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Ryanodine receptors contribute to the induction of nociceptive input-evoked long-term potentiation in the rat spinal cord slice.
Mol Pain. 2010 Jan 20; 6:1.MP

Abstract

BACKGROUND

Our previous study demonstrated that nitric oxide (NO) contributes to long-term potentiation (LTP) of C-fiber-evoked field potentials by tetanic stimulation of the sciatic nerve in the spinal cord in vivo. Ryanodine receptor (RyR) is a downstream target for NO. The present study further explored the role of RyR in synaptic plasticity of the spinal pain pathway.

RESULTS

By means of field potential recordings in the adult male rat in vivo, we showed that RyR antagonist reduced LTP of C-fiber-evoked responses in the spinal dorsal horn by tetanic stimulation of the sciatic nerve. Using spinal cord slice preparations and field potential recordings from superficial dorsal horn, high frequency stimulation of Lissauer's tract (LT) stably induced LTP of field excitatory postsynaptic potentials (fEPSPs). Perfusion of RyR antagonists blocked the induction of LT stimulation-evoked spinal LTP, while Ins(1,4,5)P3 receptor (IP(3)R) antagonist had no significant effect on LTP induction. Moreover, activation of RyRs by caffeine without high frequency stimulation induced a long-term potentiation in the presence of bicuculline methiodide and strychnine. Further, in patch-clamp recordings from superficial dorsal horn neurons, activation of RyRs resulted in a large increase in the frequency of miniature EPSCs (mEPSCs). Immunohistochemical study showed that RyRs were expressed in the dorsal root ganglion (DRG) neurons. Likewise, calcium imaging in small DRG neurons illustrated that activation of RyRs elevated [Ca(2+)]i in small DRG neurons.

CONCLUSIONS

These data indicate that activation of presynaptic RyRs play a crucial role in the induction of LTP in the spinal pain pathway, probably through enhancement of transmitter release.

Authors+Show Affiliations

Institute of Neurobiology, Institutes of Brain Science and State Key laboratory of Medical Neurobiology, Fudan University, Shanghai 200032, China. lzcheng@fudan.edu.cnNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

20089138

Citation

Cheng, Long-Zhen, et al. "Ryanodine Receptors Contribute to the Induction of Nociceptive Input-evoked Long-term Potentiation in the Rat Spinal Cord Slice." Molecular Pain, vol. 6, 2010, p. 1.
Cheng LZ, Lü N, Zhang YQ, et al. Ryanodine receptors contribute to the induction of nociceptive input-evoked long-term potentiation in the rat spinal cord slice. Mol Pain. 2010;6:1.
Cheng, L. Z., Lü, N., Zhang, Y. Q., & Zhao, Z. Q. (2010). Ryanodine receptors contribute to the induction of nociceptive input-evoked long-term potentiation in the rat spinal cord slice. Molecular Pain, 6, 1. https://doi.org/10.1186/1744-8069-6-1
Cheng LZ, et al. Ryanodine Receptors Contribute to the Induction of Nociceptive Input-evoked Long-term Potentiation in the Rat Spinal Cord Slice. Mol Pain. 2010 Jan 20;6:1. PubMed PMID: 20089138.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Ryanodine receptors contribute to the induction of nociceptive input-evoked long-term potentiation in the rat spinal cord slice. AU - Cheng,Long-Zhen, AU - Lü,Ning, AU - Zhang,Yu-Qiu, AU - Zhao,Zhi-Qi, Y1 - 2010/01/20/ PY - 2009/09/30/received PY - 2010/01/20/accepted PY - 2010/1/22/entrez PY - 2010/1/22/pubmed PY - 2010/6/11/medline SP - 1 EP - 1 JF - Molecular pain JO - Mol Pain VL - 6 N2 - BACKGROUND: Our previous study demonstrated that nitric oxide (NO) contributes to long-term potentiation (LTP) of C-fiber-evoked field potentials by tetanic stimulation of the sciatic nerve in the spinal cord in vivo. Ryanodine receptor (RyR) is a downstream target for NO. The present study further explored the role of RyR in synaptic plasticity of the spinal pain pathway. RESULTS: By means of field potential recordings in the adult male rat in vivo, we showed that RyR antagonist reduced LTP of C-fiber-evoked responses in the spinal dorsal horn by tetanic stimulation of the sciatic nerve. Using spinal cord slice preparations and field potential recordings from superficial dorsal horn, high frequency stimulation of Lissauer's tract (LT) stably induced LTP of field excitatory postsynaptic potentials (fEPSPs). Perfusion of RyR antagonists blocked the induction of LT stimulation-evoked spinal LTP, while Ins(1,4,5)P3 receptor (IP(3)R) antagonist had no significant effect on LTP induction. Moreover, activation of RyRs by caffeine without high frequency stimulation induced a long-term potentiation in the presence of bicuculline methiodide and strychnine. Further, in patch-clamp recordings from superficial dorsal horn neurons, activation of RyRs resulted in a large increase in the frequency of miniature EPSCs (mEPSCs). Immunohistochemical study showed that RyRs were expressed in the dorsal root ganglion (DRG) neurons. Likewise, calcium imaging in small DRG neurons illustrated that activation of RyRs elevated [Ca(2+)]i in small DRG neurons. CONCLUSIONS: These data indicate that activation of presynaptic RyRs play a crucial role in the induction of LTP in the spinal pain pathway, probably through enhancement of transmitter release. SN - 1744-8069 UR - https://www.unboundmedicine.com/medline/citation/20089138/Ryanodine_receptors_contribute_to_the_induction_of_nociceptive_input_evoked_long_term_potentiation_in_the_rat_spinal_cord_slice_ L2 - http://journals.sagepub.com/doi/full/10.1186/1744-8069-6-1?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -