Effects of serotonin 1A agonist on acute spinal cord injury

We evaluated the effects of serotonin (5-HT) agonists on in vitro models of spinal cord compressive injury. Evoked potentials in injured rat spinal cords (n=24) were recorded during perfusion with 5-HT agonists.

To evaluate the therapeutic effects of 5-HT agonists on the recovery of compound action potentials in injured spinal cords.

Rat dorsal columns were isolated, placed in a chamber, and injured by extradural compression with a clip. Conducting action potentials were activated by supramaximal constant current electrical stimuli and recorded during perfusion with 5-HT agonists and antagonists.

After inducing compression injuries, mean action potential amplitudes were reduced to 33.9+/-5.4% of the pre-injury level. After 120 min of perfusion with Ringer's solution, the mean amplitudes recovered to 62.8+/-8.4% of the pre-injury level. At a concentration of 100 micro M, perfusion with tandospirone (a 5-HT1A agonist) resulted in a significantly greater recovery of mean action potential amplitudes at 2 h after the injury (86.2+/-6.9% of pre-injury value) as compared with the control Ringer's solution (62.8+/-8.4% of pre-injury value, P<0.05). In contrast, quipazine (a 5-HT2A agonist) accelerated the decrease of amplitude (54.5+/-11.7% of pre-injury value). 5-HT1A and 5-HT2A agonist did not consistently alter latencies of the action potentials.

The 5-HT1A receptor agonist was effective for the recovery of spinal action potential amplitudes in a rat spinal cord injury model.