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Involvement of R‐type Ca 2+ channels in neurotransmitter release from spinal dorsolateral funiculus terminals synapsing motoneurons

Molecular studies have revealed the presence of R‐type voltage‐gated Ca 2+ channels at pre‐ and postsynaptic regions; however, no evidence for the participation of these channels in transmitter release has been presented for the spinal cord. Here we characterize the effects of SNX‐482, a selective R...

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Published in:Journal of comparative neurology (1911) 2009-03, Vol.513 (2), p.188-196
Main Authors: Castro, Alberto, Andrade, Arturo, Vergara, Paula, Segovia, Jose, Aguilar, Justo, Felix, Ricardo, Delgado‐Lezama, Rodolfo
Format: Article
Language:English
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Summary:Molecular studies have revealed the presence of R‐type voltage‐gated Ca 2+ channels at pre‐ and postsynaptic regions; however, no evidence for the participation of these channels in transmitter release has been presented for the spinal cord. Here we characterize the effects of SNX‐482, a selective R channel blocker, on the monosynaptic excitatory postsynaptic potentials (EPSPs) evoked in motoneurons by stimulation of dorsolateral funiculus (DLF) terminals in a slice preparation from the adult turtle spinal cord. SNX‐482 inhibited neurotransmission in a dose‐dependent manner, with an IC 50 of ∼9 ± 1 nM. The EPSP time course and membrane time constant of the motoneurons were not altered, suggesting a presynaptic mechanism. The toxin inhibited the residual component of the EPSPs recorded in the presence of N‐ and P/Q‐type Ca 2+ channel blockers, strongly suggesting a role for the R channels in neurotransmission at the spinal cord DLF terminals. Consistently with this, RT‐PCR analysis of turtle spinal cord segments revealed the expression of the Ca V 2.3 pore‐forming (α 1E ) subunit of R channels, whereas the use of anti‐α 1E ‐specific antibodies resulted in its localization in the DLF fibers as demonstrated by immunohistochemistry coupled with laser confocal microscopy. J. Comp. Neurol. 513:188–196, 2009. © 2009 Wiley‐Liss, Inc.
ISSN:0021-9967
1096-9861
DOI:10.1002/cne.21952