Abstract
Preliminary pharmacological studieshave suggested that the most prominent electroencephalographic events of mammalian slow-wave sleep (SWS) – slow waves and spindles – and the most prominent electroencephalographic feature of reptilian sleep – a high voltage (up to 200 µV), fast (up to 150 msec) spike – may respond similarly to centrally acting drugs. To further evaluate the correspondence between mammalian SWS and reptilian spikes, atropine sulfate, a centrally acting cholinergic blocking agent which increases slow waves in mammals, was administered to ten tortoises, Geochelone carbonaria, chronically implanted for electroencephalogram and electrocardiogram recordings. Five of these animals also received atropine methyl nitrate, a peripherally acting cholinergic blocker. Both drugs were administered in a dose of 1.0–1.5 mg/kg. Baseline recordings and recordings after saline injection were made for each animal. Recording sessions under each condition were 48 h long and were counterbalanced with respect to order.A dramatic increase in spike activity was seen within 4–12 h after atropine sulfate administration relative to saline injection (p<0.02). By hours 37–48 postinjection there was no significant statistical difference in spike rates between saline and atropine sulfate conditions. Atropine methyl nitrate had no statistically significant effect upon spike rates for the first 12 h postinjection. Baseline rates of spiking and spike rates after saline injection were not significantly different. A dissociation between electroencephalographic activity and behavior after atropine sulfate administration was not seen.These results support the analogy of mammalian SWS and reptilian spikes. Both are increased after administration of atropine sulfate, and both are centrally mediated phenomena. Whether reptilian spikes and mammalian SWS have a similar functional significance, however, cannot be determined without further study.