Effects of serotonin on fictive locomotion coordinated by a neural network deprived of NMDA receptor-mediated cellular properties.

The neural network coordinating fictive locomotion in the isolated lamprey spinal cord can be activated by either N-methyl-D-aspartate (NMDA) or kainate/AMPA receptors. Serotonin (5-HT) is known to affect the pattern of fictive locomotion induced by NMDA receptor activation by increasing spike rate within a burst, increasing burst duration, and increasing the intersegmental delay. Two cellular mechanisms contribute to these 5-HT induced effects: The after-hyperpolarization following individual action potentials is reduced and the depolarizing plateau induced by NMDA is prolonged. Both of these serve as important burst-terminating factors in the locomotor network. In order to isolate these two mechanisms, the 5-HT effect on plateau potentials was eliminated by applying 5-HT during fictive locomotion induced by activation of kainate/AMPA receptors. In the absence of NMDA-mediated plateau potentials, the 5-HT-induced increase in burst duration and cycle period was greater than that previously reported during NMDA-induced fictive locomotion. In addition, the prolonged burst period of a single side was subdivided into brief multiple bursts with a shorter cycle period than the control reciprocal burst activity. Intracellular recordings of spinal neurons combined with chloride injection to reverse inhibitory post-synaptic potentials revealed that, in a proportion of these cells, the bursting within a single side may be generated solely or predominantly by phasic excitation.