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5‐hydroxytryptamine‐mediated increase in glutamate uptake by the leech giant glial cell
Author(s) -
Hirth Ingolf C.,
Deitmer Joachim W.
Publication year - 2006
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/glia.20417
Subject(s) - glutamate receptor , biology , hirudo medicinalis , adenylyl cyclase , intracellular , neuroglia , neurotransmitter , protein kinase a , microbiology and biotechnology , biophysics , biochemistry , leech , endocrinology , central nervous system , signal transduction , kinase , receptor , world wide web , computer science
The clearance of synaptically released glutamate is one of the pivotal functions of glial cells. We have studied the role of 5‐hydroxytryptamine (5‐HT, 30 μM), a neurotransmitter and neurohormone in the leech central nervous system with a versatile action spectrum, on the efficacy of glial glutamate uptake. The activity of the glutamate uptake carrier in the giant glial cell in isolated ganglia of Hirudo medicinalis was monitored by measuring the membrane current and the change in the intracellular Na + concentration (Na + i ) as induced by the glutamate carrier substrate D ‐aspartate ( D ‐asp, 1 mM). 5‐HT increased the D ‐asp‐induced current (EC 50 at 5 μM) and rise in Na + i , an effect which was mimicked by the membrane‐permeable cyclic nucleotide analogue dibutyryl‐cyclic AMP (db‐cAMP). The adenylyl cyclase inhibitor SQ 22,536 and the protein kinase A antagonist Rp‐cAMP inhibited the effect of 5‐HT. Blocking the G protein in the giant glial cell by injecting GDP‐β‐S suppressed the effect of 5‐HT, but not the effect of db‐cAMP, on the D ‐asp‐induced current. Our results suggest that 5‐HT enhances the glial uptake of glutamate via cAMP‐ and PKA‐mediated pathway. © 2006 Wiley‐Liss, Inc.