Summary.
In decerebrate cats stretch reflexes from the ankle extensors have been studied in 100 fibres from dissected ventral root filaments. These reflexes have been maximally facilitated by post‐tetanic potentiation, as describthd by Granit (1956 a).
In the post‐tetanic or potcwtiated state the reflexes to a constant 10 mm stretch haw been found to fall into two main categories: (i) tonic reflexes which go on firing for a long duration in maintained stretch and (ii) phasic ones which only fire one or two spikes on the rising phase of stretch, in spite of any amount of post‐tetanic potentiatioit.
Analysis of spike size showed that the tonic ventral horn cells tended to fire smaller spikes than the phasic ones. From this it was concluded that the tonic motoneurones tend to group themselves among the smaller ventral horn cells.
The difference between tonic and phasic ventral horn cells was maintained when the extensor tonus was raised by decortications of the anterior lobe of the cerebellum.
In anaesthetized cats the activities of Renshaw cells (RCs) and Ia-inhibitory interneurones (IaINs) were recorded during the accumulation of tetanus toxin in the spinal cord following injection into the gastrocnemius muscle. The early response of the RCs increased during the period of development of local tetanus. With some cells there was a subsequent decrease in the early response in later periods of the observation time (16-44 hrs after intramuscular injection). The effects on the spontaneous activity of the RCs were in good correspondence to those on the early response. The hyperactivity of the RCs is proposed to be mediated mainly via disinhibited cholinergic gamma-motoneurones using muscarinic postsynaptic receptors. The "pause" which follows the early response and the recurrent inhibition of IaINs was not reduced during the development of local tetanus. These results indicate that the central action of tetanus toxin in local tetanus does not consist of a general loss of postsynaptic inhibition. It is suggested that tetanus toxin acts mainly on synaptic elements of the alpha- and gamma-motoneurones or on presynaptic nerve terminals in their vicinity. In later periods of disturbing influence on the cholinergic transmission at Renshaw cells seems to occur.
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