Journal of Neurophysiology

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Does the ascending cholinergic projection inhibit or excite neurons in the rat thalamic reticular nucleus?

Y. Kayama, I. Sumitomo, T. Ogawa


In rats anesthetized with urethan, neuronal activity was recorded in those portions of the thalamic reticular nucleus (TR) excitable by visual, somatosensory, or auditory input. Observations were made on changes in rate and pattern of discharge of these neurons during repetitive stimulation of the laterodorsal tegmental nucleus (LDT), which is composed of cholinergic neurons projecting to the thalamus. In general, TR neurons showed spontaneous activity consisting of sporadic bursts of several spikes and responded to sensory stimulation with bursts of spikes which repeated several times. Weak LDT stimulation depressed or eliminated the occurrence of both spontaneous and evoked burst discharges. When LDT stimulation was sufficiently strong, however, the majority of TR neurons resumed their tonic discharges. In some animals the cortical EEG was recorded simultaneously with unit recording in TR. Suppression of burst discharges in TR was obtained even with LDT stimulation weaker than the threshold for desynchronizing the EEG. The induction of tonic discharge, on the other hand, required stimulation strong enough to produce desynchronization. The effects of LDT stimulation, such as the suppression of bursts and the induction of tonic discharge, were mimicked by acetylcholine and were antagonized by scopolamine, both drugs being applied ionophoretically. Cooling of the visual cortex abolished LDT-induced tonic discharges of visual TR neurons. A recent report and our preliminary observation show that, when the resting potential is relatively hyperpolarized, TR neurons generated a burst of spikes superposed on a low-threshold broad spike, which is inactivated and replaced with tonic firing by depolarization. Supported by these facts, the present results suggest that cholinergic input depolarizes TR neurons directly and that further depolarization occurs indirectly via activated cortex when the LDT stimulation is sufficiently strong to desynchronize EEG.