Skeletal muscle contraction modulates carbonic anhydrase phenotype in adult mouse dorsal root ganglion neurons.

Recently carbonic anhydrase (CA) activity was demonstrated in adult mammalian proprioceptive neurons of the lumbar dorsal root ganglion (DRG). To assess if neuron-target interactions govern the neuronal CA phenotype, we examined how various experimental procedures which modify the interactions of these neurons with their central and peripheral targets, affect mouse L5 lumbar DRG CA activity. In normal mice and under central disconnection, carbonic anhydrase activity was detected in 30% of neurons. One day after sciatic nerve transaction the percentage of CA-positive neurons decreased to around 50% of that in controls, although both the total number of neurons per ganglion and glial CA content were unchanged. The pattern of CA activity then remained stable until at least 30 days post-operative. All experimental procedures used to block muscle contraction, including ventral rhizotomy, tenotomy, local application to the nerve of both tetrodotoxin and lidocaine or intramuscular injection of the botulinum toxin, produced a significant decrease in neuronal CA staining. Moreover, axonal transport block by vinblastine induced a decrease in CA-positive neurons. These results show that functional neuron-muscle interactions independent of DRG-spinal Cord influences contribute to the regulation of CA activity in lumbar DRG neurons. This modulation could be under the control of unidentified activity-dependent molecular mechanism involving stimuli through the skeletal muscle contraction, inducing in turn, the synthesis of a CA-regulating factor(s) retrogradely transported to the neuronal cell body and/or nuclei.