Activation of metabotropic glutamate receptors inhibits synapsin I phosphorylation in visceral sensory neurons

• Published in: The Journal of membrane biology 2000-12, Vol.178 (3), p.195-204
• Main Authors: Hay, M, Hoang, C J, Hasser, E M, Price, E M
• Format: Article
• Language: English
• Subjects: Aminobutyrates - pharmacology; Animals; Cycloleucine - analogs & derivatives; Cycloleucine - pharmacology; Exocytosis - drug effects; Gene Expression Regulation - drug effects; Membrane Potentials; Nerve Tissue Proteins - agonists; Nerve Tissue Proteins - antagonists & inhibitors; Nerve Tissue Proteins - classification; Nerve Tissue Proteins - genetics; Nerve Tissue Proteins - physiology; Neurons, Afferent - drug effects; Neurons, Afferent - metabolism; Nodose Ganglion - cytology; Patch-Clamp Techniques; Phosphorylation - drug effects; Potassium Chloride - pharmacology; Protein Isoforms - agonists; Protein Isoforms - antagonists & inhibitors; Protein Isoforms - genetics; Protein Isoforms - physiology; Protein Processing, Post-Translational - drug effects; Rats; Rats, Sprague-Dawley; Receptors, Metabotropic Glutamate - agonists; Receptors, Metabotropic Glutamate - antagonists & inhibitors; Receptors, Metabotropic Glutamate - classification; Receptors, Metabotropic Glutamate - genetics; Receptors, Metabotropic Glutamate - physiology; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger - analysis; Signal Transduction; Synapsins - metabolism
• ISSN: 0022-2631; 1432-1424
• DOI: 10.1007/s002320010027

Activation of glutamate metabotropic receptors (mGluRs) in nodose ganglia neurons has previously been shown to inhibit voltage-gated Ca++ currents and synaptic vesicle exocytosis. The present study describes the effects of mGluRs on depolarization-induced phosphorylation of the synaptic-vesicle-associated protein synapsin I. Depolarization of cultured nodose ganglia neurons with 60 mM KCl resulted in an increase in synapsin I phosphorylation. Application of mGluR agonists 1-aminocyclopentane-1s-3r-dicarboxylic acid (t-ACPD) and L(+)-2-Amino-4-phosphonobutyric acid (L-AP4) either in combination or independently inhibited the depolarization induced phosphorylation of synapsin I. Application of the mGluR antagonist (RS)-alpha-Methyl-4-carboxyphenylglycine (MCPG) blocked t-ACPD-induced inhibition of synapsin phosphorylation but not the effects of L-AP4. In addition, application of either t-ACPD or L-AP4 in the absence of KCl induced depolarization had no effect on resting synapsin I phosphorylation. RT-PCR analysis of mGluR subtypes in these nodose ganglia neurons revealed that these cells only express group III mGluR subtypes 7 and 8. These results suggest that activation of mGluRs modulates depolarization-induced synapsin I phosphorylation via activation of mGluR7 and/or mGluR8 and that this process may be involved in mGluR inhibition of synaptic vesicle exocytosis in visceral sensory neurons of the nodose ganglia.