Spinal motoneuron distress during experimental allergic encephalomyelitis.

The main pathophysiological feature characterizing multiple sclerosis (MS) is demyelination. However, the possibility of neural damage has recently been proposed as a mechanism in chronic disease. Experimental allergic encephalomyelitis (EAE) is the most widely used experimental model for MS. We investigated occurrences of microglial activation and astrocytosis in the spinal cord, choline acetyl-transferase (ChAT) and calcitonin gene-related peptide (CGRP) mRNA regulation in spinal motoneurones during EAE. EAE was induced in female Lewis rats by injecting guinea pig spinal cord tissue in complete Freund's adjuvant (CFA) to which heat-inactivated Mycobacterium had been added. Rats injected with CFA and uninjected rats were used as controls. ChAT and CGRP mRNAs were studied by in situ hybridization in the lumbar spinal cord and a computerized grain counting procedure was used for quantification. No differences in ChAT mRNA level were found between control and CFA-injected rats. ChAT mRNA level was strongly reduced in EAE 14 days after immunization and then recovered (29 days after immunization). CGRP mRNA increased 14 days after immunization, and then recovered to control level. Extensive long-lasting gliosis developed in the spinal cord and around motoneurones and a transient expression of p75LNGFR in motoneurones was also found. These data suggest that during EAE, gliosis induces distress in spinal cord neurones involving the synthesis enzyme for the main transmitter.