In homogenates of rabies-infected rat brain the specific binding of a tritium-labelled antagonist of muscarinic acetylcholine (mACh) to mACh receptors (mAChR) varied during the course of infection. A small increase in the binding of the antagonist, quinuclidinyl benzylate (QNB), during the first days after infection was followed by a marked decrease as the symptoms of rabies appeared. Measurements of H-labelled QNB binding in dissected brain regions, i.e. brain stem, caudatus nucleus, cortex, hippocampus, cerebellum and medulla, showed that the decrease in binding was greater in the hippocampus than in any other brain region. We conclude that in the central nervous system (CNS) of the rabies-infected rat neuronal impairment may be one manifestation of rabies pathogenesis.


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