Acetylcholinesterase activity and acetylcholine effects in the cerebello-rubro-thalamic pathway of the cat.
Unilateral transections of the brachium conjunctivum (BC) of cats resulted, after 2-3 weeks, in marked loss of acetylcholinesterase (AChE) activity from the contralateral red nucleus (RN) and ventral tier nuclei of the thalamus (VA-VL). Significant changes in activity were not observed in other locations. Sensitivity of RN neurons to iontophoretically applied acetylcholine (ACh) was studied under conditions which should maximize ACh sensitivity, including AChE inhibition, but ACh was found to have only a weak depressant effect on excitability or no effect at all. Intravenous physostigmine usually increased spontaneous activity of RN neurons, and sometimes increased potentials evoked by electrical stimulation of cerebellar nuclei, to a small extent. Anticholinergic drugs were found not to influence such evoked responses, except to reverse the effects of physostigmine. It is concluded that ACh is not a major transmitter in the excitatory cerebello-rubral tract in spite of the relationship of AChE to this pathway.
D000109:Acetylcholine / Q000494:pharmacology*; D000110:Acetylcholinesterase / Q000378:metabolism*; D000818:Animals; D002415:Cats; D002531:Cerebellum / Q000187:drug effects / Q000201:enzymology*; D003714:Denervation; D005071:Evoked Potentials / Q000187:drug effects; D006710:Homocysteine / Q000494:pharmacology; D009434:Neural Pathways / Q000201:enzymology; D009474:Neurons / Q000187:drug effects / Q000201:enzymology; D012012:Red Nucleus / Q000187:drug effects / Q000201:enzymology*; D013787:Thalamic Nuclei / Q000187:drug effects / Q000201:enzymology*
D006710:Homocysteine; D000110:Acetylcholinesterase; D000109:Acetylcholine