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Lapchak, P.A., Araujo, D.M. and Collier, B. (1989) Regulation of endogenous acetylcholine release from mammalian brain slices by opiate receptors: Hippocampus, striatum and cerebral cortex of guinea-pig and rat. Neuroscience, 31, 313-325. doi:10.1016/0306-4522(89)90376-X

has been cited by the following article:

• TITLE: Acetylcholine participates in pain modulation by influencing endogenous opiate peptides in rat spinal cord

  AUTHORS: Jun Yang, Ying Zhao, Yanjuan Pan, Guangzhou Lu, Lu Lu, Daxin Wang, Jingcheng Wang

  KEYWORDS: Achetylcholine; Endogenous Opiate Peptide; Pain Modulation; Spinal Cord

  JOURNAL NAME: World Journal of Neuroscience, Vol.2 No.1, February 29, 2012

  ABSTRACT: The spinal cord is a necessary pathway that transfers the body nociceptive inputs to the brain, and endo-genous opiate peptides (EOP) play an important role in pain modulation. Our previous work has proven that arginine vasopressin (AVP) antinociception in the caudate nucleus (CdN) relates with the acetylcholine (Ach) system mainly. The communication was de-signed to investigate the interrelations between Ach system and EOP system at the spinal level during pain process. The results showed that: 1) pain stimulation increased L-enkephalin (L-Ek), β-endorphin (β-Ep), dynorphin A1-13(DynA1-13), Ach and choline (Ch, an Ach metabolic product) concentrations in the spinal cord; 2) Ach increased L-Ek, β-Ep and DynA1-13 concentrations in the spinal cord; and 3) Atropine (M-receptor inhibitor) or hexahydric gallamine (N-receptor inhibitor) decreased L-Ek, β-Ep and DynA1-13 concentrations in the spinal cord. The data suggested that Ach antinociception was involved in the EOP system at the spinal level.