ArticleExperimental brain research1991
The posterior hypothalamus is responsible for the increase of brain temperature during paradoxical sleep.
Article in Experimental brain research, 1991. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 25 citations in OpenAlex.
- Comparative Perspectives that Challenge Brain Warming as the Primary Function of REM Sleep.iScience · 2020Article
- Cortical temperature and EEG slow-wave activity in the rat: analysis of vigilance state related changes.Pflugers Archiv : European journal of physiology · 1992Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Electroencephalogram, caudate nucleus temperature (Tc), ear skin temperature (Te) as well as cerebral blood flow (CBF) measured by a thermal clearance method, were recorded simultaneously and continuously in cats. After baseline recording in which we confirmed the increase of Tc during paradoxical sleep (PS), neuronal cell bodies of the mesencephalic reticular formation and/or the posterior hypothalamus (PH) were destroyed with ibotenic acid. Only PH lesions were followed by either a suppression of the increase or even a decrease of Tc during PS while Te variations were not modified. The decrease in CBF, which was always associated with Tc increase, was suppressed after the PH lesion. These results led us to the conclusion that the increase of Tc at the onset of PS is due to a decrease in CBF. Furthermore, it may be hypothesized that the decrease in CBF depend upon an active vasoconstriction process originating in the PH.
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