PolyADP-ribosylation of PARP-1 in the central amygdala is a prerequisite for cocaine-induced place preference

G Yadid, E Lax, A Friedman, L Abraham, L Visochek, M Cohen-Armon

Research output: Contribution to journalConference articlepeer-review

Original languageEnglish
Pages (from-to)S29-S30
Number of pages2
JournalJournal of Molecular Neuroscience
Volume53
Issue numbersuppl. 1
DOIs
StatePublished - 12 Mar 2014

Bibliographical note

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This work was supported by A DOD award number W81XWH-11-2-0111 to GRL

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Supported by NIMH R01MH090134 and NIDA R21DA034954

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Grant of the Deutsche Forschungsgemeinschaft to (BaCoFun, DFG FOR 1341).

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This work was supported by NIAAA R01 AA014366 and the State of California.

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Supported by the Israel Science Foundation grant 1593/10

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This study was supported by AFAR, NIPI, TBG supported by the Lady Davis Post doctoral fellowship

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EU7 Marie Curie grant, AK supported by the Lady Davis fellowship trust

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This work was supported by The Israel Science Foundation grant (NO. 207/11)

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This study was supported by the German Israeli Foundation.

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The research was supported by FP7-PEOPLE-2012-ITN “OLIMPIA”, IIT and Telethon – Italy

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This study was supported by the Edmond J. Safra Philanthropic Foundation

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Supported by US ONR grant # N00014-10-1063 to Y.G.

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Supported by Italian Ministry of Univ. and Resarch (PRIN project n. 2006058401)

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This work was funded by "Fondazione Grigioni per il Morbo di Parkinson" and "Regione Lombardia".

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This work has been supported by the Alzheimer’s Drug Discovery Foundation grant n. 20120601.

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This project is funded by FP7-HEALTH-2013-INNOVATION-1 (Proposal n: 602531-2); Acronym: “DESIRE”

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This study was supported by the Rosetrees Trust and by the European Research Council

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* PL holds the Jacob Gitlin Chair in Physiology at Hebrew Univ. and is affiliated and acknowledges the support by the David R. Bloom Center for Pharmacy and the Dr. Adolf and Klara Brettler Center for Research in Molecular Pharmacology and Therapeutics at The Hebrew Univ. of Jerusalem, Israel. Cohen G is supported by “Eshkol” fellowship from the Israeli Ministry of Science and Technology.

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Supported by NIH

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Supported by Italian Project of Main National Interest, Woman Health Center-Camillo Golgi Foundation

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Supported by ISF

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This work is supported by Mr. Sami Sagol PhD fellowship.

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Supported by the grodetsky center for research of higher brain functions.

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Supported by Dipartimento Politiche Antidroga

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The study was supported by NSF Grant No. DEC-2011/01/B/ HS6/01912

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This work was supported by grants from GIF and ISF

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Supported by an Israel Science Foundation (ISF) grant to IGS.

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This work is currently supported by the Israel Academy of Sciences and Humanities (1181/11).

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In a series of previous experiments (Ben-Yakov & Dudai (2011), Ben Yakov, Eshel & Dudai (2013)) we identified hippocampal activity at the offset of short episodes, presented as movie clips, using functional magnetic resonance imaging (fMRI). This activity was found to be predictive of subsequent memory performance. We have now employed a similar episodic encoding paradigm using magnetoencephalography (MEG), in order to determine the temporal dynamics of the hippocampal offline activity in higher temporal resolution. To this end, 20 subjects watched 112 short movie clips while inside the MEG scanner and were later tested about the clips' gist. We analyzed the data both at the sensor level and using a localization method. Sensor level analysis was conducted in time, frequency and spectral (time-frequency) domains. Next, we utilized a beam former localization method (SAM – synthetic aperture magnetometry, Robinson & Verba, 1998) to inspect the hippocampal response to the stimuli. The results show a clear response to clip offset at a sensory level, apparent in most MEG channels. Further investigation is now conducted to identify sources of memory predictive activity.(This project is supported by the I-CORE Program of the Planning and Budgeting Committee and The Israel Science Foundation (grant No 51/11).)

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Center for Security Science and Technology at the Technion, under grant number 2016258.

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Traumatic brain injury (TBI) causes disability and death. Cell therapy by human umbilical cord blood (HUCB) transplantation has shown promising results in animal models of TBI and is under evaluation in several clinical trials. HUCB contains different stem cell populations, but only mesenchymal stem cells were evaluated for therapy of TBI. Here we confirm and further extend the characterization of the neurotherapeutic effect of HUCB-derived mononuclear cells and demonstrate for the first time, that HUCB-derived CD45 positive (CD45+) cell subset reduced the neurobehavioral deficits which typically occur in a mouse model of closed head injury. Using magnetic sorting, a CD45+ cell population was obtained which was characterized by expression of CD45 and CD11b (96-99%). Intravenous transplantation of these cells 1 day post-trauma resulted with a significant therapeutic effect observed up to 35 days as evaluated by neurological score reflecting neurobehavioral improvement. This therapeutic effect was in a direct correlation with the decreased lesion volume. Treatment of the cells with anti-CD45 antibody decreased the beneficial neurotherapeutic effect of the cells. CD45+ cells were detected by immunohistochemistry at the site of brain injury 1.5-2 h after transplantation. Preliminary experiments suggest attenuation of astrogliosis and microglia activation by decreased immunoreactivity of glial fibrillary acidic protein (GFAP) and allograft inflammatory factor 1 (AIF1/Iba1), at the site of brain injury, 20 days after CD45+ cells transplantation. These findings indicate the neurotherapeutic potential of HUCB-derived CD45+ cell population in a mice model of brain trauma and propose their use in new clinical settings. ** PL holds the Jacob Gitlin Chair in Physiology at Hebrew Univ. and is affiliated and acknowledges the support by the David R. Bloom Center for Pharmacy, the Dr. Adolf and Klara Brettler Center for Research in Molecular Pharmacology and Therapeutics at The Hebrew Univ. of Jerusalem and the Israel Ministry of Science and Technology, Israel; First two authors equally contributed.

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Supported by the Grodetsky center fpor research of higher brain functions.

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The research leading to these results has received funding from the ERC Seventh Framework Programme

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Supported by grants from NIH and NJCSCR.

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The research leading to these results has received funding from the European Research Council ERC 1 Dept of Physiology and Cell Biology, Ben Gurion Univ. of the Negev

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Supported by ISF (311/07, 508/13), BSF (2011044), and EU 7th Program (EduGLIA)

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Supported by the Israel Science Foundation (ISF). H.H is supported by the Azrieli Foundation.

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Supported by ISF and DFG

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Funding was provided by the Legacy Heritage Bio-Medical Program of the ISF (688/10).

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The European Union Seventh Framework Program FP7 under grant agreement 269459

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Research supported by the Israeli National Science Foundation (Grant no’ 623/11)

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This work was supported by the EU Commission, 7th Frame-work Programme: EC FP7-ICT-248311 AMARSi

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This work was supported by Grant from The Ministry of Education and Science of The Perm Krai, Russia

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Stroke afflicts a large segment of population and is a leading cause of death in the western world. Stroke develops when a part of the brain is deprived of oxygen and glucose. Recently, mesenchymal stem cells have been suggested as a therapeutic approach for stroke, due to their ability to secrete a large number of protective anti-inflammatory cytokines and growth factors. Here we investigate the neuroprotective effect of PLX cells (expressing mesenchymal markers but lacking expression of hematopoietic, endothelial and trophoblastic-specific cell markers), on differentiated pheochromocytoma PC12 cells, in an OGD ischemic model. At first, we determined the optimal conditions for neuropro-tection, by exposing undifferentiated or nerve growth factor-differentiated PC12 cells to hypoglycemic and hypoxic conditions followed by reoxygenation in a trans-well system with PLX cells. Under optimal conditions, 2x105 PLX cells conferred 30% neuroprotection towards PC12 cells exposed to ischemic insult. PC12 necrotic cell death, evaluated by lactate dehydrogenase release, was reduced by PLX cells in a dose-dependent manner. Interestingly, the neuroprotective effects of PLX cells was also promoted by conditioning media of cells exposed to OGD insult and was similar to those achieved by the antioxidant 4-Hydroxy-2,2,6,6-tetramethylpiperidine-N-oxyl. Since neuroprotection is one of the prominent functions of the interleukin (IL)-6-type cytokine family and VEGF is an angiogenic factor known to confer neuroprotection, we measured their secretion from PLX cells under ischemic conditions. We found that IL-6 and VEGF secretion was higher, compared to normoxia. Furthermore, exogenous supplementation of human recombinant IL-6 and VEGF to ischemic PC12 cells conferred neuroprotection, reminiscent of PLX cells neuroprotective effect. Therefore, PLX induced-neuroprotection on PC12 neurons exposed to ischemic conditions may partly be explained by IL-6 and VEGF secretion. *PL holds the Jacob Gitlin Chair in Physiology at Hebrew Univ. and is affiliated and acknowledges the support by the David R. Bloom Center for Pharmacy, the Dr. Adolf and Klara Brettler Center for Research in Molecular Pharmacology and Therapeutics at The Hebrew Univ. of Jerusalem and the Israeli Ministry of Industry and Trade, MAGNETON program for the financial support.

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This work was supported by the research consortium (FD hope, FD foundation Inc., FD Israel foundatio

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Suported by grant from Israeli Science Foundation (ISF)

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NO and in basal synthesis of TNF-α. However, in stimulated cells, perindopril increased production of TNF-α.Exposureof the stimulated cells to captopril resulted in a dual effect regarding the release of NO and TNF-α and the expression of iNOS. Captopril concentration of 0.1mM increased NO and TNF-α synthesis and iNOS expression and at concentration of 3mM caused the opposite outcome compared to LPS-treated cells. Ang II nor selective antagonists of BK altered NO and TNF-α observed levels upon ACEI treatment. Conclusions: These results suggest that perindopril and captopril has an anti-inflammatory effect in BV2 microglia that is not mediated through BK nor Ang II. This may suggests that brain penetrating ACEI can serve as neuroprotecting agents neuroinflammation. This research was supported by the ISF (grant No. 101/11).

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Supported in part by the Ministry of Science and Technology, Israel and US Dept. of Defense.

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Study was supported by the RFBR grant #12-04-90434-Укр_а and Ukrainian NAS grant #07-0412

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This study was supported by the Israel Science Foundation.

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This study was generously supported by the Rosetrees Trust (EC) and by the European.

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* PL holds the Jacob Gitlin Chair in Physiology at Hebrew Univ. and is affiliated and acknowledges the support by the David R. Bloom Center for Pharmacy and the Dr. Adolf and Klara Brettler Center for Research in Molecular Pharmacology and Therapeutics at The Hebrew Univ. of Jerusalem, Israel.

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Heart & Stroke Foundation of Canada (CN, MFA); NIH GM-55632 (PL); Canada Research Chair (CN).

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Supported by grants from the ISF and the Israeli Ministry of Science (Israel-France collaboration)

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Supported by the I-CORE Program, (grant No. 51/11)

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Supported by the Israel Science Foundation (ISF) Grant no. 1325/08 to I.N.

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This work was supported by EU FP7 MERIDIAN grant #280778 and Marie Curie EU FP7 grant #26872.

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This study was supported by the I-CORE Program of the Planning and Budgeting Committee

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The research was sponsored by grants from FIRE-AICE and MIUR

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Support/Acknowledgment: Work funded by Fondazione Banco di Sardegna, Sassari, Italy.

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Supported by the ISF, GIF, and the National Institute of Psychobiology in Israel

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Supported by Marie Curie Grant and Rosetrees Foundation

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Study was supported in part by the Sidney and Judy Swartz fund for research in multiple sclerosis

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Background: Most of experimental studies concerning deception show that lying is a more demanding cognitive process and takes more time than telling the truth. However, some findings indicate that deceptive responding generates reaction times similar to truthful responding. The aim of our study was to re-consider the question of response latency in the context of lying and to investigate whether giving the untruthful answer took longer than telling the truth in two specific situations: when the subjects lie as participants of the events and when they lie as witnesses of the events. To reach this aim we developed a new ecological urban-gaming paradigm. Deception was the integral part of the last stage of the game and, likewise in the real life, the participants were not under any constraints to deceive the interviewer. Results: Thirty-two healthy volunteers (18 males) at the age of between 20 and 30 took part in the study. We compared the reaction times in this group when they were lying and when they were telling the truth answering two kinds of questions: addressed to participants and to the witnesses of the events during the urban gaming. We conducted the hierarchical linear modeling, which showed that the stable effect of lying and telling the truth was statistically significant. The effects of interaction showed specifically that the reaction times for lying and for telling the truth differed significantly only in the case of the questions addressed to the witnesses and not participants of the events. Conclusion: The findings suggest that the elongation of reaction times for lying as compared to telling the truth is related to the type of lying. As far as witnesses are concerned, lying takes them much longer than telling the truth - witnesses cannot lie plump. This study was supported with a grant (2011/01/B/ HS6/04611) from the Polish National Science Center.

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This work was supported by A DOD award number W81XWH-11-2-0111 to GRL.

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This study was supported by the Edmond J. Safra Philanthropic Foundation.

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This research was supported in part by I-CORE of the ISF (grant No. 51/11).

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This research was supported by the by the Israeli National Science Foundation (Grant no’ 623/11) 1 Dept. of Neurobiology, Institute of Life Sciences, HUJI 2 The Edmond and Lily Safra Center for Brain Sciences, HUJI 3 Dept. of Biology, Howard Hughes Medical Institute, Stanford Univ.

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The study was supported by grant 823/88 by the Israel Science Foundation to LYD.

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This work was supported by the Technion Autonomous Systems Program, under grant number 2017041.

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The Israel Science foundation grant

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Supported by an ERC grant to JG and an NCN grant to MS

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This research was supported by a grant from the Israeli Science Foundation (ISF, 384/10) to GA.

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Renin-Angiotensin System (RAS) is a hormonal system which mediates cardiovascular regulation and its major effector is angiotensin II (AngII). Lately this system has been discovered also in the brain. AngII is formed from angiotensin I by angiotensin converting enzyme (ACE). There is increasing evidence that RAS may contribute to neuro-inflammation associated with AD. Thereby, specific inhibition of brain RAS has been suggested as a potential therapeutic strategy for AD. In this study we examined the role of Ang II AT1 Receptor Blockers (ARBS) and angiotensin converting enzyme inhibitors (ACEI) in regulation of neuro-inflammation. The in vivo study was conducted on transgenic mice that express five Familial Alzheimer's Disease mutations (5FAD) APP (3 mutations) and PS1(2 mutations). These mice overproduce Aβ42 and exhibit amyloid plaque pathology similar to that found in AD. Results: Intranasal administration of 1mg/kg/day of Telmisartan (ARB) to two month old 5FAD mice for 3-8 weeks resulted in a significant decrease of amyloid beta plaques, an important feature of AD, and in microglial activation, as detected by CD11b immunofluorescence, in the hip-pocampuses and the cortex. Similar changes were observed in the cortex but not in the hippocampus of mice treated with the same dose of Perindopril (ACEI). Conclusions: Our results indicate that intervention in the brain renin angiotensin system with ARBs or ACEI may serve as a new approach for the treatment of brain disorders, such as AD, where inflammation plays a significant role. This research was supported by the Israel Science Foundation (grant 101/11).

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Supported by ERC (AB), ISF (YY), and the Henri J. and Erna D. Leir Chair for Research in Neurodegene

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Background: Angiotensin II receptor type 2 (AT2) agonists have been shown to limit brain ischemic insult and to improve its outcome. The activation of AT2 was also linked to induced neuronal proliferation and differentiation in vitro. Aims: In this study we examined the therapeutic potential of AT2 activation following traumatic brain injury (TBI) which has been shown to exert brain pathology similar to that of cerebral ischemia. AT2 agonist, CGP42112Awas administrated for the first three sequential days post closed head injury (CHI) in a mouse model of TBI. We have followed the functional recovery of the injured mice for 35 days post CHI, and evaluated cognitive function, lesion volume, molecular signaling and neurogenesis at different time points after the impact. Results: We found dose dependent improvement in functional recovery and cognitive performance after CGP42112A treatment that was accompanied by reduced lesion volume and induced neurogenesis in the neurogenic niches of the brain and in the injury region. In the molecular level, CGP42112A induced early activation of the neuroprotective kinases Akt and ERK1/2 as well as of the neurotrophins NGF and BDNF; all were blocked by treatment with the AT2 antagonist PD123319. Conclusions: Our results suggest that AT2 activation after TBI promotes neuroprotection and neurogenesis and may be a novel approach for the development of new drugs to treat TBI victims. This study was supported in part by grant from Dr. Miriam and Sheldon G. Adelson Medical Research Foundation (AMRF).

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Supported by Deutsche Forschungsgemeinschaft (CRC1080)

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The study was supported by an ISF grant 384/10 to GA

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