ENDOGENOUS ACTIVATION OF METABOTROPIC GLUTAMATE RECEPTORS CONTRIBUTESTO BURST FREQUENCY REGULATION IN THE LAMPREY LOCOMOTOR NETWORK

The effect of metabotropic glutamate receptor (mGluR) agonists and ant agonists on the spinal cord network underlying locomotion in the lampr ey has been analysed. The specific group I mGluR agonist (R,S)-3,5-dih ydroxyphenylglycine (DHPG) and the broad-spectrum mGluR agonist (1S,3R )-1-aminocyclopentane-1,3-dicarboxylic acid (1S,3R-ACPD) both increase d the burst frequency of N-methyl-D-aspartic acid (NMDA)induced fictiv e locomotion and depolarized grey matter neurons. The burst frequency increase induced by the mGluR agonists was counteracted by the mGluR a ntagonists (+)-alpha-methyl-4-carboxyphenylglycine ((+)-MCPG), cyclopr opan[b]chromen-1a-carboxylic acid ethylester (CPCCOEt) and (RS)-1-amin oindan-1,5-dicarboxylic acid (AIDA). Application of CPGCOEt alone redu ced the locomotor burst frequency, indicating that mGluRs are endogeno usly activated during fictive locomotion. The mGluR antagonist CPCCOEt had no effect on NMDA-, or alpha-amino-3-hydroxy-5-methyl-4-isoazolep ropionic 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.