RT Journal Article
SR Electronic
T1 NMDA Receptor Plasticity in the Hypothalamic Paraventricular Nucleus Contributes to the Elevated Blood Pressure Produced by Angiotensin II
JF The Journal of Neuroscience
JO J. Neurosci.
FD Society for Neuroscience
SP 9558
OP 9567
DO 10.1523/JNEUROSCI.2301-14.2015
VO 35
IS 26
A1 Michael J. Glass
A1 Gang Wang
A1 Christal G. Coleman
A1 June Chan
A1 Evgeny Ogorodnik
A1 Tracey A. Van Kempen
A1 Teresa A. Milner
A1 Scott D. Butler
A1 Colin N. Young
A1 Robin L. Davisson
A1 Costantino Iadecola
A1 Virginia M. Pickel
YR 2015
UL http://www.jneurosci.org/content/35/26/9558.abstract
AB Hypertension induced by angiotensin II (Ang II) is associated with glutamate-dependent dysregulation of the hypothalamic paraventricular nucleus (PVN). Many forms of glutamate-dependent plasticity are mediated by NMDA receptor GluN1 subunit expression and the distribution of functional receptor to the plasma membrane of dendrites. Here, we use a combined ultrastructural and functional analysis to examine the relationship between PVN NMDA receptors and the blood pressure increase induced by chronic infusion of a low dose of Ang II. We report that the increase in blood pressure produced by a 2 week administration of a subpressor dose of Ang II results in an elevation in plasma membrane GluN1 in dendrites of PVN neurons in adult male mice. The functional implications of these observations are further demonstrated by the finding that GluN1 deletion in PVN neurons attenuated the Ang II-induced increases in blood pressure. These results indicate that NMDA receptor plasticity in PVN neurons significantly contributes to the elevated blood pressure mediated by Ang II.