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21 in vivo, in cortex tissues. Our data together with others suggest that themember of class II and IV HDACs may act as important regulators of geneexpression in developing neural cells and tissues in murine CNS.

Abstracts / Neuroscience R

hole-cell patch-clamp recording technique. Our results show that stimu-ation of alpha-2A-AR inhibits excitatory synaptic transmission in the mPFChrough cAMP-PKA-PP1-AMPA-R and cAMP-PKA-PP1-CAMKII-AMPA-R sig-aling pathways.

oi:10.1016/j.neures.2010.07.1988

1-b09 �1- and �2-Adrenergic activations enhance exci-atoryynaptic transmission in layer V/VI pyramidal neurons ofhe medial prefrontal cortex of ratsejun Feng

Institute of Neurobiology, Fudan University, Shanghai, China

-Adrenoceptors (�-ARs) are widely distributed throughout the central ner-ous system. Our previous work showed that �-AR activation facilitatesxcitatory synaptic transmission in pyramidal cells of the medial prefrontalortex (mPFC). However, little is known about the �1- and �2-AR regulationsf synaptic transmission in the mPFC. The present study investigated �1- and2-AR modulation of glutamate synaptic transmission in layer V/VI pyrami-al cells of the rat mPFC. Our results show that (1) stimulation of �1-ARsoes not affect the frequency nor the amplitude of mEPSCs, and stimulationf �2-ARs increases the frequency but not amplitude of mEPSCs; (2) stimula-ion of �2-ARs suppresses the paired-pulse ratio of eEPSC, and stimulation of1-ARs does not; and (3) stimulations of �1- and �2-ARs both enhance themplitude of eEPSC and non-MDA-R current and NMDA-induced currents.aken together, these results suggest that �1- and �2-AR activations bothacilitate excitatory synaptic transmission in mPFC pyramidal cells.

oi:10.1016/j.neures.2010.07.1989

1-b24 Morphine has different effect on regulators of-protein signaling 4 (RGS4) protein gene expression inresence or absence of corticosterone in ratseila Satarian 1 , Fereshteh Motamedi 2, Abolhasan Ahmadiani 2,aeed Esmaeili-Mahani 3, Mohammad Javan 1

Dept. Physiol, Iran 2 Neuroscience Research Center, Shahid Beheshti Univer-ity (M.C). Tehran, Iran 3 Department of Biology and Biomolecular Researchenter, Faculty of Sciences, Shahid Bahonar University of Kerman, Kerman,

ran

egulators of G-protein signaling (RGS) proteins negatively modulate G-rotein coupled receptor signaling duration by accelerating G �-subunituanosine triphosphate hydrolysis. Since RGS4 have an important rolen morphine effects at the cellular level and the exact mechanism(s) ofdrenalectomy-induced morphine sensitization have not been fully clari-ed, the present study was designed to determine the changes in the levelsf RGS4 mRNA and protein in intact and adrenalectomized (ADX) morphine-reated rats. All experiments were carried out on male Wistar rats. Theail-flick test was used to assess the nociceptive threshold and corticosteroneevels were measured by radioimmunoassay as a marker of HPA function. Theorsal half of the lumbar spinal cord was assayed for the expression of RGS4sing semiquantitative RT-PCR and immunobloting. Results showed thathe antinociceptive effect of intrathecal morphine (5 �g) was significantlyncreased in ADX rats and these effects were reversed with corticosteroneeplacement. The levels of RGS4 mRNA and protein in ADX rats were simi-ar to those in intact animals. However, morphine could elicit a significantncrease in both mRNA and protein levels of RGS4 following adrenalectomy.n contrast, the pattern of RGS4 gene expression did not show significanthanges in the lumbar spinal cord of intact animals after morphine injection.n conclusion, our results demonstrate that the presence and absence of cor-icosterone could affect morphine-induced analgesia and change RGS4 genexpression following morphine injection.

oi:10.1016/j.neures.2010.07.1990

1-c12 Regulation of evoked vesicular release by synapto-agmins in astrocytesing Guo 1 , Yingfei Xiong 1,2, Sasa Teng 1, Tao Liu 1, ClaireXihang 1, Zhiren Rao 2, Zhuan Zhou 1

Institute of Molecular Medicine, Peking University, Beijing, China 2 Institutef Neuroscience, The Fourth Military Medical University, Xi’an, China

ynaptotagmins (syts) are a family of membrane proteins that may serves Ca2+ sensors in regulating exocytosis. Astrocytes could release different

h 68S (2010) e447–e456 e449

kinds of gliotransmitters to regulate neuronal functions through differentpathways. Glutamate release in astrocytes was proved via Ca2+-dependentexocytosis. It is still controversial for role of SytIV and sytVII in Ca2+-dependent exocytosis in astrocytes. Here we examine effects of transientover-transfected sytIV and/or sytVII, as well as sytVII-KO on the exocyto-sis process in hippocampal astrocytes. Astrocyte exocytosis was recorded byeither fluorescence FM2-10 or electrochemical carbon fiber electrode (CFE)(Chen et al., JNS, 2005). Over expression of SytVIIs prolonged time processof single vesicle release, while SytIV accelerated this process in Syt-over-expressed astrocytes. RNAi tests confirmed these results.

doi:10.1016/j.neures.2010.07.1991

P1-d09 Intravenous neural stem cell transfusion restoresfunctional defecits in 6-OHDA lesioned ratsKavita Seth , Anshi Shukla, Reyaz W. Ansari, Rajnish K. Chaturvedi,Ashok K. AgrawalDev. Tox. Div., IITR, India

We explored the possibility of migration of intravenously infused NSCs tolesioned site in 6-OHDA lesioned rat model of PD in order to restore functionaldeficits as it would be less traumatic and more useful in widely spread or mul-tifocally present lesions. In vitro expended NSCs, labeled with PKH2 linkerdye were intravenously infused through tail vein into 6-OHDA-lesioned rats.NSCs could be tracked in ipsilateral striatum indicating their migration tolesioned area. NSC infusion led to significant functional restoration as evi-dent from as evident from significant decrease in d-amphetamine inducedrotations along with recovered spontaneous locomotion and grip strengthin infused animals. This was accompanied by significant up-regulation inthe expression of tyrosine hydroxylase, its neurotrophin regulators suchas GDNF/BDNF along with restored Bcl-2 and Bax expression as assessedthrough immunohistochemistry, western blot and RT-PCR. The present studyshows that intravenously infused NSC could migrate to lesioned site lead-ing to functional restoration in rat model of PD. These findings can help inadvancing stem cell concepts toward clinical relevance leading to the lesstraumatic and cost effective PD management.

doi:10.1016/j.neures.2010.07.1992

P1-d17 Expression of class II & IV HDACs during murinebraindevelopmentAfsaneh Goudarzi , Farzam AjamianDept. Biology, Univ. of Guilan, Rasht, Iran

Histone deacetylases (HDACs) involved in the remodeling of nuclear chro-matin and thus have a key role in the regulation of gene expression in alleukaryotic cells including neural. In central nervous system (CNS) this phe-nomenon therefore, reflects their key contribution in neural cell proliferationand/or differentiation in important processes such as fetal brain formationand development. Histone hypoacetylation seems to be important to oligo-dendrocyte lineage development and a correlation between reduction inacetylation of histone core proteins and development of neural cells in CNSwas recently addressed. Using reverse transcription-polymerase chain reac-tion (RT-PCR) we investigated the expression of all known member of classII HDACs during early differentiation of embryonic murine neural progeni-tors in Vitro. Our initial screen showed that the members of this family arehighly expressed during this time window, while by far the highest expres-sion level was belonging to the HDAC9. We are currently working to measurethe expression levels of these members from tissues in vivo in distinct part ofmurine brain including cortex during pre- and post-natal development. TheZn-dependent HDAC11 in mammals is the only member of class IV HDACs. Indeveloping murine brain, HDAC11 is shown to be widely expressed postnataland its expression correlates with the maturation of neural cells. However,little is known about HDAC11 role in prenatal development of muring brain.We are currently investigating the change of HDAC11 expression levels dur-ing three main time points of mouse brain development; days 14, 18 and

doi:10.1016/j.neures.2010.07.1993