Abstract
Motoneurons (MNs) are the output neurons from the central nervous system and their activities cause muscles to contract. In addition to their peripheral axons MNs have central collaterals that contact Renshaw cells (RCs) that provide recurrent inhibition to MNs. It has been a general notion that acetylcholine is the only transmitter released from MN synapses both peripherally and centrally. In this study, we re-examined the physiological nature of the MN-RC synapse using glutamic acid decarboxylase-green fluorescence protein (GAD67-GFP) knock-in mouse neonates (Tamamaki et al. J Comp Neurol (2003) 467:60-79). We performed whole cell recordings from visually identified GABAergic neurons in the lumbar ventral horn using isolated spinal cord preparations. Patched neurons were identified as RCs as electrical stimulation of the ventral root evoked short latency (<5 ms) excitatory postsynaptic currents (EPSCs). These EPSCs were reduced to about 35% of control by blocking nicotinic receptors with mecamylamine or d-tubocurarine. Antagonists for ionotropic glutamate receptors, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and D-(-)-2-amino-5-phosphonopentanoic acid (AP5), further reduced the EPSC to 10% of control. Furthermore, by using immunohistochemical methods, we found vesicular glutamate transporter 2 (VGLUT2) colocalized with MN axon terminals. These results indicate that mammalian spinal MNs, in addition to acetylcholine, co-release glutamate to excite RCs. [Jpn J Physiol 55 Suppl:S173 (2005)]
