Spontaneous recovery of motor neuron function in the spinal cord and debilitating muscle spasms are seen following spinal cord injury. A specific subtype of serotonin receptors may contribute to recovery and can be targeted to prevent spasms, suggests a report published online in this week's Nature Medicine.
Numerous animal studies have confirmed that following spinal cord injury, motor neuron excitability ― crucial for movement ― can be recovered by stimulating serotonin receptors in the spinal cord through administrating serotonin itself or compounds which activate serotonin receptors.
David Bennett and colleagues found that following spinal cord injury in mice, motor neurons spontaneously regain the ability to support muscle contractions. The findings suggest that a specific subset of neurons may compensate for the lack of serotonin by up-regulating receptors that do not require serotonin for activity, and therefore restoring walking. However, left unabated this also leads to muscle spasms. Bennett and colleagues found that drugs which block continuous activity of these receptors can block muscle spasms in mice and as well as in patients.