Selective discharge of pontine neurons during the postural atonia produced by an anticholinesterase in the decerebrate cat
- PMID: 190961
Selective discharge of pontine neurons during the postural atonia produced by an anticholinesterase in the decerebrate cat
Abstract
I. Episodes of postural atonia associated with bursts of REM similar to those which occur spontaneously either in the intact preparation during desynchronized sleep, or in the chronic decorticate or decerebrate preparations, can be elicited in acute decerebrate cats following intravenous injection of small doses of an anticholinesterase. The present experiments were performed in precollicular decerebrate animals in order to identify the pontine neurons which show increases in their firing rate related in time with the appearance of the cataplectic episodes. In particular long-term recordings of single units were obtained before, during and after the episodes of postural atonia produced by i.v. injection of 0.03-0.1 mg/kg of eserine sulphate. Spontaneous discharge rates were used to measure the selectivity of each individual unit, i.e., the tendency of the unit to discharge more during the cataplectic episode than during the postural rigidity. The physiological data obtained from neurons histologically localized in different nuclear groups were then averaged. 2. Neurons localized in the pontine reticular formation as well as in the region of the locus coeruleus and the raphe system showed low rates of discharge when rigidity was present. The same units, however, showed a remarkable increase in firing rate which preceded by several tenths of seconds the onset of postural atonia and lasted throughout the cataplectic episodes. 3. The neurons of the pontine reticular formation had a selectivity which was higher than that of the neurons located in the locus coeruleus-raphe system; moreover the cells of the gigantocellular tegmental field (FTG) had the highest selectivity of all pontine reticular structures studied. 4. The relation of the discharge rate curves to the occurrence of the cataplectic episodes suggests that these neurons constitute output elements of a generator system for postural atonia. It is postulated that these pontine reticular neurons are directly involved in the activation of the bulbospinal inhibitory system, which is finally responsible for the abolition of the decerebrate rigidity. 5. During cataplectic episodes these pontine neurons showed some clustered discharges which appeared in association with bursts of eye movements. In most instances, however, there was no constant relationship of the unit activity to individual eye movements. Moreover large phasic increases in firing rate appeared also during the intervals between successive bursts of REM. 6. The striking increase in firing rate of the FTG neurons observed during the cataplectic episodes cannot be attributed to an increased excitatory input to these neurons. In fact excitatory influences following intense somatic stimulation are unlikely to occur during the cataplectic episodes; moreover the response of these neurons to intense somatosensory stimulations did not reach rates comparable with those occurring spontaneously during the induced cataplectic episodes...
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