Anaclet C, Pedersen NP, Lu J (2008) Medullary circuitry regulating trigeminal motor nucleus phasic activity during rapid eye movement sleep in the rat. Neuroscience 2008 Abstracts 784.16/RR67. Society for Neuroscience, Washington, DC.
Summary: Rapid Eye Movement (REM) sleep or paradoxical sleep is characterized by activation of the cortical and hippocampal EEG, atonia of postural muscles (neck and limbs), and phasic movements of cranial muscles (eyes, chin, ears and whiskers). We have previously established that glutamatergic neurons of the sublaterodorsal tegmentual nucleus (SLD) play a critical role in generating postural muscle atonia during REM sleep. It has been further proposed that the SLD produces REM motor atonia by stimulating spinal inhibitory neurons, which in turn inhibit spinal motor output neurons. It is not known however whether the SLD is also involved in the regulation of tonic and phasic events of cranial muscles during REM sleep (e.g., rapid eye movement, phasic masseter activation). Previous studies have shown that the supraolivary medulla (SOM, dorsal to the inferior olive) and parvocellular reticular (PCRt) nucleus in the medullary reticular formation project to relevant cranial motor nuclei, including: the trigeminal motor nucleus (Mo5), retroabducens region, facial nucleus (Mo7) and hypoglossal nucleus (Mo12). It is therefore possible that either the SOM or the PCRt (or both) may also be involved in regulating cranial muscle activity in REM sleep. To identify the cell groups responsible for REM phasic control of cranial motor nuclei, we examined masseter muscle EMG following cell-specific lesions (anti-orexin B IgG-saporin) of the SLD, SOM or PCRt. Following two weeks of surgical recovery, we recorded the EEG, EMG (neck and masseter muscles) and EOG continuously for two days. Control rats showed significant phasic activation of the masseter muscles, in particular during the second half of REM sleep episodes. This phasic bursting pattern was similar to eye movements during REM sleep. Neither SLD nor PCRt lesions altered the phasic activity of the masseter muscles during REM sleep, although, and as previously reported, SLD lesions did produce REM without atonia in postural muscles. By contrast, lesions in the SOM eliminated phasic activation of the masseter muscles during REM and produced myoclonic twitching of neck muscles. These results indicate that the SOM is involved in the induction of phasic REM activity of masseter muscles, likely via activation of Mo5, whereas SOM projections to the spinal cord are involved in suppression of myoclonic activity of postural muscles.
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