ABSTRACT
Ascorbic acid [ASC] is abundant in the brain. ASC is effective on synthesis and transportation of neurotransmitters. Glutamatergic system is involved in pain transduction. NMDA receptors can be inhibited, and TPRV1 and ASIC receptors are excited due to its acidity at the presence of ASC. Therefore, this study is aimed to investigate the effects of intraperitoneal [i.p] and intrathecal [i.t] administration of ASC and sodium-ascorbate on pain. Male Wistar rats [200-250 g] in eight groups [n=7] included saline [i.p], saline [i.t], ASC [1, 10, 100, 200 mg/kg, i.p], usual and neutralized ASC [0.02 mg/10 micro l, i.t] were used. Pain threshold was measured by tail-flick test and chemical pain was assessed using formalin-test. ASC [10, 100, 200 mg/kg, i.p] induced hyperalgesia in tail-flick test [P<0.01] and reduced pain in formalin-test [P<0.05], but ASC [1 mg/kg i.p] with no effect in tail-flick, decreased pain during formalin-test interphase [P<0.01]. Intrathecal ASC at 0.02 mg/10 micro1 concentration, but not sodium-ascorbate, induced hyperalgesia in tail-flick test [P<0.001]. ASC [0.02 mg/10 microl, i.t] in both forms of usual and sodium-ascorbate, decreased pain in formalin-test [P<0.001]. Lesser inhibition effects of ASC on AMPA receptors may be responsible at least in part for its hyperalgesia in tail-flick test at i.p administration. This plus the sensitivity of TRPV1 and ASIC receptors to ASC acidity can be considered for i.t administration, because sodium-ascorbate [i.t] didn't induce hyperalgesia. Inhibiting effects of i.p and i.t administration of ASC and sodium-ascorbate on NMDA receptors, release of SP and other inflammatory mediators, were probably some players of pain reduction during the formalin-test