Brain stem stimulation and the acetylcholine‐evoked inhibition of neurones in the feline nucleus reticularis thalami

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Abstract
In cats anesthetized with halothane and nitrous oxide the responses to iontophoretically applied acetylcholine (ACh) and high-frequency stimulation of the mid-brain reticular formation (MRF) were tested on spontaneously active neurons in the nucleus reticularis thalami and underlying ventrobasal complex. The initial response to MRF stimulation of 90% of the ACh-inhibited neurons found in the region of the dorsolateral nucleus reticularis was an inhibition; the initial response of 82% of the ACh-excited neurons in the ventrobasal complex was an excitation. Neurons in the rostral pole of the nucleus reticularis were inhibited by ACh and RMF stimulation. The mean latency (and standard error of the mean) for the MRF-evoked inhibition was 13.7 .+-. 3.2 ms (n = 42) and that for the MRF-evoked excitation, 44.1 .+-. 4.2 ms (n = 35). The ACh-evoked inhibitions were blocked by iontophoretic atropine in doses that did not block amino acid-evoked inhibition. In 24 ACh-inhibited neurons the effect of iontophoretic atropine was tested on MRF-evoked inhibition. In all 24 neurons atropine had no effect on the early phase of MRF-evoked inhibition, but weakly antagonized the late phase of inhibition in 9 of 14 neurons. Interspike-interval histograms showed that the firing pattern of neurons in the nucleus reticularis was characterized by periods of prolonged, high-frequency bursting. The ACh-evoked inhibitions and the late phase of MRF-evoked inhibitions were accompanied by an increased burst activity; iontophoretic atropine tended to suppress burst activity. The possibility was discussed that electrical stimulation of the MRF activates an inhibitory cholinergic projection to the nucleus reticularis. Since neurons of the nucleus reticularis inhibit thalamic relay cells, activation of this inhibitory pathway may play a role in MRF-evoked facilitation of thalamo-cortical relay transmission and the associated electrocortical desynchronization.