The cholinergic agonist carbachol was conjugated to latex microspheres that were fluorescently labeled with rhodamine and used as neuroanatomical probes that show little diffusion from their injection site and retrogradely label neurons projecting to the injection site. Microinjection of this pharmacologically active probe into the gigantocellular field of the cat pontine brain stem caused the awake cats to fall into rapid movement (REM) sleep indistinguishable from that produced by free carbachol. Three-dimensional computer reconstruction of the retrogradely labeled neurons revealed a widely distributed neuronal network in the pontine tegmentum. These pharmacologically active microspheres permit a new precision in the characterization and mapping of neurons associated with the control of behavioral state and of other cholinergic networks.
Rapid eye movement (REM) sleep is characterized by periods of profound cardiac autonomic activation evident in heart rate surges in humans and canines. Our goals were to determine whether or not the heart rate surge phenomenon occurs in cats and to characterize concurrent central nervous system activity. Cortical and hippocampal electroencephalogram, electromyogram, electrooculogram, pontogeniculooccipital (PGO) waves, subcutaneous electrocardiogram, and respiration were recorded. Bouts of sinus tachycardia lasting ≥3.5 s achieved a rate of 210 beats/min and were present predominantly during REM sleep. Heart rate during the surges rose an average of 26.4% from 132.5 ± 2.0 beats/min before the surge to 167.5 ± 2.6 beats/min ( P< 0.001) and returned to 130.7 ± 2.6 beats/min ( P < 0.001). The heart rate surges were invariably accompanied by increased incidence and frequency of hippocampal theta waves and increased PGO wave frequency and incidence of PGO wave clusters and eye movement clusters. The occurrence of surges was dramatically reduced from 0.11 ± 0.03 to 0.01 ± 0.01/15 s of REM sleep ( P = 0.02) by atenolol (0.6 mg/kg iv), indicating that the phenomenon is β1-adrenergically mediated. These findings suggest a coupling between central activation of cardiac sympathetic nerves and the generation of hippocampal theta waves and PGO activity.
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