[Neuropharmacologic and neurotoxic studies on the Renshaw mechanism].
Recurrent axon collaterals of alpha-motoneurons formed with Renshaw cells cholinergic synapses. The effects of ethanol, pyritinol-HCl and type A botulinum toxin on this central nervous cholinergic synapse were studied. Ethanol caused a marked increase in Renshaw cell activity. The excitatory influence effects above all the Renshaw cell synapses directly. Pyritinol-HCl decreased the activity of Renshaw cells. The increase of Renshaw cell activity, caused by ethanol, changed into a decrease after pyritinol-HCl application so that pyritinol-HCl has a protective effect on this cholinergic system. The injection of the neurotoxin botulinum type A into the muscle or even into the ventral root was without effect on the Renshaw cell activity during the test period. Only the direct application of botulinum toxin type A into the spinal cord led to a decrease of the early and the late response of Renshaw cells. The results are discussed and the clinical relevance is considered. The cholinergic Renshaw cell synapse is not only considered as a special synapse but also as a model for cholinergic transmission which is assumed in several parts of the central nervous system.
D000109:Acetylcholine / Q000378:metabolism; D000818:Animals; D001905:Botulinum Toxins / Q000494:pharmacology; D002415:Cats; D004336:Drug Antagonism; D000431:Ethanol / Q000494:pharmacology; D009045:Motor Endplate / Q000502:physiology; D009046:Motor Neurons / Q000502:physiology*; D011746:Pyrithioxin / Q000494:pharmacology; D011976:Receptors, Muscarinic; D011978:Receptors, Nicotinic; D013116:Spinal Cord / Q000166:cytology*; D013569:Synapses / Q000502:physiology
D011976:Receptors, Muscarinic; D011978:Receptors, Nicotinic; D000431:Ethanol; D011746:Pyrithioxin; D001905:Botulinum Toxins; D000109:Acetylcholine
Neuropharmakoligische und neurotoxische Untersuchungen am Renshaw-Mechanismus.