Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0184567 (
acute pain
)
3,962
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Most Serotonin Selective Reuptake Inhibitors (SSRIs) have been found to possess secondary binding properties, while citalopram and its S-enantiomer (escitalopram) have been reconfirmed "purest SSRIs". Using the mouse model of
acute pain
hotplate analgesia meter, we evaluated the antinociceptive properties of fluoxetine, fluvoxamine, citalopram and escitalopram, injected i.p.
Fluvoxamine
induced a dose-dependent clear antinociceptive effect (with an ED(50) value of 6.4 mg/kg). Both fluoxetine and citalopram induced (separately) only a weak antinociceptive effect with an inverse "U" shape curve. All three drug's effects were not abolished by naloxone. Escitalopram did not elicit any effect at quasi-equipotent doses. These findings show that fluoxetine, fluvoxamine and citalopram given i.p. are weak antinociceptors, (not mediated through opioid mechanisms), while escitalopram possesses no antinociceptive properties when injected i.p. This difference between citalopram and escitalopram calls for further studies in order to assess the various differences between the two enantiomers of citalopram, and between each enantiomer and the racemic mixture.
...
PMID:From selective to highly selective SSRIs: a comparison of the antinociceptive properties of fluoxetine, fluvoxamine, citalopram and escitalopram. 1641 73
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.
...
PMID:Intracerebroventricular fluvoxamine administration inhibited pain behavior but increased Fos expression in affective pain pathways. 1881 6