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[Decreased A-type potassium current mediates the hyperexcitability of nociceptive neurons in the chronically compressed dorsal root ganglia].
Sheng Li Xue Bao. 2007 Apr 25; 59(2):240-6.SL

Abstract

The excitability of nociceptive neurons increases in the intact dorsal root ganglion (DRG) after a chronic compression, but the underlying mechanisms are still unclear. The aim of this study was to investigate the ionic mechanisms underlying the hyperexcitability of nociceptive neurons in the compressed ganglion. Chronic compression of DRG (CCD) was produced in adult rats by inserting two rods through the intervertebral foramina to compress the L4 DRG and the ipsilateral L5 DRG. After 5-7 d, DRG somata were dissociated and placed in culture for 12-18 h. In sharp electrode recording model, the lower current threshold and the depolarized membrane potential in the acutely dissociated CCD neurons were detected, indicating that hyperexcitability is intrinsic to the soma. Since voltage-gated K(+) (Kv) channels in the primary sensory neurons are important for the regulation of excitability, we hypothesized that CCD would alter K(+) current properties in the primary sensory neurons. We examined the effects of 4-aminopyridine (4-AP), a specific antagonist of A-type potassium channel, on the excitability of the control DRG neurons. With 4-AP in the external solution, the control DRG neurons depolarized (with discharges in some cells) and their current threshold decreased as the CCD neurons demonstrated, indicating the involvement of decreased A-type potassium current in the hyperexcitability of the injured neurons. Furthermore, the alteration of A-type potassium current in nociceptive neurons in the compressed ganglion was investigated with the whole-cell patch-clamp recording model. CCD significantly decreased A-type potassium current density in nociceptive DRG neurons. These data suggest that a reduction in A-type potassium current contributes, at least in part, to the increase in neuron excitability that may lead to the development of pain and hyperalgesia associated with CCD.

Authors+Show Affiliations

Department of Physiology, the Second Military Medical University, Shanghai, China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

chi

PubMed ID

17437050

Citation

Yan, Ni, et al. "[Decreased A-type Potassium Current Mediates the Hyperexcitability of Nociceptive Neurons in the Chronically Compressed Dorsal Root Ganglia]." Sheng Li Xue Bao : [Acta Physiologica Sinica], vol. 59, no. 2, 2007, pp. 240-6.
Yan N, Li XH, Cheng Q, et al. [Decreased A-type potassium current mediates the hyperexcitability of nociceptive neurons in the chronically compressed dorsal root ganglia]. Sheng Li Xue Bao. 2007;59(2):240-6.
Yan, N., Li, X. H., Cheng, Q., Yan, J., Ni, X., & Sun, J. H. (2007). [Decreased A-type potassium current mediates the hyperexcitability of nociceptive neurons in the chronically compressed dorsal root ganglia]. Sheng Li Xue Bao : [Acta Physiologica Sinica], 59(2), 240-6.
Yan N, et al. [Decreased A-type Potassium Current Mediates the Hyperexcitability of Nociceptive Neurons in the Chronically Compressed Dorsal Root Ganglia]. Sheng Li Xue Bao. 2007 Apr 25;59(2):240-6. PubMed PMID: 17437050.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - [Decreased A-type potassium current mediates the hyperexcitability of nociceptive neurons in the chronically compressed dorsal root ganglia]. AU - Yan,Ni, AU - Li,Xiao-Han, AU - Cheng,Qi, AU - Yan,Jin, AU - Ni,Xin, AU - Sun,Ji-Hu, PY - 2007/4/18/pubmed PY - 2012/8/21/medline PY - 2007/4/18/entrez SP - 240 EP - 6 JF - Sheng li xue bao : [Acta physiologica Sinica] JO - Sheng Li Xue Bao VL - 59 IS - 2 N2 - The excitability of nociceptive neurons increases in the intact dorsal root ganglion (DRG) after a chronic compression, but the underlying mechanisms are still unclear. The aim of this study was to investigate the ionic mechanisms underlying the hyperexcitability of nociceptive neurons in the compressed ganglion. Chronic compression of DRG (CCD) was produced in adult rats by inserting two rods through the intervertebral foramina to compress the L4 DRG and the ipsilateral L5 DRG. After 5-7 d, DRG somata were dissociated and placed in culture for 12-18 h. In sharp electrode recording model, the lower current threshold and the depolarized membrane potential in the acutely dissociated CCD neurons were detected, indicating that hyperexcitability is intrinsic to the soma. Since voltage-gated K(+) (Kv) channels in the primary sensory neurons are important for the regulation of excitability, we hypothesized that CCD would alter K(+) current properties in the primary sensory neurons. We examined the effects of 4-aminopyridine (4-AP), a specific antagonist of A-type potassium channel, on the excitability of the control DRG neurons. With 4-AP in the external solution, the control DRG neurons depolarized (with discharges in some cells) and their current threshold decreased as the CCD neurons demonstrated, indicating the involvement of decreased A-type potassium current in the hyperexcitability of the injured neurons. Furthermore, the alteration of A-type potassium current in nociceptive neurons in the compressed ganglion was investigated with the whole-cell patch-clamp recording model. CCD significantly decreased A-type potassium current density in nociceptive DRG neurons. These data suggest that a reduction in A-type potassium current contributes, at least in part, to the increase in neuron excitability that may lead to the development of pain and hyperalgesia associated with CCD. SN - 0371-0874 UR - https://www.unboundmedicine.com/medline/citation/17437050/[Decreased_A_type_potassium_current_mediates_the_hyperexcitability_of_nociceptive_neurons_in_the_chronically_compressed_dorsal_root_ganglia]_ L2 - http://www.actaps.com.cn/qikan/manage/wenzhang/2007-2-19.pdf DB - PRIME DP - Unbound Medicine ER -