Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.1.7 (acetylcholinesterase)
 28,390 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Young adult mice were inoculated in the hind limb with rabies virus or Sindbis virus. Rabies 1820B virus antigen was detected in leg sections by immuno-fluorescence at 1 h post-inoculation at sites comparable in form and distribution to cholinesterase-positive sites, which represent motor end-plates (MEPs). Sites which were rabies virus antigen-positive by immunofluorescence were also cholinesterase- positive on double-stained slides. Rabies CVS virus detected by autoradiography was similarly distributed at 6 h post-inoculation. Uptake of rabies virus at motor nerve endings was confirmed by the detection of rabies antigen by immunofluorescence in ventral horn cells in the spinal cord at 20 h post-inoculation before involvement of dorsal root ganglia. Rabies virus antigen could not be detected at MEPs if the virus had been inactivated by beta propiolactone or mixed with antibody prior to injection or if the sciatic nerve had been cut 7 days earlier, similarly treated groups of mice survived for the observation period of 6 weeks. Rabies virus antigen was found at MEPs in mice given antibody 24 h before virus injection, but virus antigen was not found in the spinal cord, and mice similarly treated survived. Sindbis virus strain Ar86, which like rabies virus is neurotropic in adult mice, was also found at MEPs and in peripheral nerves by autoradiography at 6 h post-inoculation. In contrast to results with rabies virus-infected mice, stimulation of the sciatic nerve for the first hour post-inoculation prevented mortality. Sindbis virus strain Ar339, which is not neurotropic in adult mice, could not be detected at MEP's by immunofluorescence or autoradiography and mice injected with virus survived. The results presented here suggest that rabies virus and perhaps other neurotropic viruses can use the motor axon terminal at the neuromuscular junction as a site of entry into the nervous system.
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PMID:Entry of rabies virus into the peripheral nerves of mice. 703 Nov 82

A defect in cholinergic synaptic neurotransmission could explain the neuronal dysfunction that has been observed in rabies. The enzymatic activities of choline acetyltransferase (ChAT), acetylcholinesterase (AChE), and enolase were assessed in the brains of rabies virus strain CVS-infected and uninfected mice. No statistically significant differences in activities of ChAT, AChE, or enolase were observed in the cerebral cortex or hippocampus of moribund CVS-infected mice versus controls. Binding to muscarinic acetylcholine receptors, which was assessed with 3H-labelled quinuclidinyl benzylate (QNB), was also not significantly different in the cerebral cortex or hippocampus of CVS-infected mice and uninfected controls. The studies suggest that dysfunction of the cholinergic system is unlikely of fundamental importance in this mouse model of rabies.
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PMID:Cholinergic system in experimental rabies in mice. 801 Jan 87