WWW.JNEUROSCI.ORG
-
The Journal of Neuroscience MBF Bioscience Autoneuron
QUICK SEARCH:   [advanced]


     
-


HOME  |   SEARCH  |   ARCHIVE  |   SUBSCRIBE  |   CONTACT  |   HELP
This Article
Right arrow Full Text (PDF)
Right arrow Submit an eLetter
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Eilam, R.
Right arrow Articles by Segal, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Eilam, R.
Right arrow Articles by Segal, M.

 Previous Article  |  Next Article 

Journal of Neuroscience, Vol 14, 4891-4902, Copyright © 1994 by Society for Neuroscience

ARTICLE

Selective elimination of hypothalamic neurons by grafted hypertension- inducing neural tissue

R Eilam, R Malach and M Segal
Department of Neurobiology, Weizmann Institute, Rehovot, Israel.

Embryonic hypothalamic tissue originating from spontaneously hypertensive rats (SHR) was implanted in young normotensive Wistar Kyoto rats in an attempt to localize hypothalamic regions directly responsible for the induction of hypertension. A 25% increase in host systolic blood pressure as compared with the controls was recorded 3 months after implantation in the animals receiving rostral hypothalamic tissue (R-SHR), whereas blood pressure was not affected in the animals grafted with caudal hypothalamic tissue (C-SHR). The hypertension in the R-SHR group was accompanied by hypertrophy of the heart and kidneys. The number of vasopressin-immunopositive (VPi) parvocellular cells in the hypothalamic paraventricular nucleus (PVN) of the R-SHR group was massively reduced (by 72%), while that of the tyrosine hydroxylase-immunopositive cells displayed no change. In the suprachiasmatic nucleus of these animals the VPi cell number was unaltered. In the C-SHR, the amount of parvocellular VPi cells was also unaltered. Likewise, oxytocin-containing cells were the same in all groups. DNA nick-end labeling of the tissue revealed that PVN cells are undergoing programmed cell death. These results implicate a selective degeneration by hypothalamic PVN cells in the pathogenesis of hypertension.


This article has been cited by other articles:


Home page
 J. Neurophysiol.Home page
K. J. Latchford and A. V. Ferguson
Angiotensin II Activates a Nitric-Oxide-Driven Inhibitory Feedback in the Rat Paraventricular Nucleus
J Neurophysiol, March 1, 2003; 89(3): 1238 - 1244.
[Abstract] [Full Text] [PDF]

Home page
 Physiol. Rev.Home page
H. E. De Wardener
The Hypothalamus and Hypertension
Physiol Rev, October 1, 2001; 81(4): 1599 - 1658.
[Abstract] [Full Text] [PDF]

Home page
 HypertensionHome page
A. Blume, C. J. Lebrun, T. Herdegen, R. Bravo, W. Linz, E. Mollenhoff, and T. Unger
Increased Brain Transcription Factor Expression by Angiotensin in Genetic Hypertension
Hypertension, February 1, 1997; 29(2): 592 - 598.
[Abstract] [Full Text]


-

Home  |   Search  |   Archive  |   Subscribe  |   Contact  |   Help
-
Copyright 2008 by Society for Neuroscience ONLINE ISSN: 1529-2401
-