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NMDA Receptor Plasticity in the Hypothalamic Paraventricular Nucleus Contributes to the Elevated Blood Pressure Produced by Angiotensin II.

TitleNMDA Receptor Plasticity in the Hypothalamic Paraventricular Nucleus Contributes to the Elevated Blood Pressure Produced by Angiotensin II.
Publication TypeJournal Article
Year of Publication2015
AuthorsGlass MJ, Wang G, Coleman CG, Chan J, Ogorodnik E, Van Kempen TA, Milner TA, Butler SD, Young CN, Davisson RL, Iadecola C, Pickel VM
JournalJ Neurosci
Volume35
Issue26
Pagination9558-67
Date Published2015 Jul 01
ISSN1529-2401
KeywordsAnalysis of Variance, Angiotensin II, Animals, Blood Pressure, Functional Laterality, Green Fluorescent Proteins, Male, Mice, Mice, Inbred C57BL, Mice, Transgenic, Microscopy, Immunoelectron, N-Methylaspartate, Nerve Tissue Proteins, Neurons, Nitric Oxide Synthase Type I, Paraventricular Hypothalamic Nucleus, Plethysmography, Reactive Oxygen Species, Receptors, N-Methyl-D-Aspartate, RNA, Messenger, Vasoconstrictor Agents
Abstract

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.

DOI10.1523/JNEUROSCI.2301-14.2015
Alternate JournalJ. Neurosci.
PubMed ID26134639
PubMed Central IDPMC4571498
Grant ListHL09657 / HL / NHLBI NIH HHS / United States
MH40342 / MH / NIMH NIH HHS / United States
R01 DA004600 / DA / NIDA NIH HHS / United States
R01 MH040342 / MH / NIMH NIH HHS / United States
NS89323 / NS / NINDS NIH HHS / United States
HL063887 / HL / NHLBI NIH HHS / United States
R01 HL063887 / HL / NHLBI NIH HHS / United States
R01 HL098351 / HL / NHLBI NIH HHS / United States
P01 HL084207 / HL / NHLBI NIH HHS / United States
DA04600 / DA / NIDA NIH HHS / United States
DA024030 / DA / NIDA NIH HHS / United States
R37 MH040342 / MH / NIMH NIH HHS / United States
F32 HL009657 / HL / NHLBI NIH HHS / United States
HL098351 / HL / NHLBI NIH HHS / United States
R37 NS089323 / NS / NINDS NIH HHS / United States
P01 HL096571 / HL / NHLBI NIH HHS / United States
R01 DA024030 / DA / NIDA NIH HHS / United States