Journal of Neuroscience, Vol 12, 1640-1646, Copyright © 1992 by Society for Neuroscience
Activity of medial mesopontine units during cataplexy and sleep-waking states in the narcoleptic dog
JM Siegel, R Nienhuis, HM Fahringer, C Chiu, WC Dement, E Mignot and R Lufkin
VAMC, Sepulveda, California 91343.
Narcolepsy has been hypothesized to be a disease of rapid eye movement
(REM) sleep. According to this hypothesis, cataplexy is a result of the
triggering during waking of the mechanism that normally serves to suppress
muscle tone in REM sleep. REM sleep control mechanisms have been localized
to the pons. Narcoleptic dogs have increased numbers of cholinergic
receptors in the medial pons. These findings suggest that neurons mediating
the triggering of cataplexy might be located in medial pontine regions. In
the present study, this hypothesis has been investigated by recording the
discharge of units in the medial mesopontine region of the narcoleptic dog.
Unit activity was examined in the nucleus reticularis pontis oralis,
caudalis, and central gray, with each cell being recorded during both
cataplexy and sleep states. Maximal discharge rates were observed, in all
of these regions, during active waking states (mean rate, 45.3/sec) and REM
sleep (16.0/sec), with minimal discharge rates in non-REM sleep (8.3/sec).
Unit discharge was reduced in cataplexy relative to precataplexy periods.
Cataplexy discharge rates were 8.3/sec, 52% of the mean REM sleep rate.
Cataplexy discharge rates were also significantly lower than those at REM
sleep onset. Cataplexy discharge rates were comparable to rates in quiet
waking and non-REM sleep. While medial mesopontine neurons discharge at
high rates in REM sleep, they have little or no activity in cataplexy. We
interpret the lack of activation of medial mesopontine units in cataplexy
as indicating that the characteristic phasic motor activation of REM sleep
does not occur in this state.(ABSTRACT TRUNCATED AT 250 WORDS)
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