Aglycemia and ischemia depress monosynaptic and polysynaptic reflexes in neonatal rat spinal cord in vitro by involving different types of 5-hydroxytryptamine receptors

Abstract

Involvement of 5-hydroxytryptaminergic (5-HT) system for aglycemia- and ischemia-induced depression of the spinal reflexes was evaluated. The monosynaptic (MSR) and polysynaptic (PSR) reflex potentials were elicited in the ventral root by stimulating the corresponding dorsal root in an isolated spinal cord from neonatal rat. Superfusion of aglycemic (glucose-free) or ischemic (glucose- and O 2-free) solution produced a time-dependent depression of the spinal reflexes and abolished them within 35 min. The time required to produce 50% depression of the reflexes (T-50) was around 19 and 13 min for aglycemia and ischemia, respectively. Spiperone (5-HT 2A antagonist) and ketanserin, (5-HT 2A/2C antagonist) blocked the aglycemia-induced depression of the reflexes completely while ondansetron (5-HT 3 antagonist) attenuated it partially (as abolition times were around 50 min). Ischemia-induced depression was blocked up to 50 min by ketanserin or ondansetron but not by spiperone. In the presence of ketanserin or ondansetron, the reflexes were abolished by 60 min while in spiperone the reflexes were abolished by 30 min. In 5,7-dihydroxytryptamine treated rats, aglycemia depressed the reflexes by 45 min (greater than control, P < 0.05) while the time for ischemia-induced depression was not different from the control response. The results indicate that aglycemia involves mainly 5-HT 2 receptors while ischemia involves 5-HT 3 receptors.