Corticofugal action on transmission of group I input from the hindlimb to the pericruciate cortex in the cat.

AUTOR(ES)

McIntyre, A K

RESUMO

1. In cats anaesthetized with alpha-chloralose, evidence was sought for a corticofugal action on input from muscle group I afferents projecting to the cerebral cortex via the brain stem relay at nucleus Z. 2. Extracellular recordings were made of responses of thirty-four nucleus Z neurones which could be activated by stimuli at group I strength applied to each of a variety of hindlimb muscle nerves. Afferent input to each nucleus Z neurone was restricted to a single muscle. 3. Nucleus Z neurones typically showed a resting discharge which could be increased or decreased by altering the amount of stretch on the muscle which was the source of the afferent input. Ventral root stimulation gave response patterns which showed these neurones to be driven by input from either tendon organs or muscle spindles, but not both. 4. A brief train of focal, cathodal stimuli applied to a discrete region of pericruciate cortex could consistently inhibit the maintained activity evoked by muscle stretch in nucleus Z neurones, or the response evoked by stimulation of the muscle nerve at group I strength. The inhibition was powerful and lasted 50-400 ms. The effective stimulating site corresponded to area 3a, the main cortical receiving area for hindlimb muscle group I input. 5. Since the ascending spinal axons which project to nucleus Z are collaterals of dorsal spinocerebellar tract fibres, it was possible to stimulate the parent axons at their termination in the anterior lobe of the cerebellum. Cortical stimulation was found to have little or no effect on activity in nucleus Z neurones evoked by cerebellar stimulation over conditioning-test intervals in the range 10-200 ms. 6. It is concluded that over the time intervals for which it has been tested, corticofugal inhibitory action appears to be largely operating at the first spinal segmental relay, in Clarke's column. Thus the inhibitory action arising in area 3a of the cerebral cortex will suppress the action of input from hindlimb group I fibres at the level both of the cerebellum and the cerebral cortex.

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