PT  - JOURNAL ARTICLE
AU  - Michael J. Glass
AU  - Gang Wang
AU  - Christal G. Coleman
AU  - June Chan
AU  - Evgeny Ogorodnik
AU  - Tracey A. Van Kempen
AU  - Teresa A. Milner
AU  - Scott D. Butler
AU  - Colin N. Young
AU  - Robin L. Davisson
AU  - Costantino Iadecola
AU  - Virginia M. Pickel
TI  - NMDA Receptor Plasticity in the Hypothalamic Paraventricular Nucleus Contributes to the Elevated Blood Pressure Produced by Angiotensin II
AID  - 10.1523/JNEUROSCI.2301-14.2015
DP  - 2015 Jul 01
TA  - The Journal of Neuroscience
PG  - 9558--9567
VI  - 35
IP  - 26
4099  - http://www.jneurosci.org/content/35/26/9558.short
4100  - http://www.jneurosci.org/content/35/26/9558.full
SO  - J. Neurosci.2015 Jul 01; 35
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.