title: Norepinephrine plays an important role in antinociceptive modulation of hypothalamic paraventricular nucleus in the rat.
abstract: Our previous study has proven that hypothalamic paraventricular nucleus (PVN) plays a role in antinociception. The effects of studied classical neurotransmitter on PVN antinociceptive modulation were investigated in the rat. The results showed: (1) Pain stimulation increased norepinephrine (NE), but not epinephrine, dopamine (DA), 3,4-dihydroxyphenylacetic acid (DA metabolic product), homovanilic acid (DA metabolic product), serotonin (5-HT), 5-hydroxyindoleacetic acid (5-HT metabolic product), acetycholine (Ach), choline (Ach metabolic product), gamma-aminobutyric acid (GABA), and L-glutamate acid concentrations in the PVN perfusion liquid; (2) PVN stimulation with L-glutamate sodium, which excited local neurons only, did not influence the concentrations of the studied classical neurotransmitter and metabolic product in the PVN perfusion liquid; (3) Microinjection of NE, epinephrine, or L-glutamate sodium into the PVN elevated pain threshold, and local administration of GABA decreased pain threshold in a dose-dependent manner, but PVN administration of Ach, DA, or 5-HT did not change pain threshold; (4) Microinjection of phentolamine (alpha-receptor antagonist) or MK801 [NMDA-receptor antagonist] into the PVN reduced pain threshold, and local administration of bicuculline (GABA-receptor antagonist) raised pain threshold, but PVN administration of propranolol (beta-receptor antagonist), atropine (Muscarinic cholinergic receptor antagonist), 6-OH gallamine (Nicotinic cholinergic receptor antagonist), fluperidol (DA-receptor antagonist), or cyproheptadine (5-HT-receptor antagonist) did not alter pain threshold. The data suggested that endogenous NE, not epinephrine, 5-HT, Ach, GABA, and L-glutamate acid played an important role in the PVN antinociceptive modulation.
authors.affiliation: Wuxi 101 Hospital of People Liberty Army, Wuxi, Jiangsu, China.
authors.forename: Xi-Jian
authors.initials: XJ
authors.lastname: Zhou
authors.forename: Jun
authors.initials: J
authors.lastname: Yang
authors.forename: Fu-Lin
authors.initials: FL
authors.lastname: Yan
authors.forename: Da-Xin
authors.initials: DX
authors.lastname: Wang
authors.forename: Xiang-Yong
authors.initials: XY
authors.lastname: Li
authors.forename: Xiao-Qiang
authors.initials: XQ
authors.lastname: Fan
authors.forename: Fang
authors.initials: F
authors.lastname: Hao
authors.forename: Xi-Qing
authors.initials: XQ
authors.lastname: Yan
authors.forename: Xue-Ping
authors.initials: XP
authors.lastname: Li
authors.forename: Hui
authors.initials: H
authors.lastname: Li
authors.forename: Wen-Yan
authors.initials: WY
authors.lastname: Liu
authors.forename: Bao-Cheng
authors.initials: BC
authors.lastname: Lin
mesh_terms: D000818:Animals; D018698:Glutamic Acid / Q000378:metabolism; D008297:Male; D018377:Neurotransmitter Agents / Q000378:metabolism; D009638:Norepinephrine / Q000378:metabolism*; D010146:Pain / Q000378:metabolism*; D010147:Pain Measurement; D017288:Pain Threshold / Q000187:drug effects / Q000502:physiology; D010286:Paraventricular Hypothalamic Nucleus / Q000187:drug effects / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D017981:Receptors, Neurotransmitter / Q000037:antagonists & inhibitors / Q000378:metabolism
chemical_list: D018377:Neurotransmitter Agents; D017981:Receptors, Neurotransmitter; D018698:Glutamic Acid; D009638:Norepinephrine