S286 P.1.d. Basic and clinical neuroscience − Animal behaviour reduction of GABA-ergic interneurons in the cortex and the hippocampus (2). Dysfunctional cortical inhibition has been sug- gested as a mechanism through which symptoms of schizophrenia are mediated. Our previous studies have demonstrated selective deficit of parvalbumin- and reelin-positive interneurons in CA1 and CA3 subregions of hippocampus of adult rats after perinatal PCP administration. The aim of this study was to determine GABAergic synaptic coverage of hippocampal principal cells after perinatal phencyclidine treatment. Animals were treated on 2nd, 6th, 9th and 12th postnatal (PN) day, with either PCP (10mg/kg) or vehicle (0.9% saline) subcutaneously and sacrificied on PN70. Coronal brain sections of the hippocampus were stained for vesicular GABA transporter (VGAT) and stacks of 1-mm-thick images (pyramidal cells in CA1 and CA3 and granulle cells in the dentate gyrus (DG)) were obtained on confocal microscope using a 63 × oil immersion objective and digital resolution of 1024×1024 pixel. Four bilateral sections 250 mm apart were analyzed per animal. One image per principal cell at the level of the largest cell body cross-sectional area was used to measure soma area, perimeter, and number of perisomatic VGAT terminals. Areas and perimeters were measured using the Image Tool 2.0 software program (University of Texas, San Antonio, TX). Linear density was calculated as number of perisomatic terminals per unit length. Mean values of individual animals (n = 5 per group) were used to calculate group mean values. All numerical data are presented as group mean values with standard deviation of mean (SD) and were analyzed using the one-way ANOVA with the Bonferroni’s post hoc test. After perinatal PCP administration there was no change in soma size of pyramidal cells in CA1 and CA3 subregions of hip- pocampus, while soma area of granule cells in DG was increased (table 1). In congruence, we found no difference in the density of perisomatic VGAT terminals around pyramidal cells in CA1 and CA3 regions, while the density of perisomatic VGAT terminals around granule cells in DG was increased (table 1). The cortical and hippocampal GABAergic system consists of many different subclasses of interneurons which differ in their morphological, electrophysiological and neurochemical features. Results obtained in this study demonstrate a long term effect of perinatal PCP treatment on GABAergic innervation of granule cells of DG. To the best of our knowledge, this is first report on the effect of perinatal PCP treatment on synaptic coverage of principal cells in the hippocampus in the rat model of schizophrenia. Dentate gyrus CA1 CA3 saline PCP saline PCP saline PCP Area size (mm 2 ) 135.75 ±9.94 150.75 ±4.92* 181.5±5 190 ±15.28 264.5 ±25.68 292.6 ±20.4 Number of perisomatic VGAT terminals (mm −1 ) 329.25 ±18.31 421.25 ±13.12* 339.5 ±24.47 336.8 ±25.79 332.5 ±8.1 319 ±16.18 References [1] Daskalakis, Z.J., Fitzgerald, P.B., Christensen, B.K.,2007. The role of cortical inhibition in the pathophysiology and treatment of schizo- phrenia. Brain Res Rev 56, 427−42. [2] Benes, F.M., McSparren, J., Bird, E.D., SanGiovanni, J.P., Vincent, S.L., 1991. Deficits in small interneurons in prefrontal and cingulate cortices of schizophrenic and schizoaffective patients. Arch Gen Psychiatry 48, 996–1001. P.1.d.023 Effect of sex hormones on pain-related behaviour in rats E. Shekunova 1 ° , A. Malyshkin 1 , I. Belozertseva 1 . 1 Pavlov Medical State University, Pharmacology, St. Petersburg, Russia A number of chronic pain conditions is more prevalent in women than in men. Research has suggested that the sex hormones may have a pivotal role in mediating sex differences in pain. Experi- mental studies have demonstrated activational role of estrogen on pain behavior in rats (the model of inflammatory pain). However in the experimental literature exists a lack of consensus as to the direction of hormonal influence in the pain modulation. The first set of experiments was aimed to estimate the role of sex steroids in pain modulation using two models of chronic pain: neuropathic pain (chronic constriction injury (CCI) and inflammatory pain (Complete Freud’s adjuvant inoculation, CFA). Mechanical and cold allodynia was estimated weekly during 28 days (CCI model) and daily during 7 days (CFA model) after surgery. Females (CCI model) demonstrated increased sensitivity to mechanical and cold stimuli as compared to males. Three groups of rats were compared: ovariectomized (OVX) female chronically treated with estradiol (1) or vehicle (2) and the cycling females (3). OVX females were less sensitive to mechanical stim- uli than cycling females (both models). Estradiol administration increased pain sensitivity in OVX rats 48h after CFA inoculation. In CCI model sensitivity to cold stimuli was significantly higher (P < 0.01) in both cycling and estradiol-treated OVX females com- pared to vehicle-treated OVX females until day 28 after surgery. Thus, estradiol administration resulted in increased sensitivity to cold (CCI model) and mechanical stimuli (CFA model) in female rats. Second set of experiment was aimed to estimate the role of sex hormones in the behavioral alteration induced by chronic pain. It has been shown previously that the behavior of rats with CCI indicates the presence of spontaneous (i.e., not induced by apparent external stimuli) pain. It is known that depression and anxiety often coexist with chronic pain status. In our laboratory the model based on social interaction paradigm was developed for simultaneous estimation of a spon- taneous pain and depressive-like behavioral alteration induced by chronic pain. Behavior of males and females before and after CCI was compared in social interaction test. Individual, social behaviors and signs of spontaneous pain (foot lifting, vibration-like scratching) were monitored via data acquisition system (“Ethograph”, 2.07, Russia). Group-housed males and OVX females were served as opponents. Behavior of rats with neuropathy was compared with behavior of sham-operated ani- mals. Male and female rats with neuropathic pain demonstrated diminished sociability and exploratory activity; however females demonstrated less pronounced spontaneous pain behavior. All groups of CCI females (OVX treated with estradiol or vehicle, and cycling) also demonstrated diminished sociability and exploratory activity compared to sham-operated females. Most pronounced decreasing in sociability was observed in cycling female rats compared to OVX females. Duration of spontaneous pain behavior was greater in OVX females treated with vehicle than in estradiol- treated and cycling females, indicating an influence of estradiol on spontaneous pain behavior. Thus, estradiol can modulate the development or expression of behavioral alteration induced by chronic pain. The involvement of estradiol in modulation of pain sensitivity depends on pain model used.