Anti-nociceptive effects of
fluvoxamine, administered by intracerebroventricular (i.c.v.) injection, include inhibited
pain behavior in both
formalin-induced
acute pain (p<0.05-0.01) and sciatic nerve
ligation-
allodynia (p<0.03). A
5-HT1 receptor antagonist (WAY-100635) and a 5-HT2 receptor antagonist (
ketanserin), injected i.c.v., induced
hyperalgesia and inhibited
fluvoxamine's anti-nociceptive effects. We also investigated how
fluvoxamine affects neural activities in brain areas involved in affectional
pain using Fos-like
protein immunohistochemistry. The
acute pain and
allodynia increased Fos-positive cells in the prefrontal cortex (PFC), basolateral nucleus (BL) and central nucleus of the amygdala (Ce), indicating that these areas are involved in
pain processing.
Fluvoxamine did not block the Fos expression, though it did produce anti-nociception. Moreover,
fluvoxamine alone increased Fos in the BL and PFC.
Ketanserin did not decrease the Fos expression induced by
fluvoxamine. The results indicated that 5-HT2 receptor activities participate minimally in Fos induction by
fluvoxamine in the PFC and BL. In contrast,
WAY-100635 affected the Fos expression produced by
fluvoxamine. In the portion of the brain with affectional
pain pathways,
5-HT1 receptor activities induced anti-nociceptive effects and decreased Fos expression with
fluvoxamine, while 5-HT2 receptor activation affected to anti-nociceptive effects but did not induce Fos expression.