Long-lasting excitability changes of soleus alpha-motoneuron induced by midpontine stimulation in decerebrate,...

Stimulation of the dorsal portion of the caudal tegmental field (DTF) in the pons resulted in hyperpolarization of extensor alpha-motoneurons (alpha-MNs) that persisted for several minutes after cessation of the stimulation. The resulting inhibition of alpha-MN discharge led to a progressive reduction in the number of active motor units. Renshaw cells, persistently active at high levels of extensor muscle tone, were abruptly silenced by DTF stimulation. Active discharge was renewed at the time of cessation of the stimulation but at a frequency reduced in proportion to the persistently lowered level of extensor muscle tone. Ia primary afferents were tonically active during the high extensor tonus of reflex standing. DTF stimulation was accompanied by a brief, slight increase in Ia discharge frequency followed by a reduction in frequency variably correlated to the magnitude of extensor force reduction. Orthodromically elicited Ia EPSPs in the soleus alpha-MNs were reduced in peak voltage, time to peak, and half width during the hyperpolarization accompanying DTF stimulation. All of these parameters recovered beyond their prestimulus values with the cessation of DTF stimulation in spite of the persisting hyperpolarization. Antidromically initiated invasion of the somatodendritic (SD) segment of the motoneuron membrane was delayed and sometimes blocked during DTF stimulation. At the same time, the peak voltage of the SD action potential was reduced. There was an immediate recovery of these changes on termination of DTF stimulation, although the poststimulus hyperpolarization persisted. Intracellular injection of depolarizing current steps during DTF stimulation revealed a depression of membrane excitability that persisted during the hyperpolarization that followed the termination of the DTF stimulation. Depolarizing and hyperpolarizing steps of intracellular current were used to demonstrate a reduction of cellular input resistance during DTF stimulation. The resistance values rapidly returned to prestimulus levels following the cessation of DTF stimulation. It was demonstrated that the degree of resistance change is greater and that the magnitude of DTF-induced hyperpolarization is smaller for low-resistance cells than for high-resistance cells. Iontophoretically induced increase in intracellular Cl- resulted in a reversal of both Ia IPSPs and the hyperpolarization induced by DTF stimulation. The hyperpolarization enduring after DTF stimulation was not affected by the Cl- injection.