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Vol. 53, Issue 1, 6-13, January 1998
Department of Pharmacology, University of Innsbruck, 6020 Innsbruck, Austria
Receptor autoradiography with the Y2 receptor ligand
125I-peptide YY3-36 and in situ
hybridization were applied to investigate changes in neuropeptide
tyrosine-Y2 receptor expression after kainic acid-induced
recurrent seizures in the rat hippocampus. In the strata oriens and
radiatum of CA1 to CA3, which are densely innervated by Y2
receptor-bearing Schaffer collateral terminals, a transient 2-fold
increase in Y2 receptor affinity was observed after 4-12
hr, with a later slow decline. No change was seen in Y2
mRNA expression in CA2/CA3 pyramidal cells, from which Schaffer collaterals originate. Conversely, in granule cells of the dentate gyrus, markedly elevated Y2 mRNA concentrations were
observed (by 740% in the dorsal hippocampus) 24-48 hr after kainate
injection. At the same time, a marked and lasting (up to 6 months)
increase in the number of Y2 receptor sites (by 800%) was
seen in the dentate hilus, which is innervated densely by mossy fibers.
The early increase in Y2 receptor affinity in Schaffer
collaterals was accompanied by a 60% decrease in the EC50
of peptide YY3-36 in inhibiting K+-stimulated
glutamate release in hippocampal slices from kainic acid-treated rats.
Our data indicate transient up-regulation of presynaptic Y2
receptors in Schaffer collaterals by a change in affinity and a
permanent de novo synthesis of presynaptic
Y2 receptors in granule cells/mossy fibers. These changes
may cause augmented presynaptic inhibition of glutamate release from
different hippocampal sites and, in conjunction with increased
concentrations of neuropeptide tyrosine in mossy fibers, may represent
an endogenous reactive anticonvulsant mechanism.
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