Abstract
Recent studies reported that a recovery of motoneurons after spinal cord transection at the sacrocaudal level may depend on adaptive alterations of the serotonin 2C (5-HT 2CR) and 2A (5-HT 2CR) receptor function via changes in mRNA editing or protein expression, respectively. It has been suggested that depletion of serotonergic input may drive these adaptations. Here, mRNA editing and/or expression of 5-HT 2CR and 5-HT 2AR was evaluated in rats that sustained a complete transection at the thoracic (T10) level. While 5-HT 2AR mRNA expression was upregulated below the site of spinal cord injury (SCI), no changes in 5-HT 2CR mRNA editing or expression were detected. These findings argue against the hypothesis that 5-HT 2CR editing is regulated by extracellular serotonin levels. Rather, it appears that the editing process is just one of the ways in which excitability of motor neurons can be restored following SCI. To this end, the influence of excitatory locomotor circuits on motor neurons in the thoracic spinal cord of rats requires further exploration.
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