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Kainate receptor subunits underlying presynaptic regulation of transmitter release in the dorsal horn.
J Neurosci. 2002 Sep 15; 22(18):8010-7.JN

Abstract

Presynaptic kainate (KA) receptors regulate synaptic transmission at both excitatory and inhibitory synapses in the spinal cord dorsal horn. Previous work has demonstrated pharmacological differences between the KA receptors expressed by rat dorsal horn neurons and those expressed by the primary afferent sensory neurons that innervate the dorsal horn. Here, neurons isolated from KA receptor subunit-deficient mice were used to evaluate the contribution of glutamate receptor subunit 5 (GluR5) and GluR6 to the presynaptic control of transmitter release and to KA receptor-mediated whole-cell currents in these two cell populations [corrected]. Deletion of GluR6 produced a significant reduction in KA receptor-mediated current density in dorsal horn neurons, whereas GluR5 deletion caused no change in current density but removed sensitivity to GluR5-selective antagonists. Presynaptic modulation of inhibitory transmission between dorsal horn neurons was preserved in cells from either GluR5- or GluR6-deficient mice. In DRG neurons, in contrast, GluR5 deletion abolished KA receptor function, whereas deletion of GluR6 had little effect on peak current density but increased the rate and extent of desensitization. These results highlight fundamental differences in KA receptor physiology between the two cell types and suggest possible strategies for the pharmacological modulation of nociception.

Authors+Show Affiliations

Washington University Pain Center and Departments of Anesthesiology, Anatomy and Neurobiology, and Psychiatry, Washington University School of Medicine, St. Louis, Missouri 63110, USA.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

12223554

Citation

Kerchner, Geoffrey A., et al. "Kainate Receptor Subunits Underlying Presynaptic Regulation of Transmitter Release in the Dorsal Horn." The Journal of Neuroscience : the Official Journal of the Society for Neuroscience, vol. 22, no. 18, 2002, pp. 8010-7.
Kerchner GA, Wilding TJ, Huettner JE, et al. Kainate receptor subunits underlying presynaptic regulation of transmitter release in the dorsal horn. J Neurosci. 2002;22(18):8010-7.
Kerchner, G. A., Wilding, T. J., Huettner, J. E., & Zhuo, M. (2002). Kainate receptor subunits underlying presynaptic regulation of transmitter release in the dorsal horn. The Journal of Neuroscience : the Official Journal of the Society for Neuroscience, 22(18), 8010-7.
Kerchner GA, et al. Kainate Receptor Subunits Underlying Presynaptic Regulation of Transmitter Release in the Dorsal Horn. J Neurosci. 2002 Sep 15;22(18):8010-7. PubMed PMID: 12223554.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Kainate receptor subunits underlying presynaptic regulation of transmitter release in the dorsal horn. AU - Kerchner,Geoffrey A, AU - Wilding,Timothy J, AU - Huettner,James E, AU - Zhuo,Min, PY - 2002/9/12/pubmed PY - 2002/10/4/medline PY - 2002/9/12/entrez SP - 8010 EP - 7 JF - The Journal of neuroscience : the official journal of the Society for Neuroscience JO - J. Neurosci. VL - 22 IS - 18 N2 - Presynaptic kainate (KA) receptors regulate synaptic transmission at both excitatory and inhibitory synapses in the spinal cord dorsal horn. Previous work has demonstrated pharmacological differences between the KA receptors expressed by rat dorsal horn neurons and those expressed by the primary afferent sensory neurons that innervate the dorsal horn. Here, neurons isolated from KA receptor subunit-deficient mice were used to evaluate the contribution of glutamate receptor subunit 5 (GluR5) and GluR6 to the presynaptic control of transmitter release and to KA receptor-mediated whole-cell currents in these two cell populations [corrected]. Deletion of GluR6 produced a significant reduction in KA receptor-mediated current density in dorsal horn neurons, whereas GluR5 deletion caused no change in current density but removed sensitivity to GluR5-selective antagonists. Presynaptic modulation of inhibitory transmission between dorsal horn neurons was preserved in cells from either GluR5- or GluR6-deficient mice. In DRG neurons, in contrast, GluR5 deletion abolished KA receptor function, whereas deletion of GluR6 had little effect on peak current density but increased the rate and extent of desensitization. These results highlight fundamental differences in KA receptor physiology between the two cell types and suggest possible strategies for the pharmacological modulation of nociception. SN - 1529-2401 UR - https://www.unboundmedicine.com/medline/citation/12223554/Kainate_receptor_subunits_underlying_presynaptic_regulation_of_transmitter_release_in_the_dorsal_horn_ L2 - http://www.jneurosci.org/cgi/pmidlookup?view=long&pmid=12223554 DB - PRIME DP - Unbound Medicine ER -