The lateral septal area is involved in mediation of immobilization stress-induced blood pressure increase in rats

Immobilization stress increased the number of neurons with Fos immunoreactivity, mainly in the ventral zone of the rostral part of the lateral septal nucleus (LSV) in rats. Immobilization stress caused an increase in blood pressure, and the stress-induced pressor response was inhibited by the GABAA...

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Bibliographic Details
Published in:Neuroscience letters 2002-01, Vol.318 (1), p.25-28
Main Authors: Kubo, Takao, Kanaya, Tomohiro, Numakura, Hiroyuki, Okajima, Hideaki, Hagiwara, Yukihiko, Fukumori, Ryuji
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Blood Pressure - drug effects
Blood Pressure - physiology
Fos immunoreactivity
Fundamental and applied biological sciences. Psychology
GABA Agonists - pharmacology
Immobilization stress
Injections, Intraventricular
Lateral septal area
Male
Motor control and motor pathways. Reflexes. Control centers of vegetative functions. Vestibular system and equilibration
Muscimol
Muscimol - pharmacology
Neurons - chemistry
Neurons - physiology
Pressor response
Proto-Oncogene Proteins c-fos - analysis
Rat
Rats
Rats, Wistar
Restraint, Physical
Septal Nuclei - cytology
Septal Nuclei - physiology
Stress, Physiological - physiopathology
Vertebrates: nervous system and sense organs
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Summary:Immobilization stress increased the number of neurons with Fos immunoreactivity, mainly in the ventral zone of the rostral part of the lateral septal nucleus (LSV) in rats. Immobilization stress caused an increase in blood pressure, and the stress-induced pressor response was inhibited by the GABAA receptor agonist, muscimol (8 and 80 pmol), injected bilaterally into the rostral part of the LSV in a dose-dependent manner. Intracerebroventricular injection of muscimol (16 pmol) did not affect the immobilization stress-induced pressor response. These findings suggest that the rostral part of the LSV is involved in mediation of the stress-induced pressor response.
ISSN:0304-3940
1872-7972
DOI:10.1016/S0304-3940(01)02463-6