PMID- 15527827
OWN - NLM
STAT- MEDLINE
DCOM- 20050113
LR  - 20191210
IS  - 0028-3908 (Print)
IS  - 0028-3908 (Linking)
VI  - 47
IP  - 6
DP  - 2004 Nov
TI  - Role of intracellular calcium in acute thermal pain perception.
PG  - 935-44
AB  - The role of intracellular calcium in acute thermal nociception was investigated 
      in the mouse hot-plate test. Intracerebroventricular (i.c.v.) administration of 
      TMB-8, a blocker of Ca++ release from intracellular stores, produced 
      hypernociception. By contrast, i.c.v. pretreatment with thapsigargin, a depletor 
      of Ca++ intracellular stores, produced an increase of the mouse pain threshold. 
      Furthermore, non-analgesic doses of thapsigargin prevented the hypernociception 
      produced by TMB-8. In mice undergoing treatment with heparin, an InsP3-receptor 
      antagonist, or ryanodine, a ryanodine receptor (RyR) antagonist, a dose-dependent 
      reduction of the pain threshold was observed. Pretreatment with D-myo inositol, 
      compound which produces InsP3, and 4-chloro-m-cresol, a RyR agonist, induced an 
      antinociceptive effect. The heparin hypernociception was prevented by D-myo 
      inositol, but not by L-myo inositol, used as negative control. In the same 
      experimental conditions, the antinociception induced by D-myo inositol was 
      prevented by a non-hyperalgesic dose of heparin. Similarly, the reduction of pain 
      threshold produced by ryanodine was reversed by non-analgesic doses of 
      4-chloro-m-cresol, whereas the antinocicpetion induced by 4-chloro-m-cresol was 
      prevented by non-hyperalgesic doses of ryanodine. The pharmacological treatments 
      employed did not produce any behavioral impairment of mice as revealed by the 
      rota-rod and hole-board tests. These results indicate that a variation of 
      intracellular calcium contents at a supraspinal level is involved in the 
      modulation of acute thermal nociception. In particular, the stimulation of both 
      InsP3- and Ry-receptors appears to play an important role in the induction of 
      antinociception in mice, whereas a blockade of these receptors is involved in an 
      hypernociceptive response to acute thermal pain.
FAU - Galeotti, Nicoletta
AU  - Galeotti N
AD  - Department of Preclinical and Clinical Pharmacology, University of Florence, 
      Viale G. Pieraccini 6, 50139 Florence, Italy. nicoletta.galeotti@unifi.it
FAU - Bartolini, Alessandro
AU  - Bartolini A
FAU - Ghelardini, Carla
AU  - Ghelardini C
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Neuropharmacology
JT  - Neuropharmacology
JID - 0236217
RN  - 0 (Calcium Channel Blockers)
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (Ryanodine Receptor Calcium Release Channel)
RN  - 57818-92-5 (8-(N,N-diethylamino)octyl-3,4,5-trimethoxybenzoate)
RN  - 632XD903SP (Gallic Acid)
RN  - 67526-95-8 (Thapsigargin)
RN  - 85166-31-0 (Inositol 1,4,5-Trisphosphate)
RN  - EC 7.2.2.10 (Calcium-Transporting ATPases)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Acute Disease
MH  - Animals
MH  - Behavior, Animal/drug effects
MH  - Calcium/pharmacology/*physiology
MH  - Calcium Channel Blockers/pharmacology
MH  - Calcium-Transporting ATPases/antagonists & inhibitors
MH  - Dose-Response Relationship, Drug
MH  - Enzyme Inhibitors/pharmacology
MH  - Gallic Acid/*analogs & derivatives/pharmacology
MH  - Hot Temperature
MH  - Hyperalgesia/drug therapy
MH  - Injections, Intraventricular
MH  - Inositol 1,4,5-Trisphosphate/antagonists & inhibitors/pharmacology
MH  - Male
MH  - Mice
MH  - Pain/*psychology
MH  - Pain Threshold/drug effects
MH  - Postural Balance/drug effects
MH  - Reaction Time/drug effects
MH  - Ryanodine Receptor Calcium Release Channel/drug effects
MH  - Thapsigargin/pharmacology
EDAT- 2004/11/06 09:00
MHDA- 2005/01/14 09:00
CRDT- 2004/11/06 09:00
PHST- 2004/04/07 00:00 [received]
PHST- 2004/06/11 00:00 [revised]
PHST- 2004/06/30 00:00 [accepted]
PHST- 2004/11/06 09:00 [pubmed]
PHST- 2005/01/14 09:00 [medline]
PHST- 2004/11/06 09:00 [entrez]
AID - S0028390804001832 [pii]
AID - 10.1016/j.neuropharm.2004.07.001 [doi]
PST - ppublish
SO  - Neuropharmacology. 2004 Nov;47(6):935-44. doi: 10.1016/j.neuropharm.2004.07.001.