Endogenous activation of metabotropic glutamate receptors contributes to burst frequency regulation in the lamprey locomotor network.

The effect of metabotropic glutamate receptor (mGluR) agonists and antagonists on the spinal cord network underlying locomotion in the lamprey has been analysed. The specific group I mGluR agonist (R,S)-3,5-dihydroxyphenylglycine (DHPG) and the broad-spectrum mGluR agonist (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid (1S,3R-ACPD) both increased the burst frequency of N-methyl-D-aspartic acid (NMDA)-induced fictive locomotion and depolarized grey matter neurons. The burst frequency increase induced by the mGluR agonists was counteracted by the mGluR antagonists (+)-alpha-methyl-4-carboxyphenylglycine ((+)-MCPG), cyclopropan[b]chromen-1a-carboxylic acid ethylester (CPCCOEt) and (RS)-1-aminoindan-1,5-dicarboxylic acid (AIDA). Application of CPCCOEt alone reduced the locomotor burst frequency, indicating that mGluRs are endogenously activated during fictive locomotion. The mGluR antagonist CPCCOEt had no effect on NMDA-, or (S)-alpha-amino-3-hydroxy-5-methyl-4-isoazolepropionic acid (AMPA)-induced depolarizations. The mGluR agonists 1S,3R-ACPD and DHPG increased the amplitude of NMDA-induced depolarizations, a mechanism which could account for the increase in burst frequency. The group III mGluR agonist L-2-amino-4-phosphonobutyric acid reduced intraspinal synaptic transmission and burst frequency.