐dependently decreased the firing activity with a significant hyperpolarization in 12 of 26 neurons tested. Blockade of A1 receptors with DPCPX or intracellular dialysis of GDP‐β‐s eliminated the inhibitory effects of adenosine. Also, blocking ATP‐dependent K+ (KATP) channel with glibenclamide (50 μM) or tolbutamide (200 μM) abolished the effect of adenosine on the firing activity of PVN neurons. Furthermore, glibenclamide or tolbutamide significantly decreased the outward K+ current elicited by adenosine. In addition, adenosine decreased the frequency of glutamatergic and GABAergic postsynaptic currents in labeled PVN neurons. Collectively, these data suggested that adenosine inhibits the excitability of PVN presympathetic neurons mainly through postsynaptic A1 receptors and opening of KATP channels.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
