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Long‐term potentiation of glutamatergic synaptic transmission induced by activation of presynaptic P2Y receptors in the rat medial habenula nucleus
Author(s) -
Price Gareth D.,
Robertson Susan J.,
Edwards Frances A.
Publication year - 2003
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1046/j.1460-9568.2003.02501.x
Subject(s) - long term potentiation , uridine , chemistry , neurotransmission , glutamatergic , biophysics , uridine triphosphate , glutamate receptor , receptor , neuroscience , microbiology and biotechnology , biochemistry , biology , nucleotide , rna , gene
A novel form of long‐term potentiation of glutamatergic synaptic transmission is described in the rat medial habenula nucleus. It occurs when uridine 5′‐triphosphate is bath applied at low micromolar concentrations and is prevented by Reactive Blue 2, suggesting that it is mediated by P2Y 4 receptors. Uridine 5′‐diphosphate can also cause such a Reactive Blue 2‐sensitive potentiation, but at higher concentrations (200 µ m ), suggesting that this might also be an effect on the relatively uridine 5′‐diphosphate‐insensitive P2Y 4 receptor. The potentiation is due to an increase in presynaptic release probability. It requires neither depolarization nor calcium influx postsynaptically and is thus probably non‐Hebbian. When potentiation due to low concentrations of uridine 5′‐triphosphate is inhibited in the presence of Reactive Blue 2, uridine 5′‐triphosphate causes instead a significant inhibition of glutamate release. We suggest that this inhibition may be mediated by a Reactive Blue 2‐insensitive P2Y 2 ‐like receptor. At higher concentrations of uridine 5′‐triphosphate (200 µ m ), the inhibitory effect dominates such that even in the absence of Reactive Blue 2 no potentiation is seen.