SEAN D. STOCKER,1,2 JOHNNY R. SIMMONS,3 RUTH L. STORNETTA,3*
GLENN M. TONEY,2 AND PATRICE G. GUYENET3
1Department of Physiology, University of Kentucky College of Medicine,
Lexington, Kentucky 40536-0298
2Department of Physiology, University of Texas Health Science Center,
San Antonio, Texas 78229
3Department of Pharmacology, University of Virginia, Charlottesville, Virginia 22908
THE JOURNAL OF COMPARATIVE NEUROLOGY 494:673–685 (2006)
This study examined compensatory mechanisms within the medullary circuit in response to water deprivation. As we already know (or should know) the PVN generally plays a greater role in cardiovascular regulation under non-normotensive conditions. This study sought to see the role of PVN in the case of water deprivation, particularly in regards to its projections to RVLM. They sought to determine whether the PVN-RVLM projections activated by water deprivation were glutamatergic and/or contained vasopressin or oxytocin. Adult male Sprague-Dawley rats were injected with several retrograde tracers into both their PVN and RVLM, as a means to track the projections between the two areas. They were first microinjected with CTB into their RVLM (wow that’s cool), and then exposed to a water deprivation protocol or not (control). Following a period of about two weeks these rats were sacrificed and then perfused. After the brain tissue was retrieved and fixed, they conducted in-situ hybridization to quantify mRNA in PVN to determine whether or not PVN had glutamatergic or GABAergic projections to RVLM. As a result of measuring the VGLUT2 in PVN, they were able to deduce that PVN actually had glutamatergic projections to RVLM, and were particularly activated during water deprivation. This once again suggests that PVN plays a role in non-normotensive conditions and that it may project glutamate onto RVLM in the case of hypertension and other CVD.
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