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 lam prey spinal cord can be activated by either N-methyl-D-aspartate (NMDA ) or kainate/AMPA receptors. Serotonin (5-HT) is known to affect the p attern of fictive locomotion induced by NMDA receptor activation by in creasing spike rate within a burst, increasing burst duration, and inc reasing the intersegmental delay. Two cellular mechanisms contribute t o these 5-HT induced effects: The after-hyperpolarization following in dividual action potentials is reduced and the depolarizing plateau ind uced by NMDA is prolonged. Both of these serve as important burst-term inating factors in the locomotor network. In order to isolate these tw o mechanisms, the 5-HT effect on plateau potentials was eliminated by applying 5-HT during fictive locomotion induced by activation of kaina te/AMPA receptors. In the absence of NMDA-mediated plateau potentials, the 5-HT-induced increase in burst duration and cycle period was grea ter than that previously reported during NMDA-induced fictive locomoti on. In addition, the prolonged burst period of a single side was subdi vided 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-sy naptic potentials revealed that, in a proportion of these cells, the b ursting within a single side may be generated solely or predominantely by phasic excitation.