Abstract(s)
The main axons of mammalian sensory neurons are usually viewed as passive transmitters of sensory information. However, the spindle
afferents of jaw-closing muscles behave as if action potential traffic along their central axons is phasically regulated during rhythmic jaw
movements. In this paper, we used brainstem slices containing the cell bodies, stem axons, and central axons of these sensory afferents to
show that GABA applied to the descending central (caudal) axon often abolished antidromic action potentials that were elicited by
electrical stimulation of the tract containing the caudal axons of the recorded cells. This effect ofGABAwas most often not associated with
a change in membrane potential of the soma and was still present in a calcium-free medium. It was mimicked by local applications of
muscimol on the axons and was blocked by bath applications of picrotoxin, suggesting activation of GABAA receptors located on the
descending axon. Antidromic action potentials could also be blocked by electrical stimulation of local interneurons, and this effect was
prevented by bath application of picrotoxin, suggesting that it results from the activation of GABAA receptors after the release of
endogenous GABA. We suggest that blockage is caused mainly by shunting within the caudal axon and that motor command circuits use
this mechanism to disconnect the rostral and caudal compartments of the central axon, which allows the two parts of the neuron to
perform different functions during movement.