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Increased nociceptive input rapidly modulates spinal GABAergic transmission through endogenously released glutamate.
J Neurophysiol. 2007 Jan; 97(1):871-82.JN

Abstract

Stimulation of nociceptive primary afferents elicits pain by promoting glutamatergic transmission in the spinal cord. Little is known about how increased nociceptive input controls GABAergic tone in the spinal dorsal horn. In this study, we determined how increased nociceptive inflow affects GABAergic spontaneous inhibitory postsynaptic currents (sIPSCs) of lamina II neurons by using whole cell recordings in rat spinal cord slices. Bath application of capsaicin for 3 min induced a long-lasting inhibition of sIPSCs in 50% of the neurons tested. In the other half of the neurons, capsaicin either increased the frequency of sIPSCs (34.6%) or had no effect on sIPSCs (15.4%). The GABA(A) current elicited by puff application of GABA was not altered by capsaicin. Capsaicin did not inhibit sIPSCs in rats treated with intrathecal pertussis toxin. Also, capsaicin failed to inhibit sIPSCs in the presence of ionotropic glutamate receptor antagonists or in the presence of both LY341495 and CPPG (group II and group III metabotropic glutamate receptor antagonists, respectively). However, when LY341495 or CPPG was used alone, capsaicin still decreased the frequency of sIPSCs in some neurons. Additionally, bradykinin significantly inhibited sIPSCs in a population of lamina II neurons and this inhibitory effect was also abolished by LY341495 and CPPG. Our study provides novel information that stimulation of nociceptive primary afferents rapidly suppresses GABAergic input to many dorsal horn neurons through endogenous glutamate and activation of presynaptic group II and group III metabotropic glutamate receptors. These findings extend our understanding of the microcircuitry of the spinal dorsal horn involved in nociception.

Authors+Show Affiliations

Department of Anesthesiology and Pain Medicine, Unit 409, The University of Texas M. D. Anderson Cancer Center, 1400 Holcombe Blvd., Houston, TX 77030, USA.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural

Language

eng

PubMed ID

17108089

Citation

Zhou, Hong-Yi, et al. "Increased Nociceptive Input Rapidly Modulates Spinal GABAergic Transmission Through Endogenously Released Glutamate." Journal of Neurophysiology, vol. 97, no. 1, 2007, pp. 871-82.
Zhou HY, Zhang HM, Chen SR, et al. Increased nociceptive input rapidly modulates spinal GABAergic transmission through endogenously released glutamate. J Neurophysiol. 2007;97(1):871-82.
Zhou, H. Y., Zhang, H. M., Chen, S. R., & Pan, H. L. (2007). Increased nociceptive input rapidly modulates spinal GABAergic transmission through endogenously released glutamate. Journal of Neurophysiology, 97(1), 871-82.
Zhou HY, et al. Increased Nociceptive Input Rapidly Modulates Spinal GABAergic Transmission Through Endogenously Released Glutamate. J Neurophysiol. 2007;97(1):871-82. PubMed PMID: 17108089.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Increased nociceptive input rapidly modulates spinal GABAergic transmission through endogenously released glutamate. AU - Zhou,Hong-Yi, AU - Zhang,Hong-Mei, AU - Chen,Shao-Rui, AU - Pan,Hui-Lin, Y1 - 2006/11/15/ PY - 2006/11/17/pubmed PY - 2007/3/10/medline PY - 2006/11/17/entrez SP - 871 EP - 82 JF - Journal of neurophysiology JO - J. Neurophysiol. VL - 97 IS - 1 N2 - Stimulation of nociceptive primary afferents elicits pain by promoting glutamatergic transmission in the spinal cord. Little is known about how increased nociceptive input controls GABAergic tone in the spinal dorsal horn. In this study, we determined how increased nociceptive inflow affects GABAergic spontaneous inhibitory postsynaptic currents (sIPSCs) of lamina II neurons by using whole cell recordings in rat spinal cord slices. Bath application of capsaicin for 3 min induced a long-lasting inhibition of sIPSCs in 50% of the neurons tested. In the other half of the neurons, capsaicin either increased the frequency of sIPSCs (34.6%) or had no effect on sIPSCs (15.4%). The GABA(A) current elicited by puff application of GABA was not altered by capsaicin. Capsaicin did not inhibit sIPSCs in rats treated with intrathecal pertussis toxin. Also, capsaicin failed to inhibit sIPSCs in the presence of ionotropic glutamate receptor antagonists or in the presence of both LY341495 and CPPG (group II and group III metabotropic glutamate receptor antagonists, respectively). However, when LY341495 or CPPG was used alone, capsaicin still decreased the frequency of sIPSCs in some neurons. Additionally, bradykinin significantly inhibited sIPSCs in a population of lamina II neurons and this inhibitory effect was also abolished by LY341495 and CPPG. Our study provides novel information that stimulation of nociceptive primary afferents rapidly suppresses GABAergic input to many dorsal horn neurons through endogenous glutamate and activation of presynaptic group II and group III metabotropic glutamate receptors. These findings extend our understanding of the microcircuitry of the spinal dorsal horn involved in nociception. SN - 0022-3077 UR - https://www.unboundmedicine.com/medline/citation/17108089/Increased_nociceptive_input_rapidly_modulates_spinal_GABAergic_transmission_through_endogenously_released_glutamate_ L2 - http://www.physiology.org/doi/full/10.1152/jn.00964.2006?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -