LOCOMOTOR-RELATED PRESYNAPTIC MODULATION OF PRIMARY AFFERENTS IN THE LAMPREY

Presynaptic modulation of sensory afferent transmission during rhythmi c motor activity was investigated in the lamprey spinal cord in vitro. Intracellular recordings were performed from the somata and axons of the glutamatergic sensory neurons from the skin (dorsal cells) during locomotor activity induced by N-methyl-D-aspartate (NMDA). Dorsal cell s were phasically depolarized during each ipsilateral ventral root bur st. In some soma recordings no or only small amplitude depolarizations were seen, although intracellular recording of their axons revealed t he existence of large depolarizations, suggesting that the input synap ses are located on the axons. The amplitude of the depolarizations inc reased during intracellular injection of hyperpolarizing current. The amplitude of the depolarizations increased when the frequency of the l ocomotor rhythm was increased by elevating the NMDA concentration. The depolarizations were not blocked by specific GABA(A) (bicuculline) or GABA(B) (phaclofen and saclofen) antagonists. To investigate whether the phasic depolarization may influence the monosynaptic excitatory tr ansmission to giant interneurons, the amplitude of the monosynaptic ex citatory postsynaptic potential (EPSP) was compared between the onset of the ipsilateral locomotor burst and the burst mid-point. The compou nd monosynaptic EPSP evoked from dorsal column was significantly small er during the peak depolarization than at burst onset. The reduction o f the amplitude of the EPSPs was not associated with any change of the membrane potential or input resistance of the giant interneurons, sug gesting that this effect is mediated by a presynaptic mechanism. Phase -dependent effects were also seen on burst and cycle duration followin g dorsal column stimulation. Thus, the locomotor-related depolarizatio ns in dorsal cell axons may represent a mechanism for a phasic gain co ntrol of sensory transmission during fictive locomotion.