ELECTRICAL-STIMULATION OF THE CHOLINERGIC LATERODORSAL TEGMENTAL NUCLEUS ELICITS SCOPOLAMINE-SENSITIVE EXCITATORY POSTSYNAPTIC POTENTIALS IN MEDIAL PONTINE RETICULAR-FORMATION NEURONS

A large and consistent body of data implicates mesopontine cholinergic neurons in the production of rapid eye movement sleep, and indicates that many rapid eye movement sleep events are mediated by activation o f pontine reticular formation neurons. There is anatomical evidence fo r projections from the mesopontine cholinergic nuclei to the pontine r eticular formation, but no study has shown that stimulation of this ch olinergic zone produces excitatory postsynaptic potentials in pontine reticular formation neurons. In the present study, intracellular recor dings were made from 168 pontine reticular formation neurons, identifi ed by antidromic activation from the bulbar reticular formation and by neurobiotin intracellular labeling, in acutely anesthetized cats. The effects of single-pulse electrical stimulation of the laterodorsal te gmental nucleus portion of the ipsilateral mesopontine cholinergic zon e were evaluated in these neurons. Under urethane anesthesia this stim ulation produced, in 21 of 22 recorded neurons, long-latency excitator y postsynaptic potentials (mean = 3 ms), consistent with the conductio n velocity of unmyelinated cholinergic fibers (measured conduction vel ocity was 2 m/s). This excitatory postsynaptic potential was virtually abolished by intravenous administration of the muscarinic cholinergic receptor blocker scopolamine (n = 40 neurons), and by acute cuts sepa rating the laterodorsal tegmental nucleus and the recorded neurons (n = 40). In contrast, a short-latency excitatory postsynaptic potential (0.7-1.5 ms) was not reduced in amplitude by scopolamine and could sti ll be elicited following acute transverse cuts. Unlike the longer-late ncy excitatory postsynaptic potential, its amplitude was not reduced b y barbiturate anesthesia. These data, suggesting the presence of an ex citatory, cholinergic laterodorsal tegmental nucleus projection to the pontine reticular formation, provide further support to other lines o f evidence implicating mesopontine cholinergic neurons in the producti on of rapid eye movement sleep, and are compatible with a model of rap id eye movement sleep generation in which a key element is mesopontine cholinergic input depolarizing and increasing the excitability of ret icular core neurons.