HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 554/1/100    most recent jphysiol.2003.053371v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Li, D.-P. Articles by Pan, H.-L. Search for Related Content PubMed PubMed Citation Articles by Li, D.-P. Articles by Pan, H.-L.

Department of Anaesthesiology, The Pennsylvania State University College of Medicine, The Milton S. Hershey Medical Center, Hershey, PA 17033, USA

In the paraventricular nucleus (PVN) of the hypothalamus, nitric oxide (NO) inhibits sympathetic outflow through increased GABA release. However, the signal transduction pathways involved in its action remain unclear. In the present study, we determined the role of cGMP, soluble guanylyl cyclase, and protein kinase G in the potentiating effect of NO on synaptic GABA release to spinally projecting PVN neurones. The PVN neurones were retrogradely labelled by a fluorescent tracer injected into the thoracic spinal cord of rats. Whole-cell voltage-clamp recordings were performed on labelled PVN neurones in the hypothalamic slice. Bath application of the NO donor, S-nitroso-N-acetyl-penicillamine (SNAP), reproducibly increased the frequency of miniature GABAergic inhibitory postsynaptic currents (mIPSCs) without changing the amplitude and the decay time constant. Neither replacement of Ca²⁺ with Co²⁺ nor application of Cd²⁺ to block the Ca²⁺ channel altered the effect of SNAP on mIPSCs. Also, the effect of SNAP on mIPSCs was not significantly affected by thapsigargin, a Ca²⁺-ATPase inhibitor that depletes intracellular Ca²⁺ stores. Application of a membrane-permeant cGMP analogue, pCPT–cGMP, mimicked the effect of SNAP on mIPSCs in the presence of a phosphodiesterase inhibitor, IBMX. Furthermore, both the soluble guanylyl cyclase inhibitor, ODQ, and the specific protein kinase G inhibitor, Rp pCPT cGMP, abolished the effect of SNAP on mIPSCs. Thus, these data provide substantial new information that NO potentiates GABAergic synaptic inputs to spinally projecting PVN neurones through a cGMP–protein kinase G pathway.

(Received 14 August 2003; accepted after revision 10 October 2003; first published online 10 October 2003)
Corresponding author H.-L. Pan: Department of Anaesthesiology, The Pennsylvania State University College of Medicine, The Milton S. Hershey Medical Center, Hershey, PA 17033, USA.  Email: hpan{at}psu.edu

This article has been cited by other articles:

				K. Powers-Martin, J. K. Phillip, V. C. Biancardi, and J. E. Stern Heterogeneous distribution of basal cyclic guanosine monophosphate within distinct neuronal populations in the hypothalamic paraventricular nucleus Am J Physiol Regulatory Integrative Comp Physiol, October 1, 2008; 295(4): R1341 - R1350. [Abstract] [Full Text] [PDF]

				S. Yang and C. L. Cox Excitatory and anti-oscillatory actions of nitric oxide in thalamus J. Physiol., August 1, 2008; 586(15): 3617 - 3628. [Abstract] [Full Text] [PDF]

				M. K. Kelm, H. E. Criswell, and G. R. Breese Calcium Release from Presynaptic Internal Stores Is Required for Ethanol to Increase Spontaneous {gamma}-Aminobutyric Acid Release onto Cerebellum Purkinje Neurons J. Pharmacol. Exp. Ther., October 1, 2007; 323(1): 356 - 364. [Abstract] [Full Text] [PDF]

				E. Szabadits, C. Cserep, A. Ludanyi, I. Katona, J. Gracia-Llanes, T. F. Freund, and G. Nyiri Hippocampal GABAergic Synapses Possess the Molecular Machinery for Retrograde Nitric Oxide Signaling J. Neurosci., July 25, 2007; 27(30): 8101 - 8111. [Abstract] [Full Text] [PDF]

				Q. Chen and H.-L. Pan Signaling Mechanisms of Angiotensin II-Induced Attenuation of GABAergic Input to Hypothalamic Presympathetic Neurons J Neurophysiol, May 1, 2007; 97(5): 3279 - 3287. [Abstract] [Full Text] [PDF]

				S. Yang and C. L. Cox Modulation of Inhibitory Activity by Nitric Oxide in the Thalamus J Neurophysiol, May 1, 2007; 97(5): 3386 - 3395. [Abstract] [Full Text] [PDF]

				Y.-F. Li, K. L. Jackson, J. E. Stern, B. Rabeler, and K. P. Patel Interaction between glutamate and GABA systems in the integration of sympathetic outflow by the paraventricular nucleus of the hypothalamus Am J Physiol Heart Circ Physiol, December 1, 2006; 291(6): H2847 - H2856. [Abstract] [Full Text] [PDF]

				H. Waki, D. Murphy, S. T. Yao, S. Kasparov, and J. F.R. Paton Endothelial NO Synthase Activity in Nucleus Tractus Solitarii Contributes to Hypertension in Spontaneously Hypertensive Rats Hypertension, October 1, 2006; 48(4): 644 - 650. [Abstract] [Full Text] [PDF]

				D.-P. Li, L. M. Atnip, S.-R. Chen, and H.-L. Pan Regulation of Synaptic Inputs to Paraventricular-Spinal Output Neurons by {alpha}2 Adrenergic Receptors J Neurophysiol, January 1, 2005; 93(1): 393 - 402. [Abstract] [Full Text] [PDF]

				D.-P. Li, S.-R. Chen, and H.-L. Pan VR1 Receptor Activation Induces Glutamate Release and Postsynaptic Firing in the Paraventricular Nucleus J Neurophysiol, September 1, 2004; 92(3): 1807 - 1816. [Abstract] [Full Text] [PDF]