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Am J Physiol Regul Integr Comp Physiol 279: R1590-R1598, 2000;
0363-6119/00 $5.00
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Vol. 279, Issue 5, R1590-R1598, November 2000

An ether stressor increases REM sleep in rats: possible role of prolactin

B. Bodosi1, F. Obál Jr.1, J. Gardi2, J. Komlódi1, J. Fang2, and J. M. Krueger2

1 Department of Physiology, Albert Szent-Györgyi Medical University, 6720 Szeged, Hungary; and 2 Department of Veterinary and Comparative Anatomy, Pharmacology and Physiology, Washington State University, Pullman, Washington 99164-6520

Sleep alterations after a 1-min exposure to ether vapor were studied in rats to determine if this stressor increases rapid eye-movement (REM) sleep as does an immobilization stressor. Ether exposure before light onset or dark onset was followed by significant increases in REM sleep starting ~3-4 h later and lasting for several hours. Non-REM (NREM) sleep and electroencephalographic slow-wave activity during NREM sleep were not altered. Exposure to ether vapor elicited prolactin (Prl) secretion. REM sleep was not promoted after ether exposure in hypophysectomized rats. If the hypophysectomy was partial and the rats secreted Prl after ether exposure, then increases in REM sleep were observed. Intracerebroventricular administration of an antiserum to Prl decreased spontaneous REM sleep and inhibited ether exposure-induced REM sleep. The results indicate that a brief exposure to ether vapor is followed by increases in REM sleep if the Prl response associated with stress is unimpaired. This suggests that Prl, which is a previously documented REM sleep-promoting hormone, may contribute to the stimulation of REM sleep after ether exposure.

hypophysectomy; immunoneutralization; pituitary


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