Differentiation of Acupuncture and Nonacupuncture Points by Difference of Associated Opioids in the Spinal Cord in Productton of Analgesia by Acupuncture and Nonacupuncture Point Stimulation,and Relations between Sodium and those Opioids
Restricted accessResearch articleFirst published online November, 1990
Differentiation of Acupuncture and Nonacupuncture Points by Difference of Associated Opioids in the Spinal Cord in Productton of Analgesia by Acupuncture and Nonacupuncture Point Stimulation,and Relations between Sodium and those Opioids
Antiserum of methionine-enkephalin (Met-Enk) applied Intrathecally abolished acupuncture analgesia (AA) caused by low frequency stimulation of an acupuncture point (tibial muscle, APS) of rats, but antisera of leucine-enkephalin (Leu-Enk) and dynorphin (Dyn) did not. Antiserum of Dyn applied intrathecally abolished analgesia (NAA) produced by stimulation of a nonacupuncture point (NAPS) which was revealed by lesion in the analgesia inhibitory system (AIS), whereas antisera of Met-Enk and Leu-Enk did not. NAA was antagonized by the k-receptor antagonist, Mr2266, and analgesia was produced by the k-agonist, U50-488H, In the AIS lesioned rats. Potentials in the dorsal periaqueductal central gray (D-PAG) evoked by APS were antagonized by naloxone and antiserum of Met-Enk. and those in the lateral PAG (L-PAG) evoked by NAPS were antagonized by Mr2266 and antiserum of Dyn. After adrenalectomy, AA, potentials in the D-PAG, and analgesia caused by stimulation (SPA) of the D-PAG were abolished 12 hour; and NAA, potentials in the L-PAG, and SPA of the L-PAG were abolished in 24 hour. All were then restored one hour after intravenous application of 1 ml of 5% NaCl solution. AA and NAA which were augmented for several hours before their abolition after adrenalectomy were not antagonized by naloxone nor Mr2266, respectively. However naloxone and Mr22G6 did antagonize AA and NAA, respectively, one hour after treatment with 1 ml of 5% NaCl solution.
OkuboK.Effect of the pituitary or adrenal gland ablation on analgesia caused by the acupuncture point stimulation or non-acupuncture point stimulation after lesion of the analgesia inhibitory system. J. Showa Med. Assoc., 47: 99–106, 1987. (In Japanese)
2.
TakeshigeC.Differentiation between acupuncture and non-acupuncture points by association with analgesia inhibitory system. Acupuncture & Electro-therapeutics Res., Int. J., 10: 195–203, 1985.
3.
SatoT. and TakeshigeC.Morphine analgesia caused by activation of spinal acupuncture afferent pathway in the anterolateral tract. J. Showa Med. Assoc., 41: 663–673, 1981. (In Japanese)
4.
TakeshigeC.MuraiM.. TanakaM. and HachisuM.Parallel Individual variation in effectiveness of electro-acupuncture, morphine analgesia, and dorsal PAG-SPA and their abolition by D-phenylalanine. Adv. Pain Res. Ther., 5: 563–569, 1983.
5.
TanakaM.Studies in analgesia enhancement by D-phenylalanlne. J. Showa Med. Assoc., 42: 433–440, 1982. (In Japanese)
6.
TsuchiyaM. and TakeshigeC.Relation between hypothalamic arcuate nucleus and pituitary gland in production of acupuncture and non-acupuncture point stimulation- produced analgesia. J. Showa Med. Assoc., 49: 338–350. 1989. (In Japanese)
7.
PatersonS.J.RobsonL.E. and KosterlltzH.W. Classification of opioid receptors. Br. Med. Bull., 39: 31–36, 1983.
8.
PertC.B.PasternakG. and SnyderS.H. Opiate agonists and antagonists discriminated by receptor binding in brain. Science.182: 1359–1361, 1973.
9.
PellegrinoL.J. and CushmanA.J. A stereotaxic atlas of the rat brain. Appelten Centary Crafts, New York.1967.
10.
TakeshigeC.Inhibition associated with acupuncture analgesia. Neurol. Neuroblol., 28:255–262, 1987.
11.
HanJ.S.XieG.X. and ZhouZ.F. Acupuncture mechanisms in rabbits studied with microinjection of antibodies against B-endorphln, enkephalin and substance P. Neuropharmacol., 23: 1–5. 1984.
12.
HanJ.S.XieG.X. Dynorphln: important mediator for electroacupuncture analgesia in the spinal cord of the rabbit. Pain, 18: 357–376, 1984.
13.
ChengR.PomeranzB. and YuG.Dexamethasone partially reduces and saline-treatment abolished electroacupuncture analgesia: these findings implicate pituitary endorphins. Life Sci., 24: 1481–1486, 1979.
14.
LewisJ.W. Multiple neurochemical and hormonal mechanisms of stress-induced analgesia. Ann NY Acad. Sci., 457: 194–204, 1986.
15.
UsamiS. and TakeshigeC.The difference in analgesia producing central pathway of stress induced analgesia and that of acupuncture point and non-polnt stimulation- produced analgesia. J. Showa Med. Assoc., 43: 629–638, 1983. (In Japanese)
16.
SatoT.HishidaF.LuoC.P.TsuchiyaM. and TakeshigeC.Relations of adrenal gland and sodium Ions In production of acupuncture and non-acupuncture points stimulation-produced analgesia. J. Showa Med. Assoc., 49: 286–294, 1989. (In Japanese)
17.
GuoS.SatoT.TanakaM and TakeshigeC.Acupuncture afferent and efferent pathways in the hypothalamic arcuate nucleus. J. Showa Med. Assoc., 48: 493–499, 1988. (In Japanese)
18.
MacLennanA.J.CruganR.C.HysonR.L. and MaierS.F. Corticosterone: a critical factor in opioid form of stress-induced analgesia. Science. 215: 1530–1532, 1982.
19.
SlmantovR.KuharM.J.PasternakG.W. and Snyder. S.H. The regional distribution of a morphlne-llke factor enkephalin in monkey brain. Brain Res., 106: 189–197, 1976.
20.
GramschC.HolltV.MehraelnP.PasiA. and HerzA.Regional distribution of methlonine-enkephalln and beta-endorphin like Immunoreactivity in human brain and pituitary. Brain Res., 171: 261–270, 1979.
21.
PertC.B.KuharM.J. and SnyderS.H. Autoradiographic localization of the opiate receptor in rat brain. Life Sci., 16: 1849–1854, 1975.
22.
KuharM.J.PertC.B. and SnyderS.H. Regional distribution of opiate receptor binding In monkey and human brain. Nature, 245: 447–450, 1973.
23.
JessellT.M. and IversenL.L. Opiate analgesia inhibit substance P released from rat trigeminal nucleus. Nature, 268: 549–551, 1977.
24.
MudgeW.LeemanS.E. and FischbachG.D. Enkephalin inhibits release of substance P released of substance P from sensory neurons in culture and decreases action potential duration. Proc. Natl. Acad. Sci. U.S.A., 76: 526–530, 1979.
25.
DugganA.W.HallJ.G. and HeadleyP.M. Suppression of transmission of nociceptive impulses by morphine administrated in the region of the substantia gelatinosa. Br. J. Pharmacol.61: 65–76, 1977.
26.
BarsD.L.MenetreyD.ConseillerC.. Depressive effects of morphine upon lamina V cell activities in the dorsal horn of the spinal cat. Brain Res., 98: 261–277, 1975.
27.
WlllcocksonW.S.KimJ.ShinH.K.. Action of opioids on primate spinothalamic tract neurons. J. Neuroscl., 6: 2509–2520. 1986.
28.
SumalK.K.PlckelV.M.MillerR.J.. Enkephalln- contalnlng neurons in substantia gelatinosa of spinal trigeminal complex, ultrastructure and synaptic interaction with primary sensory afferents. Brain Res., 248: 223–236, 1982.
29.
ConrathV.M.DietlM.ArluisonM.. Localization of Met-enkephalln-1ike immunoreactivity within pain-related nuclei of cervical spinal cord, brainstem and midbrain in the cat. Brain Res., 11: 587–604, 1983.
30.
GlazerE.J. and BasbaumA.I. Immunohistochemical localization of leucine-enkephalln in the spinal cord of the cat, enkephaline-contalning marginal neurons and pain modulation. J. Comp. Neurol., 196: 377–389, 1981.
31.
HuntS.P.KellyJ.S. and EmsonP.C. The electron microscopic localization of Methlonlne-enkephalin within the superficial layers (I and II) of the spinal cord. Neurosci.5: 1871–1890, 1980.
32.
BotticelliL.J., CoxB.M. and GoldsteinA.Immunoreactive dynorphln in mammalian spinal cord and dorsal root ganglia. Proc. Nat. Acad. Sci. (Wash), 78: 7783–7786, 1981.
33.
de GroatW.C., LoweI.P., KawataniM., . Identification of enkephalin ImmunorcactIvlty in sensory ganglion cells. J. Auton. Nerv. Sys. [Suppl]:361–368, 1986.
34.
KawataniM.NagelJ. and de GroatW.C.Identification of neuropeptides in pelvic and pudendal nerve afferent pathways to the sacral spinal cord of the cat. J. Comp. Neurol., 249: 117–132, 1986.
35.
BasbaumA.I.CruzL. and WeberE.Immunoreactive dynorphln B In sacral primary afferent fibers of the cat. J. Ncurosci., 5: 127–133, 1986.
