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Cholinergic system in experimental rabies in mice

¹Department of Medicine, Queen's University, Kingston, Ontario, Canada.

Acta Virologica

|December 1, 1993

Summary

Cholinergic system dysfunction is unlikely in rabies, as studies found no significant differences in key enzyme activities or receptor binding in infected mouse brains. This research impacts understanding of rabies neuropathology.

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Area of Science:

Neuroscience
Virology
Biochemistry

Background:

Neuronal dysfunction is a hallmark of rabies.
Cholinergic synaptic neurotransmission defects have been hypothesized as a cause.

Purpose of the Study:

To investigate the role of the cholinergic system in rabies neuropathology.
To assess enzymatic activities and receptor binding in a mouse model.

Main Methods:

Assessed enzymatic activities of choline acetyltransferase (ChAT), acetylcholinesterase (AChE), and enolase.
Measured muscarinic acetylcholine receptor binding using 3H-quinuclidinyl benzylate (QNB).
Compared CVS-infected mice with uninfected controls.

Main Results:

No statistically significant differences in ChAT, AChE, or enolase activities were found in the cerebral cortex or hippocampus.
Muscarinic acetylcholine receptor binding was not significantly different between infected and control groups.

Conclusions:

Cholinergic system dysfunction is unlikely to be fundamentally important in this mouse model of rabies.
The findings suggest alternative mechanisms for neuronal dysfunction in rabies.

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