DISCHARGE PROPERTIES OF MEDULLARY RETICULOSPINAL NEURONS DURING POSTURAL CHANGES INDUCED BY INTRAPONTINE INJECTIONS OF CARBACHOL, ATROPINE AND SEROTONIN, AND THEIR FUNCTIONAL LINKAGES TO HINDLIMB MOTONEURONS IN CATS

The present study was aimed at elucidating the pontomedullary and spin al cord mechanisms of postural atonia induced by microinjection of car bachol and restored by microinjections of serotonin or atropine sulfat e into the nucleus reticularis pontis oralis (NRPo). Medullary reticul ospinal neurons (n = 132) antidromically activated by stimulating the L1 spinal cord segment were recorded extracellularly. Seventy-eight of them were orthodromically activated with mono- or disynaptic latencie s by stimulating the NRPo area at the site where carbachol injections effectively induced postural atonia. Most of these reticulospinal neur ons (71 of 78) were located in the nucleus reticularis gigantocellular is (NRGc). Following carbachol injection into the NRPo, discharge rate s of the NRGc reticulospinal neurons (29 of 34) increased, while the a ctivity of soleus muscles decreased bilaterally. Serotonin or atropine injections into the same NRPo area resulted in a decrease in the disc harge rates of the reticulospinal neurons with a concomitant increase in the levels of hindlimb muscle tone. Membrane potentials of hindlimb extensor and flexor alpha motoneurons (MNs) were hyperpolarized and d epolarized by carbachol and serotonin or atropine injections, respecti vely. In all pairs of reticulospinal neurons and MNs (n = 11), there w as a high correlation between the increase in the discharge rates and the degree of membrane hyperpolarization of the MNs. Spike-triggered a veraging during carbachol-induced atonia revealed that inhibitory post synaptic potentials (IPSPs) were evoked in 15 MNs by the discharges of nine reticulospinal neurons. Four of them evoked IPSPs in more than o ne MN. The mean segmental delay and the mean time to the peak of IPSPs were 1.6 ms and 2.0 ms, respectively. Axonal trajectories of reticulo spinal neurons (n = 6), which evoked IPSPs in MNs, were investigated i n the lumbosacral segments (L1-S1) by antidromic threshold mapping. Th e stem axons descended through the ventral (n = 2) and ventrolateral ( n = 4) funiculi in the lumbar segments. All axons projected their coll aterals to the intermediate region (laminae V, VI) and ventromedial pa rt (laminae VII, VIII) of the gray matter. All these results suggest t hat the reticulospinal pathway originating from the NRGc is involved i n postural atonia induced by pontine microinjection of carbachol, and that the pathway is inactivated during the postural restoration induce d by subsequent injections of serotonin or atropine. It is further sug gested that the pontine inhibitory effect is mediated via segmental in hibitory interneurons projecting to MNs.