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First published online on December 6, 2002.
Copyright © 2002 by The Physiological Society
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2002.031773v1
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Received August 29, 2002
Accepted after revision November 12, 2002

Parallel decrease in {omega}-conotoxin-sensitive transmission and dopamine-induced inhibition at the striatal synapse of developing rats

Toshihiko Momiyama1*

1 Division of Cerebral Structure, National Institute for Physiological Sciences, Myodaiji, Okazaki 444-8585, Japan

* To whom correspondence should be addressed. E-mail: tmomi{at}nips.ac.jp.

Whole-cell patch-clamp recordings of GABAergic IPSCs were made from cholinergic interneurones in slices of striatum from developing rats aged 21-60 days postnatal. In addition, the Ca2+ channel subtypes involved in synaptic transmission, as well as dopamine (DA)-induced presynaptic inhibition, were investigated pharmacologically with development by bath application of Ca2+ channel blockers and DA receptor agonists. The IPSC amplitude was reduced by {omega}-conotoxin GVIA ({omega}-CgTX) or {omega}-agatoxin TK ({omega}-Aga-TK) across the whole age range, suggesting that multiple types of Ca2+ channels mediate transmission of the synapse. The IPSC fraction reduced by {omega}-CgTX significantly decreased, whereas that reduced by {omega}-Aga-TK remained unchanged with development. DA or quinpirole, a D2-like receptor agonist, presynaptically reduced the IPSC amplitude throughout development. The DA-induced inhibition decreased with age in parallel with the decrease in N-type Ca2+ channels. DA showed no further inhibition of IPSCs after the inhibitory effect of {omega}-CgTX had reached steady state throughout development. These results demonstrate that there is a functional link between presynaptic N-type Ca2+ channels and D2-like DA receptors at inhibitory synapses in the striatum. They also demonstrate that the suppression of GABAergic transmission by D2-like receptors is mediated by modulation of N-type Ca2+ channels and decreases in parallel with the developmental decline in the contribution of N-type Ca2+ channels to exocytosis.




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