Lesions of the pedunculopontine tegmental nucleus reduce paradoxical sleep(PS) propensity: evidence from a short-term PS deprivation study in rats

Citation
S. Deurveilher et E. Hennevin, Lesions of the pedunculopontine tegmental nucleus reduce paradoxical sleep(PS) propensity: evidence from a short-term PS deprivation study in rats, EUR J NEURO, 13(10), 2001, pp. 1963-1976
Citations number
74
Categorie Soggetti
Neurosciences & Behavoir
Journal title
EUROPEAN JOURNAL OF NEUROSCIENCE
ISSN journal
0953816X → ACNP
Volume
13
Issue
10
Year of publication
2001
Pages
1963 - 1976
Database
ISI
SICI code
0953-816X(200105)13:10<1963:LOTPTN>2.0.ZU;2-Z
Abstract
Cholinergic neurons in the mesopontine tegmentum are thought to play a crit ical role in the generation of paradoxical sleep (PS). However, no study ha s yet examined whether lesions of these neurons cause deficits of PS in the rat. We describe here the effects of lesions of the pedunculopontine tegme ntal nucleus (PPT) on spontaneous PS and on PS propensity, expressed during and after a short period of PS deprivation. Lesions were induced by bilate ral injections of ibotenate. PS deprivation was performed manually by gentl y waking rats each time they showed polygraphic signs of PS. Two weeks afte r lesions, an 8-h baseline recording was performed; the following day, rats were PS deprived for 6 h and polygraphic recordings were then continued fo r 2 h, to examine recovery sleep. The same protocol was repeated 1 week lat er. Compared with controls and with rats with limited PPT lesions, rats bea ring > 60% NADPH-diaphorase-positive cell loss within the PPT showed unaffe cted PS under baseline conditions. However, they made fewer attempts to ent er PS during deprivation and they exhibited an attenuated rebound increase in PS time after deprivation. The number of PS attempts and the magnitude o f PS rebound were negatively correlated with the percent loss of diaphorase -positive neurons within the PPT. Thus, PS propensity that accumulated as a result of PS deprivation was reduced after extensive PPT lesions. In summa ry, although spontaneous PS was found to be unaltered, the PS deprivation p rocedure used in this study demonstrated the dysfunctioning of PS caused by PPT lesions.