Play a critical role in the development of inflammatory hyperalgesia, we studied the effects of mineralocorticoid receptor antagonist spironolactone. Our results shown that intrathecal injection of spironolactone significantly down-regulated the expression and phosyphorylation of NMDA receptors in the spinal dorsal horn and DRG, while Wang and his colleagues found that spironolactone had no effects on the expression of NMDA receptors in the spinal cord. The anti-inflammatory effect of spironolactone may underlie the main mechanisms contributing to its inhibitory action on the expression and phosphorylation of NMDA receptors in the superficial dorsal horn. Our data showed that, as revealed by western blot experiments, spironolactone significantly down-regulated pNR1 and t-NR1 on Day 4 and 7 after CCD surgery. Notably, the time-course of NMDA receptor expression and phosphorylation generally parallel that of proinflammatory cytokines, microglia and pain behaviors changes after intrathecal injection of spironolactone in rats. Numerous in vitro and in vivo evidences also suggest the existence of a functional interaction among microglia, proinflammatory cytokines and NMDA receptors. Individuals with schizophrenia display changes in auditory event-related potentials including decreased amplitude of the P50 and N100 components and disrupted gating of the P50, and these are assumed to reflect deficits in elementary information processing. Nicotine has been shown to enhance P50 gating in people with schizophrenia and their first degree relatives, suggesting that nicotinic agents could be useful for the treatment of schizophrenia. Evidence from studies assessing pharmacological response, changes in response to parametric manipulations and response to novelty suggest that the mouse P20 and N40 are analogous to the human P50 and N100, respectively. In particular numerous studies have demonstrated increases in mouse P20 amplitude following nicotine administration, as well as nicotine-induced decreases in mouse N40 amplitude. Thus, rodent ERP methodologies have great potential for translational drug discovery in schizophrenia. In addition to changes in the ERP, nicotine has been shown to enhance power in the gamma frequency range of the EEG. Gamma oscillations are thought to be generated in part by parvalbumin expressing GABAergic interneurons, a cell population that is disrupted in schizophrenia. As such, gamma oscillations have been proposed as an important biomarker of the integrity of this cell population. Numerous studies have demonstrated reduced or altered gamma power in schizophrenia and in physiologically relevant animal models of schizophrenia. Increases in gamma power have been demonstrated during performance of cognitive tasks in MDV3100 control subjects, especially during attention and working memory, suggesting that enhanced gamma activity may serve as a mechanism through which nicotine influences schizophrenia symptomology and cognition. Recent studies have attempted to identify the specific nicotinic acetylcholinergic receptor subtypes responsible for regulating the effects of nicotine on ERPs.