Differential effects of sodium butyrate and physostigmine upon the activities of para-sleep in acute brain stem preparations
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TL;DR
The electrical stimulation to NRPO suppressed the NRPC spikes during PS which appeared spontaneously or were induced by injection of physostigmine or butyrate in the prepontine cat.
Abstract
The differential effects of sodium butyrate and physostigmine sulfate in inducing the pontine (NRPC) spike bursts and REM characteristic of PS were studied in cats with transections or lesions at different levels of the pons. The preparations were made by: (1) transection at the midpontine pretrigeminal level (MPT cat); (2) prepontine decerebration and transection between the pons and the medulla (IP preparation); and (3) prepontine decelebration (prepontine cat). The pontine-lesioned preparations were also made by bilateral electrolytic destructions of the rostroventral portions (RPL cat) or the caudodorsal portions (CPL cat) of the pons. The bursts of NRPC spikes and REM were induced by intravenous injection of physostigmine (0.05 mg/kg) and continued for 10–150 min (mean= 67 min; N = 69) in the MPT cat, for 17–120 min (mean= 44 min; N = 25) in the RPL cat and for 40–170 min (mean= 80 Min; N = 23) in the IP preparation. A similar phase of NRPC spike bursts with a duration of 7–73 min (mean= 26 min; N = 22) was induced by injection of butyrate (1.5mM/kg) in the IP preparation but not in the MPT and RPL cats. This effect of butyrate of physostigmine in inducing NRPC spike burst and REM was suppressed by injection of atropine sulfate (0.1 mg/kg) in the IP preparation. The electrical stimulation to NRPO suppressed the NRPC spikes during PS which appeared spontaneously or were induced by injection of physostigmine or butyrate in the prepontine cat. The mechanisms of induction of the activities characteristic of PS are discussed.
