There were no differences between the left and right sides of the brainstem. == Conversation == The present paper deals with sleep organization and control mechanisms related to PS/REM sleep after acute MI. was counted in the second, parallel experiment on DC_AC50 6 MI and 6 sham rats. Compared to the sham controls, MI rats displayed longer latency to sleep onset, shorter latency to paradoxical sleep (PS), and curtailed PS period. The number of ChAT-positive neurons in the pedunculopontine tegmentum (PPT) area of MI rats was significantly decreased compared to the sham DC_AC50 controls, while the quantity of laterodorsal tegmentum (LDT) cholinergic neurons was not different. == Conclusion: == Acute MI is usually accompanied, within 2 weeks, by PS-specific insomnia that can be explained, at least partly, by a specific loss of cholinergic neurons in an area known to control PS. == Citation: == Bah TM; Laplante F; Wann BP; Sullivan R; Rousseau G; Godbout R. Paradoxical sleep insomnia and decreased cholinergic neurons after myocardial infarction in rats.SLEEP2010;33(12):1703-1710. Keywords:Paradoxical sleep, myocardial infarction, acetylcholine, depressive disorder, rat, model ACUTE MYOCARDIAL INFARCTION (MI) Is usually FOLLOWED, WITHIN A FEW MONTHS, BY MAJOR Depressive disorder IN 15% to 30% OF PATIENTS.1WE RECENTLY replicated this phenomenon in a rat model in which behavioral signs of depression, such as despair and anhedonia, were encountered 2 weeks after MI and reversed by antidepressant treatments.24In humans, depression is also accompanied by sleep disorders, including difficulties initiating and maintaining sleep, less slow wave sleep (SWS) together with facilitation of quick eye movement (REM) sleep, also identified as paradoxical sleep (PS).5These sleep disorders have also been documented in rat models of depression, such as learned helplessness,6chronic moderate stress,7olfactory bulbectomy,8the Flinders Sensitive Line,9and the neonatal clomipramine model of endogenous depression.10The present studies were undertaken to verify if the post-MI rat model of depression3replicates the sleep findings reported in other animal models of depression and whether brainstem cholinergic neurons, known to be involved in PS control, are also targeted. Our hypotheses were that 2 weeks after MI and compared to sham-operated controls, MI rats would show: (a) increased sleep latency; (b) decreased total sleep time; (c) diminished SWS; (d) reduced latency to PS; and (e) greater total time spent in PS. == METHODS == == Experiment 1: Sleep Recording == This experiment was performed to characterize sleep architecture after MI in rats. == Animals == Sixteen adult male Sprague-Dawley rats weighing 350-375 g were acquired through regular trade (Charles Rivers, St-Constant, Quebec, Canada) and housed individually under standard conditions of 12/12-h light/dark cycles with light onset at 08:00, heat 21-25C, relative humidity 40%-50%, food and waterad libitum. All procedures described below were conducted according to Canadian Council on F2RL1 Animal Care guidelines and were approved by the animal ethics committee of the Biomedical Research Centre at Hpital du Sacr-Coeur de Montral. == Surgical Procedures == == Sleep == The animals were first anesthetized with ketamine/xylazine (50 mg/kg i.m. and 5 mg/kg i.m., respectively), then managed on isoflurane (1%-1.5%) ventilation. Body temperature was controlled by rectal probe connected to a thermostat-equipped heating pad set at 37C. EEG electrodes were situated bilaterally with stainless steel screws (diameter = 1.2 mm) DC_AC50 in the skull bone over the sensorimotor and frontal cortices; a reference electrode was placed at midline over the cerebellum. Three EMG electrodes, made of fine, flexible, Teflon-coated wire loops (diameter = 0.2 mm, bared 2 mm along the loop), were sown between the levator scapulae dorsalis and acromiotrapezius neck muscle tissue; pairs of EMG electrodes were.