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Intrathecal administration of a gap junction decoupler, an inhibitor of Na(+)-K(+)-2Cl(-) cotransporter 1, or a GABA(A) receptor agonist attenuates mechanical pain hypersensitivity induced by REM sleep deprivation in the rat.
Pharmacol Biochem Behav. 2010 Dec; 97(2):377-83.PB

Abstract

We studied the hypothesis that some of the spinal mechanisms that are involved in neuropathic hypersensitivity play a role in hypersensitivity induced by REM sleep deprivation (REMSD). Rats with a chronic intrathecal (i.t.) catheter had REMSD of 48h duration that induced hypersensitivity to mechanical stimulation. After REMSD, the animals were treated i.t. with carbenoxolone (a gap junction decoupler), bumetanide (a blocker of Na(+)-K(+)-2Cl(-) cotransporter 1 or NKCC1), muscimol (a GABA(A) receptor agonist), or pretreated intraperitoneally with minocycline (an inhibitor of microglia activation). Previously, all these treatments attenuated neuropathic hypersensitivity. Following REMSD, carbenoxolone, bumetanide and muscimol had a strong antihypersensitivity effect, whereas pretreatment with minocycline failed to prevent development of hypersensitivity. The results suggest that among spinal pain facilitatory mechanisms that are common to REMSD and neuropathy are NKCC1 blocker- and gap junction decoupler-reversible mechanisms. Moreover, there is a net pain inhibitory effect by spinal administration of an exogenous GABA(A) receptor agonist following REMSD as shown earlier in neuropathy. In contrast, activation of spinal microglia may not be as important for the development of hypersensitivity induced by REMSD as following nerve injury.

Authors+Show Affiliations

King's Lab, School of Pharmacy, Shanghai Jiao Tong University, Shanghai, PR China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo 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

20851713

Citation

Wei, Hong, et al. "Intrathecal Administration of a Gap Junction Decoupler, an Inhibitor of Na(+)-K(+)-2Cl(-) Cotransporter 1, or a GABA(A) Receptor Agonist Attenuates Mechanical Pain Hypersensitivity Induced By REM Sleep Deprivation in the Rat." Pharmacology, Biochemistry, and Behavior, vol. 97, no. 2, 2010, pp. 377-83.
Wei H, Hao B, Huang JL, et al. Intrathecal administration of a gap junction decoupler, an inhibitor of Na(+)-K(+)-2Cl(-) cotransporter 1, or a GABA(A) receptor agonist attenuates mechanical pain hypersensitivity induced by REM sleep deprivation in the rat. Pharmacol Biochem Behav. 2010;97(2):377-83.
Wei, H., Hao, B., Huang, J. L., Ma, A. N., Li, X. Y., Wang, Y. X., & Pertovaara, A. (2010). Intrathecal administration of a gap junction decoupler, an inhibitor of Na(+)-K(+)-2Cl(-) cotransporter 1, or a GABA(A) receptor agonist attenuates mechanical pain hypersensitivity induced by REM sleep deprivation in the rat. Pharmacology, Biochemistry, and Behavior, 97(2), 377-83. https://doi.org/10.1016/j.pbb.2010.09.007
Wei H, et al. Intrathecal Administration of a Gap Junction Decoupler, an Inhibitor of Na(+)-K(+)-2Cl(-) Cotransporter 1, or a GABA(A) Receptor Agonist Attenuates Mechanical Pain Hypersensitivity Induced By REM Sleep Deprivation in the Rat. Pharmacol Biochem Behav. 2010;97(2):377-83. PubMed PMID: 20851713.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Intrathecal administration of a gap junction decoupler, an inhibitor of Na(+)-K(+)-2Cl(-) cotransporter 1, or a GABA(A) receptor agonist attenuates mechanical pain hypersensitivity induced by REM sleep deprivation in the rat. AU - Wei,Hong, AU - Hao,Bin, AU - Huang,Jin-Lu, AU - Ma,Ai-Niu, AU - Li,Xin-Yan, AU - Wang,Yong-Xiang, AU - Pertovaara,Antti, Y1 - 2010/09/16/ PY - 2010/06/30/received PY - 2010/09/07/revised PY - 2010/09/07/accepted PY - 2010/9/21/entrez PY - 2010/9/21/pubmed PY - 2011/2/4/medline SP - 377 EP - 83 JF - Pharmacology, biochemistry, and behavior JO - Pharmacol Biochem Behav VL - 97 IS - 2 N2 - We studied the hypothesis that some of the spinal mechanisms that are involved in neuropathic hypersensitivity play a role in hypersensitivity induced by REM sleep deprivation (REMSD). Rats with a chronic intrathecal (i.t.) catheter had REMSD of 48h duration that induced hypersensitivity to mechanical stimulation. After REMSD, the animals were treated i.t. with carbenoxolone (a gap junction decoupler), bumetanide (a blocker of Na(+)-K(+)-2Cl(-) cotransporter 1 or NKCC1), muscimol (a GABA(A) receptor agonist), or pretreated intraperitoneally with minocycline (an inhibitor of microglia activation). Previously, all these treatments attenuated neuropathic hypersensitivity. Following REMSD, carbenoxolone, bumetanide and muscimol had a strong antihypersensitivity effect, whereas pretreatment with minocycline failed to prevent development of hypersensitivity. The results suggest that among spinal pain facilitatory mechanisms that are common to REMSD and neuropathy are NKCC1 blocker- and gap junction decoupler-reversible mechanisms. Moreover, there is a net pain inhibitory effect by spinal administration of an exogenous GABA(A) receptor agonist following REMSD as shown earlier in neuropathy. In contrast, activation of spinal microglia may not be as important for the development of hypersensitivity induced by REMSD as following nerve injury. SN - 1873-5177 UR - https://www.unboundmedicine.com/medline/citation/20851713/Intrathecal_administration_of_a_gap_junction_decoupler_an_inhibitor_of_Na_+__K_+__2Cl____cotransporter_1_or_a_GABA_A__receptor_agonist_attenuates_mechanical_pain_hypersensitivity_induced_by_REM_sleep_deprivation_in_the_rat_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0091-3057(10)00271-6 DB - PRIME DP - Unbound Medicine ER -