05) decreased pain sensitivity in all stages of estrous cycle, and the analgesic effect was higher during proestrus and estrus stages of estrous cycle than that during metestrus and diestrus stages. Picrotoxin significantly (P<0.05) increased pain sensitivity in all stages of estrous cycle, and such a hyperalgesic effect was lower during proestrus and estrus stages of estrous cycle than that during metestrus and diestrus stages. Conclusion: The findings of the present study indicate that the role of hippocampal GABAA receptor in the control of the pain sensitivity

can be modulated by variation in gonadal Inhibitors,research,lifescience,medical steroids during different stages of the estrous cycle. Key Words: Pain, estrous cycle, muscimol, picrotoxin, hippocampus Introduction There is now strong evidence for sex differences in sensitivity to pain and analgesia. These differences imply that gonadal steroid hormones such as estradiol and testosterone modulate the sensitivity to pain and analgesia.1 Terner et al suggested that Inhibitors,research,lifescience,medical the phase of the menstrual cycle might alter the effectiveness of certain opioids administered to relieve pain in women.2 Shekunova and Bespalov suggested that pain management Inhibitors,research,lifescience,medical strategies could be optimized through the use of sex- and estrous cycle-specific techniques.   Inhibitory mechanisms are essential in suppressing the development

of allodynia and hyperalgesia in a normal animal, and there is evidence that loss of selleckbio inhibition can lead to the development of neuropathic pain. A great deal of effort has been expended in attempting to define the role of GABA in mediating the transmission and perception of pain.4 Lovick and colleagues reported that the plasticity of GABAA receptor Inhibitors,research,lifescience,medical subunit expression occurs during the estrous cycle of the rat.5 In addition, GABA neurons and receptors are found in supraspinal sites known to coordinate the perception and response to more painful stimuli, and this neurotransmitter system has been shown to regulate the control of sensory information processing in the spinal

cord.6 Behavioral studies have indicated Inhibitors,research,lifescience,medical that GABAergic modulation is involved in the opioid-induced antinociception in the ventrolateral orbital cortex.7 Lee and co-workers suggested that although the impairment in spinal GABAergic inhibition may play a role in the mediation of neuropathic pain, it is not accomplished by the quantitative change in spinal elements for GABAergic inhibition, and therefore these elements are not related to the generation of neuropathic GSK-3 pain following peripheral nerve injury.8 There are now several reports that a rapid decline in progesterone is associated with changes in GABAA receptor subunit expression in diverse regions of the female rat brain.9 There is a sex difference in response to GABAA receptor-mediated injury in the developing hippocampus, also endogenous estradiol concentrations are the same in neonatal male and female hippocampus.10 Hippocampal volume was increased by either pain or stress, which may be due to edema.