These effects were not due to cholinergic neurotransmission, persisted during partial blockade of gap junctions and were mediated, in part, by AMPAergic transmission. When the light was turned off motoneuron firing and locomotor frequency both transiently increased. Illumination of the lumbar cord in mice expressing eNpHR or Arch in ChAT + or Isl1 + neurons, depressed motoneuron discharge, transiently decreased the frequency, and perturbed the phasing of the locomotor-like rhythm. We assessed the role of motoneuron firing during ongoing locomotor-like activity in neonatal mice expressing archaerhopsin-3 (Arch), halorhodopsin (eNpHR), or channelrhodopsin-2 (ChR2) in Choline acetyltransferase neurons (ChAT +) or Arch in LIM-homeodomain transcription factor Isl1 + neurons. Motoneurons are traditionally viewed as the output of the spinal cord that do not influence locomotor rhythmogenesis.
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