PMID- 30339810
OWN - NLM
STAT- MEDLINE
DCOM- 20200211
LR  - 20200211
IS  - 1872-6240 (Electronic)
IS  - 0006-8993 (Linking)
VI  - 1704
DP  - 2019 Feb 1
TI  - Stimulating muscarinic M(1) receptors in the anterior cingulate cortex reduces 
      mechanical hypersensitivity via GABAergic transmission in nerve injury rats.
PG  - 187-195
LID - S0006-8993(18)30525-0 [pii]
LID - 10.1016/j.brainres.2018.10.013 [doi]
AB  - Cholinergic systems modulate synaptic transmission across the neuraxis and play 
      an important role in higher brain function including cognition, arousal and 
      nociception. The anterior cingulate cortex (ACC) is a fundamental brain region 
      for nociception and chronic pain, and receives cholinergic projections mainly 
      from basal forebrain. Recently, we found that the activation of muscarinic M(1) 
      receptors in the ACC produced antinociceptive behavior in response to mechanical 
      stimulation. However, it has not been tested whether stimulating muscarinic 
      receptors in the ACC can reduce mechanical hypersensitivity in animal models of 
      chronic pain. Here, we tested whether the activation of muscarinic M(1) receptors 
      in the ACC can alleviate mechanical hypersensitivity in a nerve injury model. The 
      activation of muscarinic M(1)/M(4) receptors by McN-A-343 injected into the 
      contralateral side of the ACC, but not into the ventral posterolateral nucleus, 
      was found to dose-dependently reduce mechanical hypersensitivity 7 days following 
      partial sciatic nerve ligation in rats. The reduction of mechanical 
      hypersensitivity by McN-A-343, was blocked by a selective muscarinic M(1) 
      antagonist, but not a M(4) receptor antagonist. Importantly, the nerve injury 
      model did not change the protein expression of muscarinic M(1) receptors in the 
      ACC. Additionally, a type A gamma-aminobutyric acid (GABA(A)) receptor agonist 
      injected into the ACC reduced the mechanical hypersensitivity in this injury 
      model. Finally, a GABA(A) receptor antagonist blocked the reduction of mechanical 
      hypersensitivity by McN-A-343 in the injury model. Collectively, these results 
      suggest that activations of muscarinic M(1) receptors in the ACC reduce nerve 
      injury-induced mechanical hypersensitivity through GABAergic transmission via 
      GABA(A) receptors.
CI  - Copyright (c) 2018 Elsevier B.V. All rights reserved.
FAU - Koga, Kohei
AU  - Koga K
AD  - Department of Neurophysiology, Hyogo College of Medicine, Hyogo 663-8501, Japan. 
      Electronic address: kkoga@hotmail.co.jp.
FAU - Matsuzaki, Yu
AU  - Matsuzaki Y
AD  - Department of Physiology and Pharmacology, Faculty of Pharmaceutical Sciences, 
      Fukuoka University, Fukuoka 814-0180, Japan.
FAU - Migita, Keisuke
AU  - Migita K
AD  - Department of Drug Informatics, Faculty of Pharmaceutical Sciences, Fukuoka 
      University, Fukuoka 814-0180, Japan.
FAU - Shimoyama, Shuji
AU  - Shimoyama S
AD  - Department of Neurophysiology, Graduate School of Medicine, Hirosaki University, 
      Hirosaki 036-8562, Japan.
FAU - Eto, Fumihiro
AU  - Eto F
AD  - Department of Physiology and Pharmacology, Faculty of Pharmaceutical Sciences, 
      Fukuoka University, Fukuoka 814-0180, Japan.
FAU - Nakagawa, Tatsuki
AU  - Nakagawa T
AD  - Department of Neurophysiology, Hyogo College of Medicine, Hyogo 663-8501, Japan.
FAU - Matsumoto, Taichi
AU  - Matsumoto T
AD  - Department of Drug Informatics, Faculty of Pharmaceutical Sciences, Fukuoka 
      University, Fukuoka 814-0180, Japan.
FAU - Terada, Kazuki
AU  - Terada K
AD  - Laboratory of Drug Design and Drug Delivery, Faculty of Pharmaceutical Sciences, 
      Fukuoka University, Fukuoka 814-0180, Japan.
FAU - Mishima, Kenichi
AU  - Mishima K
AD  - Department of Physiology and Pharmacology, Faculty of Pharmaceutical Sciences, 
      Fukuoka University, Fukuoka 814-0180, Japan.
FAU - Furue, Hidemasa
AU  - Furue H
AD  - Department of Neurophysiology, Hyogo College of Medicine, Hyogo 663-8501, Japan.
FAU - Honda, Kenji
AU  - Honda K
AD  - Department of Physiology and Pharmacology, Faculty of Pharmaceutical Sciences, 
      Fukuoka University, Fukuoka 814-0180, Japan. Electronic address: 
      khonda@fukuoka-u.ac.jp.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20181017
PL  - Netherlands
TA  - Brain Res
JT  - Brain research
JID - 0045503
RN  - 0 (Muscarinic Agonists)
RN  - 55-45-8 ((4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethylammonium Chloride)
RN  - 56-12-2 (gamma-Aminobutyric Acid)
SB  - IM
MH  - (4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethylammonium 
      Chloride/*pharmacology/therapeutic use
MH  - Animals
MH  - GABAergic Neurons/*drug effects/metabolism
MH  - Gyrus Cinguli/*drug effects/metabolism/physiopathology
MH  - Hyperalgesia/*drug therapy/metabolism/physiopathology
MH  - Male
MH  - Muscarinic Agonists/*pharmacology/therapeutic use
MH  - Peripheral Nerve Injuries/*metabolism/physiopathology
MH  - Rats
MH  - Rats, Wistar
MH  - Sciatic Nerve/injuries
MH  - Synaptic Transmission/*drug effects/physiology
MH  - gamma-Aminobutyric Acid/metabolism
OTO - NOTNLM
OT  - Anterior cingulate cortex
OT  - GABA(A) receptors
OT  - Mechanical hypersensitivity
OT  - Muscarinic M(1) receptor
OT  - Nerve injury
EDAT- 2018/10/20 06:00
MHDA- 2020/02/12 06:00
CRDT- 2018/10/20 06:00
PHST- 2018/02/14 00:00 [received]
PHST- 2018/08/28 00:00 [revised]
PHST- 2018/10/11 00:00 [accepted]
PHST- 2018/10/20 06:00 [pubmed]
PHST- 2020/02/12 06:00 [medline]
PHST- 2018/10/20 06:00 [entrez]
AID - S0006-8993(18)30525-0 [pii]
AID - 10.1016/j.brainres.2018.10.013 [doi]
PST - ppublish
SO  - Brain Res. 2019 Feb 1;1704:187-195. doi: 10.1016/j.brainres.2018.10.013. Epub 
      2018 Oct 17.