Abstract
The midbrain locomotor region (MLR) is located in the lateral part of the mesopontine tegmentum. Either electrical or chemical stimulation of the MLR first increases the level of postural muscle tone and then initiates locomotion. The MLR receives GABAergic basal ganglia output from the substantia nigra pars reticulata (SNr). The present study was designed to understand synaptic mechanisms acting on motoneurons involved in the basal ganglia control of locomotion. Intracellular recording was made from hindlimb motoneurons (n=47) in two types of decerebrate cats (n=11). One was mesencephalic cats decerebrate at precollicular-postmammilarly level, and the other was hypothalamic cats decerebrated at precollicular-premammilarly level. In mesencephalic cats, short trains of stimuli applied to the MLR (3 pulses, 5 ms intervals, 30-50 μA) induced a sequence of EPSPs and IPSPs. Although stimulation of the SNr (20-60 μA, 50-100 Hz) alone neither changed membrane potentials nor input resistance of motoneurons, it greatly reduced the amplitude of the MLR-induced IPSPs, resulting in an enhancement of the EPSPs. In hypothalamic cats, fictive locomotion, sequences of membrane oscillations with depolarizing and hyperpolarizing phases, was induced in motoneurons. SNr stimuli reduced the hyperpolarizing phases and finally stopped the oscillations of both extensor and flexor motoneurons. These results suggest that enhancement of the basal ganglia output to the brainstem may stop locomotion by suppression of the postsynaptic inhibitory drive acting on motoneurons and initiate locomotion by removal of the inhibition. [J Physiol Sci. 2006;56 Suppl:S93]
