Some characteristics of the long‐latency component of the evoked muscle response induced by administration of catechol to the anaesthetized rat: a neurophysiological and neuropharmacological investigation

Abstract

1 Administration of catechol to rats anaesthetized with urethane produces a central excitatory state during which an EMG consisting of three temporally distinct components (Ml, M2 and M3) can be recorded from forelimb and hindlimb muscles to electrical stimulation of cutaneous afferents. 2 The probability of occurrence of all three components was measured in flexor and extensor muscles of fore-and hindlimb and showed that the long latency component (M3) occurred less frequently in hindlimb muscles than forelimb and that its probability of occurrence in hindlimb extensors was significantly reduced as compared to flexors. A possible reflex pathway for this long latency component of the EMG is suggested. 3 Phenobarbitone (5 mg kg-l i.v.) had no significant effect on the probability of occurrence of M1, M2orM3. 4 These results suggest that the long latency component (M3) is not due to activation of a spino-bulbo-spinal reflex as has been previously suggested. 5 Cholinoceptor blocking drugs were found to reduce significantly the probability of occurrence of M2 and M3 and anticholinesterases to increase the probability of M2. None of the drugs was found to affect the short latency Ml component of the EMG. These results are discussed in relation to the possible reflex pathways of all three components of the EMG.

Non involvement of γ‐aminobutyric acid in catechol‐induced seizures

“…The characteristics of these three components (M1, M2 and M3) have been described previously (Angel & Dewhurst, 1978;Dewhurst, 1984) and in this study each component was identified by its latency: Ml (4-7ms), M2 (12-18ms), and M3 (30-50ms).…”

“…These resonses which are absent in the non-catechol treated, anaesthetized animal are probably the result of an increased transmission in the dorsal column sensory pathway at the level of the ventrobasal thalamus (Angel, 1969). Ml is probably a propriospinal reflex; M2 is dependent on a long-loop reflex involving the sensorimotor cortex and M3 is possibly a cerebellar reflex (Angel & Lemon, 1973;Dewhurst, 1984).…”

“…Low doses produce a stimulus-sensitive excitatory state during which a variety ofsensory stimuli, e.g. tactile, electrical and auditory, will evoke brief myoclonic jerks (Angel & Lemon, 1973;Dewhurst, 1984). The evoked electromyographic activity associated with these convulsions can be recorded from both flexor and extensor muscles of fore and hindlimbs and typically consists of three temporally distinct components (M 1, M2 and M3), each resulting from activation of a different reflex pathway.…”

“…The mechanism of action of catechol is still largely unknown, although both spontaneous catechol convulsions and those components of the sensory-evoked jerks dependent on supra-spinal structures (M2 and M3) are partially blocked by cholinoceptor blocking drugs (Angel et al, 1977;Angel & Dewhurst, 1978;Dewhurst, 1984) indicating a possible central cholinergic involvement. Several convulsants e.g.…”

Sites and mechanisms of action of catechol (1,2‐dihydroxybenzene) in the rat olfactory cortex slice

“…In rodents, the convulsions evoked by parenterally administered catechol, which are of central origin, occur either spontaneously or in response to sensory stimuli and are characterized by a severe body tremor and brief clonic jerking of the body musculature (Angel & Lemon, 1973a, b;Dewhurst, 1984). Such convulsions are antagonized by cholinoceptor blockers and potentiated by anticholinesterases suggesting that catechol may affect central cholinergic transmission (Angel et al, 1977; Angel & Dewhurst, 1978): this conclusion is indirectly supported by the finding that catechol increases acetylcholine release at the mammalian neuromuscularjunction (Gallagher & Blaber, 1973).…”