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, R Lufkin
1992 Journal of Neuroscience  
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
more » ... d 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. We found that eye movements were significantly reduced in cataplexy relative to eye movements in waking periods preceding cataplectic attacks and relative to eye movements at REM sleep onset and during REM sleep. We hypothesize that cataplexy is a result of the pathological waking activity of neurons that are normally selectively active in relation to the muscle tone suppression of REM sleep, combined with the sudden reduction of activity in brainstem neurons that are active in both REM sleep and waking. We have found REM-cataplexy-on cells in the medial
doi:10.1523/jneurosci.12-05-01640.1992 pmid:1578258 fatcat:77cusxg37naqxav3g5otp23mfe