Activity of Renshaw cells during locomotor-like rhythmic activity in the isolated spinal cord of neonatal mice.
In the present study, we examine the activity patterns of and synaptic inputs to Renshaw cells (RCs) during fictive locomotion in the newborn mouse using visually guided recordings from GABAergic cells expressing glutamic acid decarboxylase 67-green fluorescent protein (GFP). Among the GFP-positive neurons in the lumbar ventral horn, RCs were uniquely identified as receiving ventral root-evoked short-latency EPSPs that were markedly reduced in amplitude by nicotinic receptor blockers mecamylamine or tubocurarine. During locomotor-like rhythmic activity evoked by bath application of 5-HT and NMDA, 50% of the recorded RCs fired in-phase with the ipsilateral L2 flexor-related rhythm, whereas the rest fired in the extensor phase. Each population of RCs fired throughout the corresponding locomotor phase. All RCs received both excitatory and inhibitory synaptic inputs during the locomotor-like rhythmic activity. Blocking nicotinic receptors with mecamylamine markedly reduced the rhythmic excitatory drive, indicating that these rhythmic inputs originate mainly from motor neurons (MNs). Inhibitory synaptic inputs persisted in the presence of the nicotinic blocker. Part of this inhibitory drive and remaining excitatory drive could be from commissural interneurons because the present study also shows that RCs receive direct crossed inhibitory and excitatory synaptic inputs. However, rhythmic synaptic inputs in RCs were also observed in hemicord preparations in the presence of mecamylamine. These results show that, during locomotor activity, RC firing properties are modulated not only by MNs but also by the ipsilateral and contralateral locomotor networks.
Nishimaru
Hiroshi
H
Department of Neuroscience, Karolinska Institute, Stockholm S-171 77, Sweden.
Restrepo
Carlos E
CE
Kiehn
Ole
O
D000200:Action Potentials / Q000187:drug effects / Q000502:physiology*; D000818:Animals; D000831:Animals, Newborn; D018690:Excitatory Amino Acid Agonists / Q000494:pharmacology; D019706:Excitatory Postsynaptic Potentials / Q000187:drug effects / Q000502:physiology; D005968:Glutamate Decarboxylase / Q000378:metabolism; D049452:Green Fluorescent Proteins; D007395:Interneurons / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D007527:Isoenzymes / Q000378:metabolism; D008124:Locomotion / Q000187:drug effects / Q000502:physiology*; D051379:Mice; D008822:Mice, Transgenic; D009415:Nerve Net / Q000033:anatomy & histology / Q000187:drug effects / Q000502:physiology*; D009433:Neural Inhibition / Q000187:drug effects / Q000502:physiology; D009434:Neural Pathways / Q000033:anatomy & histology / Q000187:drug effects / Q000502:physiology*; D018733:Nicotinic Antagonists / Q000494:pharmacology; D009924:Organ Culture Techniques; D010507:Periodicity; D012701:Serotonin / Q000494:pharmacology; D013116:Spinal Cord / Q000033:anatomy & histology / Q000187:drug effects / Q000502:physiology*; D013569:Synapses / Q000187:drug effects / Q000502:physiology; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
D018690:Excitatory Amino Acid Agonists; D007527:Isoenzymes; D018733:Nicotinic Antagonists; D049452:Green Fluorescent Proteins; D012701:Serotonin; D005680:gamma-Aminobutyric Acid; D005968:Glutamate Decarboxylase; C402565:glutamate decarboxylase 1