EFFECTS OF INTRATHECAL INJECTION OF NIMODIPINE, OMEGA-CONOTOXIN GVIA,CALMIDAZOLIUM, AND KN-62 ON THE ANTINOCICEPTION INDUCED BY COLD-WATERSWIMMING STRESS IN THE MOUSE
Hw. Suh et al., EFFECTS OF INTRATHECAL INJECTION OF NIMODIPINE, OMEGA-CONOTOXIN GVIA,CALMIDAZOLIUM, AND KN-62 ON THE ANTINOCICEPTION INDUCED BY COLD-WATERSWIMMING STRESS IN THE MOUSE, Brain research, 767(1), 1997, pp. 144-147
The present study was designed to determine if spinal calcium channels
, calmodulin, and calcium/calmodulin-dependent protein kinase II were
involved in the production of antinociception induced by cold water sw
imming stress (CWSS). The effects of intrathecal (i.t.) injection of n
imodipine, omega-conotoxin GVIA, calmidazolium, or (S)-5-isoquinolines
ulfonic acid, nolinyl-sulfonyl)methylamino]-3-oxo-3-(4-phenyl-1- piper
azinyl)-propyl]phenyl ester (KN-62) on CWSS-induced antinociception we
re studied in ICR mice. The antinociception was assessed by the tail-f
lick test. CWSS produced inhibition of the tail-flick response. Variou
s doses of nimodipine (10-40 ng), omega-conotoxin GVIA (5-40 ng), calm
idazolium (10-40 ng), or KN-62 (5-40 ng) injected i.t. alone did not s
how any antinociceptive effect in the tail-flick test. I.t. pretreatme
nt with omega-conotoxin GVIA, calmidazolium, or KN-62 dose dependently
attenuated the CWSS-induced inhibition of the tail-flick response. Ho
wever, i.t. pretreatment with nimodipine did not affect the inhibition
of the tail-flick response induced by CWSS. Our results suggest that
spinal N-type calcium channel, calmodulin and. calcium/calmodulin-depe
ndent protein kinase II may be involved in the production of antinocic
eption induced by CWSS. On the other hand, CWSS-induced antinociceptio
n appears not to be mediated via the spinal L-type calcium channel. (C
) 1997 Elsevier Science B.V.