Active medullary control of atonia in week-old rats.
Muscle atonia is a central feature of adult REM sleep which has recently been demonstrated to be a component of sleep in rats as young as 2 days of age (P2). The neural generation of atonia, which depends on mesopontine and medullary structures, is not fully understood in adults and has never been described in infants. In the present experiments we used electrical stimulation in decerebrated pups to identify an inhibitory area within the medial medulla of P7-10 rats. Muscle tone inhibition was consistently found on or near the midline within the ventromedial medulla, dorsal to the inferior olive, in an area that includes the nucleus gigantocellularis, nucleus paramedianus, and raphe obscurus. Chemical infusions in the same region revealed inhibitory responses to quisqualic acid but not to carbachol or corticotropin-releasing factor. Next, extracellular recordings within the medullary inhibitory area revealed neurons with atonia-on profiles; tone-on neurons were also found, typically at more lateral sites. Finally, in non-decerebrated pups, chemical lesions within the inhibitory area resulted in significant reductions in atonia durations, as well as decoupling of atonia from a second component of infant sleep, myoclonic twitching; specifically, twitches occasionally occurred during periods of high muscle tone, a condition reminiscent of "REM without atonia" as described in adults. In summary, we document the existence of an area within the ventromedial medulla of infant rats that (i) causes atonia when stimulated; (ii) contains units that exhibit atonia-related discharge profiles during sleep-wake cycling; and (iii) when lesioned, results in the partial loss of atonia and decoupling of the components of sleep. All together, these findings demonstrate that muscle atonia is actively regulated very early in ontogeny.
Karlsson
K A
KA
Program in Behavioral and Cognitive Neuroscience, Department of Psychology, E11 Seashore Hall, University of Iowa, Iowa City, IA 52242, USA.
Blumberg
M S
MS
D000200:Action Potentials / Q000187:drug effects / Q000528:radiation effects; D000704:Analysis of Variance; D000818:Animals; D000831:Animals, Newborn; D003346:Corticotropin-Releasing Hormone / Q000494:pharmacology; D003655:Decerebrate State / Q000503:physiopathology; D004558:Electric Stimulation / Q000379:methods; D004576:Electromyography / Q000379:methods; D018690:Excitatory Amino Acid Agonists / Q000494:pharmacology; D005260:Female; D008297:Male; D008526:Medulla Oblongata / Q000187:drug effects / Q000502:physiology* / Q000528:radiation effects; D009123:Muscle Hypotonia / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology; D009129:Muscle Tonus / Q000187:drug effects / Q000502:physiology* / Q000528:radiation effects; D009433:Neural Inhibition / Q000187:drug effects / Q000502:physiology / Q000528:radiation effects; D016318:Quisqualic Acid / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D011930:Reaction Time / Q000187:drug effects / Q000502:physiology / Q000528:radiation effects; D013268:Stimulation, Chemical
D018690:Excitatory Amino Acid Agonists; D016318:Quisqualic Acid; D003346:Corticotropin-Releasing Hormone