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Medial septal lesion enhances general anesthesia response.

Authors :
Leung, L. Stan
Ma, Jingyi
Shen, Bixia
Nachim, Ilan
Luo, Tao
Source :
Experimental Neurology. Sep2013, Vol. 247, p419-428. 10p.
Publication Year :
2013

Abstract

Abstract: Electrolytic lesion of the medial septum, a basal forebrain nucleus that projects to the hippocampus, prolonged the emergence from general anesthesia in rats. Septal lesioned rats required a longer time to recover from a loss of righting reflex (LORR) and a loss of tail-pinch response after injectable (20mg/kg i.p. pentobarbital, 5mg/kg i.v. propofol) or volatile (1.5% halothane, 2% isoflurane) anesthetic. When incremental doses of propofol were given i.p., septal lesioned rats as compared to control rats showed LORR at a lower dose of propofol. Similarly, when the rats were exposed to increasing concentrations of isoflurane, the percent of rats showing LORR was leftward shifted for lesioned rats as compared to control rats. Septal lesioned rats as compared to control rats showed decreased locomotor activity when exposed to 1.5% halothane. Lesion of the medial septum was confirmed by thionin-stained histological sections as well as loss of acetylcholinesterase (AchE) staining in the hippocampus, indicating a depletion of septohippocampal cholinergic afferents. Medial septal lesion resulted in a near complete loss of hippocampal theta rhythm during walking and a general decrease in power of the hippocampal EEG at all frequencies (0–100Hz), during walking or immobility. It is concluded that lesion of medial septum, in part through a loss of septohippocampal cholinergic afferents, increased the anesthesia response to volatile and injectable general anesthetics, during both induction and emergence. It is suggested that the septohippocampal system participates in many components of general anesthesia including hypnosis, immobility, and analgesia. [Copyright &y& Elsevier]

Details

Language :
English
ISSN :
00144886
Volume :
247
Database :
Academic Search Index
Journal :
Experimental Neurology
Publication Type :
Academic Journal
Accession number :
89704799
Full Text :
https://doi.org/10.1016/j.expneurol.2013.01.010