| Abstract: | 1. Experiments performed in precollicular decerebrate cats indicate that neurons located in the caudal part of the locus coeruleus and locus subcoeruleus as well as in the surrounding reticular formation were greatly depressed during the cataplectic episodes induced by i.v. injection of 0.1 mg/kg of eserine sulphate. 2. These units actually showed a slow regular firing rate when the rigidity was present. Moreover their firing rate greatly decreased during the episodes of postural atonia produced by the anticholinesterase. In some instances a complete abolition of firing occurred during these episodes. The depression of unit discharge anticipated the onset of postural atonia and lasted throughout the episodes. 3. Some of the neurons described above responded with steady changes in their discharge rate to natural stimulation of macular labyrinthine receptors during postural rigidity. However, the response of these neurons to lateral tilts was suppressed during the episodes of postural atonia induced by the anticholinesterase, This and other arguments suggested that these units were tonically inhibited during the induced cataplectic episodes. 4. The time course of the rate deceleration shown by these neurons during transition from postural rigidity to muscular atonia represents a mirror image of the rate acceleration which affects most of the pontine reticular neurons located in the gigantocellular tegmental field (FTG) during the induced cataplectic episodes. These reciprocal rate relations suggest that a functional interaction exists between the two cell groups. In particular it is postulated that the pontine FTG neurons are self-excitatory and excitatory to the locus coeruleus neurons, while the last neurons may be self-inhibitory and inhibitory to FTG neurons. These findings can be related to previous observations showing that neurons located in the region of locus coeruleus undergo a rate deceleration during desynchronized sleep which mimics the time course of firing to the pontine reticular neurons. 5. In conclusion it appears that the decerebrate rigidity is present in so far as the cholinergic reticular neurons, which trigger the bulbospinal inhibitory system, are tonically inhibited by neurons located in the monoaminergic structures of the dorsolateral pontine tegmentum. On the other hand the suppression of the decerebrate rigidity ,which occurs during the cholinergically induced cataplectic episodes results from activation of the cholinergic reticular neurons, which escape tonic inhibition from monoaminergic structures. |
