MUSCLE ATONIA CAN BE INDUCED BY CARBACHOL INJECTIONS INTO THE NUCLEUSPONTIS ORALIS IN CATS ANESTHETIZED WITH ALPHA-CHLORALOSE

Cholinegic excitation of structures in the pontine reticular formation appears to be a key step in the generation of active sleep. For examp le, muscle atonia which occurs as a result of the postsynaptic inhibit ion of motoneurons during active sleep is also present after carbachol , a cholinergic agonist, is injected into the nucleus pontis oralis. I n the present study, in order to obtain information regarding the mech anisms that generate atonia during active sleep and to provide a parad igm for studying atonia in anesthetized cats, we determined whether ch olinergically induced atonia could be generated in an animal that was anesthetized with alpha-chloralose. Cats which were initially anesthet ized with Lu-chloralose(40 mg/kg, I.V.) exhibited spikes in the EEG, h ippocampus and lateral geniculate nuclei. Muscle atonia occurred after carbachol (200 mM) was injected by microiontophoresis (300-500 nA) in to the nucleus pontis oralis; the spikes in the EEG, hippocampus and l ateral geniculate nuclei were still present. We believe that the atoni a induced by carbachol in alpha-chloralose-anesthetized cats is mediat ed by the same mechanisms that operate during active sleep in the unan esthetized animal for the following reasons. First, in the same cats w hen they were not anesthetized with alpha-chloralose, carbachol inject ions in the identical brainstem sites induced active sleep with its ac companying pattern of muscle atonia. Second, after carbachol was injec ted into the same sites in alpha-chloralose-anesthetized cats, intrace llular recordings from lumbar motoneurons revealed that inhibitory pos tsynaptic potentials were bombarding motoneurons; these inhibitory pot entials were similar to those which are present during naturally occur ring active sleep. In addition, stimulation of the nucleus reticularis gigantocellularis (NRGc) was found to induce large amplitude depolari zing potentials in lumbar motoneurons in alpha-chloralose-anesthetized cats prior to the administration of carbachol, whereas after its admi nistration, accompanying muscle atonia there were large amplitude hype rpolarizing potentials and a reduction in the amplitude of depolarizin g potentials. We therefore conclude that the cholinergically induced p rocesses that initiate and maintain muscle atonia are not blocked by t he actions of alpha-chloralose.