AJP - Regulatory, Integrative and Comparative Physiology, Vol 267, Issue 5 1397-R1407, Copyright © 1994 by American Physiological Society

ARTICLES

Alterations of synaptic transmission in sympathetic ganglia of spontaneously hypertensive rats

J. C. Magee and G. G. Schofield
Department of Physiology, Tulane University Medical School, New Orleans, Louisiana 70112.

An enhanced sympathetic nerve activity (SNA) has been implicated in the development and maintenance of the hypertension observed in experimental animal models such as the spontaneously hypertensive rat (SHR). Recent evidence suggests that an alteration of sympathetic synaptic transmission could also play a significant role in the elevation of SNA observed in the SHR (J. C. Magee and G. G. Schofield. Hypertension Dallas 20: 367-373, 1992). To test this hypothesis, we used intracellular recordings from superior cervical ganglion (SCG) neurons to compare properties of synaptic transmission between SHRs and two normotensive controls [Wistar-Kyoto (WKY) and Wistar rats]. Supramaximal preganglionic stimulation elicited larger amplitude fast excitatory postsynaptic potentials (EPSPs) and currents (EPSCs) in SHR sympathetic neurons compared with the normotensive controls. Analysis of variance of both compound and unitary EPSC amplitudes suggests that an increase in transmitter release is responsible for the elevated EPSP amplitude in these neurons. Also, a diminished short-term facilitation and an elevated synaptic depression limit the ability of SHR preganglionic neurons to increase transmitter release during short trains of repetitive stimuli. It is hypothesized that an enhanced transmitter depletion results in the altered synaptic plasticity of SHR sympathetic ganglion neurons. Intracellular recordings in low-Ca2+, high-Mg2+ external solutions support this idea. Therefore, synaptic transmission between the preganglionic and postganglionic neurons of SCGs from hypertensive rats was found to be altered in a manner that would tend to enhance sympathetic nervous activity, further implicating an exaggerated SNA in the pathogenesis of hypertension in the SHR model.

This article has been cited by other articles:

				K. A Alkadhi, S. A Otoom, F. L Tanner, D. Sockwell, and Y. H Hogan Inhibition of Ganglionic Long-Term Potentiation Decreases Blood Pressure in Spontaneously Hypertensive Rats Experimental Biology and Medicine, December 1, 2001; 226(11): 1024 - 1030. [Abstract] [Full Text] [PDF]

				A. A. Aileru, A. De Albuquerque, J. M. Hamlyn, P. Manunta, J. R. Shah, M. J. Hamilton, and D. Weinreich Synaptic plasticity in sympathetic ganglia from acquired and inherited forms of ouabain-dependent hypertension Am J Physiol Regulatory Integrative Comp Physiol, August 1, 2001; 281(2): R635 - R644. [Abstract] [Full Text] [PDF]

				W. P. Robertson and G. G. Schofield Primary and adaptive changes of A-type K+ currents in sympathetic neurons from hypertensive rats Am J Physiol Regulatory Integrative Comp Physiol, June 1, 1999; 276(6): R1758 - R1765. [Abstract] [Full Text] [PDF]

				D. Ely, A. Caplea, G. Dunphy, H. Daneshvar, M. Turner, A. Milsted, and M. Takiyyuddin Spontaneously Hypertensive Rat Y Chromosome Increases Indexes of Sympathetic Nervous System Activity Hypertension, February 1, 1997; 29(2): 613 - 618. [Abstract] [Full Text]