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Berlin Brandenburg

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  • 1
    Language: English
    In: The Journal of Headache and Pain, 2015, Vol.16(Supplement 1), pp.1-1
    Description: Kynurenine pathway (KP), the quantitatively main branch of tryptophan metabolism, has long been considered a source of nicotinamide adenine dinucleotide, although several of its products, the so-called kynurenines, are endowed with the capacity to activate glutamate receptors, thus potentially influencing a large group of functions in the central nervous system (CNS). In fact, Kynurenic Acid and Quinolinic Acid are able to interact with ionotropic glutamate receptors and Cinnabarinic Acid has been reported as an orthosteric agonist of metabotropic glutamate receptors (mGlu4), and Xanthurenic Acid has been recently demonstrated to be a putative agonist of metabotropic glutamate receptors 2/3 (mGlu2/3). Moreover, 3-HK and 3-HANA have mainly been studied, since they have been shown to induce neurotoxic effects by increasing oxidative stress and the production of free radicals or through excitotoxicity. Migraine has a complex pathophysiology in which both central and peripheral components of the trigeminal pain pathway play a central role. The trigemino-vascular activation during the attack has largely been described, and recently the brainstem nuclei, called “migraine generators”, have been reported to be involved in migraine. Moreover, a series of destabilizing events within the brain trigger a cortical spreading depression (CSD), responsible for the aura phenomena and for trigeminal activation. The role of glutamate is heavily supported both in the trigemino-vascular as well as in brainstem nuclei activation, and furthermore in the CSD initiation and propagation. Some of the KP metabolites able to interact both with ionotropic and metabotropic glutamate receptors might be involved in migraine pathophysiology. Despite the large number of studies conducted on migraine etiopathology, the KP has only been recently linked to this disease. Nonetheless, some evidence suggests an intriguing role for some kynurenines, and an exploratory study on the serum kynurenine levels has been helpful to better understand possible alterations of the kynurenine pathway in patients suffering from migraine.
    Keywords: Medicine;
    ISSN: 1129-2369
    E-ISSN: 1129-2377
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  • 2
    In: Medicine & Science in Sports & Exercise, 2013, Vol.45(1), pp.29-35
    Description: PURPOSE: Anabolic androgenic steroids (AAS) are synthetic androgen-like compounds that are abused in sport communities despite their adverse effects. Nerve growth factor (NGF) influences neuronal differentiation and survival, and it also mediates higher brain functions such as learning and memory. Changes in NGF expression have been implicated in neurodegenerative disorders, including Alzheimer disease. Hence, we decided to study the effect of chronic AAS exposure on brain NGF profile, NGF-dependent cholinergic function, and related behavioral performance. METHODS: Male Wistar rats were injected for 4 wk with either nandrolone or stanozolol at daily doses (5.0 mg·kg, s.c.) that are considered equivalent to those abused by humans. NGF levels and NGF receptor (TrkA and p75NTR) expression were measured in the hippocampus and in the basal forebrain. Choline acetyltransferase expression was evaluated in basal forebrain. Spatial learning and memory were assessed using the Morris water maze. RESULTS: AAS treatment caused region-specific changes in the expression of NGF and its receptors. Both nandrolone and stanozolol increased NGF levels in the hippocampus and reduced NGF levels in the basal forebrain, reduced p75NTR expression in the hippocampus, and failed to affect TrkA expression in the basal forebrain. Finally, AAS treatment reduced the expression of choline acetyltransferase in the basal forebrain and impaired the behavioral performance in the Morris water maze. CONCLUSION: The evidence that supraphysiological doses of AAS cause neurotrophic unbalance and related behavioral disturbances raises the concern that AAS abuse in humans may affect mechanisms that lie at the core of neuronal plasticity.
    Keywords: Anabolic Agents -- Adverse Effects ; Androgens -- Adverse Effects ; Hippocampus -- Drug Effects ; Nandrolone -- Adverse Effects ; Nerve Growth Factor -- Metabolism ; Performance-Enhancing Substances -- Adverse Effects ; Stanozolol -- Adverse Effects;
    ISSN: 0195-9131
    E-ISSN: 15300315
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  • 3
    Language: English
    In: Proceedings of the National Academy of Sciences of the United States, March 19, 2013, Vol.110(12), p.4804(6)
    Description: Epigenetic mechanisms are involved in the pathophysiology of depressive disorders and are unique potential targets for therapeutic intervention. The acetylating agent L-acetylcarnitine (LAC), a well-tolerated drug, behaves as an antidepressant by the epigenetic regulation of type 2 metabotropic glutamate (mGlu2) receptors. It caused a rapid and long-lasting antidepressant effect in Flinders Sensitive Line rats and in mice exposed to chronic unpredictable stress, which, respectively, model genetic and environmentally induced depression. In both models, LAC increased levels of acetylated H3K27 bound to the Grm2 promoter and also increased acetylation of NF-KB-p65 subunit, thereby enhancing the transcription of Grm2 gene encoding for the mGlu2 receptor in hippocampus and prefrontal cortex. Importantly, LAC reduced the immobility time in the forced swim test and increased sucrose preference as early as 3 d of treatment, whereas 14 d of treatment were needed for the antidepressant effect of chlorimipramine. Moreover, there was no tolerance to the action of LAC, and the antidepressant effect was still seen 2 wk after drug withdrawal. Conversely, NF-kB inhibition prevented the increase in mGlu2 expression induced by LAC, whereas the use of a histone deacetylase inhibitor supported the epigenetic control of mGlu2 expression. Finally, LAC had no effect on mGlu2 knockout mice exposed to chronic unpredictable stress, and a single injection of the mGlu2/3 receptor antagonist LY341495 partially blocked LAC action. The rapid and long-lasting antidepressant action of LAC strongly suggests a unique approach to examine the epigenetic hypothesis of depressive disorders in humans, paving the way for more efficient antidepressants with faster onset of action. doi/10.1073/pnas.1216100110
    Keywords: Antidepressants -- Research ; Antidepressants -- Analysis ; Depression (Mood disorder) -- Research ; Depression (Mood disorder) -- Analysis
    ISSN: 0027-8424
    Source: Cengage Learning, Inc.
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  • 4
    Language: English
    In: The Journal of Headache and Pain, Dec, 2015, Vol.16(1), p.1(1)
    Description: To access, purchase, authenticate, or subscribe to the full-text of this article, please visit this link: http://dx.doi.org/10.1186/1129-2377-16-S1-A1 Byline: Ferdinando Nicoletti (1) Author Affiliation: (1) Dipartimento di Fisiologia Umana e Farmacologia "V. Erspamer", Universita Sapienza di Roma, Rome, Italy Article History: Registration Date: 28/09/2015 Online Date: 28/09/2015
    ISSN: 1129-2369
    Source: Cengage Learning, Inc.
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  • 5
    In: Neuropsychopharmacology, 2011, Vol.37(4), p.929
    Description: Prenatal exposure to restraint stress causes long-lasting changes in neuroplasticity that likely reflect pathological modifications triggered by early-life stress. We found that the offspring of dams exposed to repeated episodes of restraint stress during pregnancy (here named 'prenatal restraint stress mice' or 'PRS mice') developed a schizophrenia-like phenotype, characterized by a decreased expression of brain-derived neurotrophic factor and glutamic acid decarboxylase 67, an increased expression of type-1 DNA methyl transferase (DNMT1) in the frontal cortex, and a deficit in social interaction, locomotor activity, and prepulse inhibition. PRS mice also showed a marked decrease in metabotropic glutamate 2 (mGlu2) and mGlu3 receptor mRNA and protein levels in the frontal cortex, which was manifested at birth and persisted in adult life. This decrease was associated with an increased binding of DNMT1 to CpG-rich regions of mGlu2 and mGlu3 receptor promoters and an increased binding of MeCP2 to the mGlu2 receptor promoter. Systemic treatment with the selective mGlu2/3 receptor agonist LY379268 (0.5 mg/kg, i.p., twice daily for 5 days), corrected all the biochemical and behavioral abnormalities shown in PRS mice. Our data show for the first time that PRS induces a schizophrenia-like phenotype in mice, and suggest that epigenetic changes in mGlu2 and mGlu3 receptors lie at the core of the pathological programming induced by early-life stress.
    Keywords: Medicine ; Pharmacy, Therapeutics, & Pharmacology ; Anatomy & Physiology;
    ISSN: 0893-133X
    E-ISSN: 1740634X
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  • 6
    Language: English
    In: European Journal of Pharmacology, Jan 10, 2010, Vol.626(1), p.64(8)
    Description: To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ejphar.2009.10.022 Byline: Filippo Caraci (a), Agata Copani (a)(b), Ferdinando Nicoletti (c)(d), Filippo Drago (e) Keywords: Major depression; Alzheimer's disease; Chronic inflammation; [beta]-amyloid; Transforming-growth-factor-[beta]1; Brain-derived neurotrophic factor; Neuroprotection Abstract: Depression is one of the most prevalent and life-threatening forms of mental illnesses, whereas Alzheimer's disease is a neurodegenerative disorder that affects more than 37 million people worldwide. Recent evidence suggests a strong relationship between depression and Alzheimer's disease. A lifetime history of major depression has been considered as a risk factor for later development of Alzheimer's disease. The presence of depressive symptoms can affect the conversion of mild cognitive impairment into Alzheimer's disease. Neuritic plaques and neurofibrillary tangles, the two major hallmarks of Alzheimer's disease brain, are more pronounced in the brains of Alzheimer's disease patients with comorbid depression as compared with Alzheimer's disease patients without depression. On the other hand, neurodegenerative phenomena have been observed in different brain regions of patients with a history of depression. Recent evidence suggests that molecular mechanisms and cascades that underlie the pathogenesis of major depression, such as chronic inflammation and hyperactivation of hypothalamic-pituitary-adrenal (HPA) axis, are also involved in the pathogenesis of Alzheimer's disease. In particular, a specific impairment in the signaling of some neurotrophins such as transforming-growth-factor [beta]1 (TGF-[beta]1) and brain-derived neurotrophic factor (BDNF) has been observed both in depression and Alzheimer's disease. In the present review we will examine the evidence on the common molecular pathways between depression and Alzheimer's disease and we will discuss these pathways as new pharmacological targets for the treatment of both major depression and Alzheimer's disease. Author Affiliation: (a) Department of Pharmaceutical Sciences, University of Catania, 95125, Catania, Italy (b) I.B.B., CNR-Catania, 95125, Catania, Italy (c) I.N.M. Neuromed, Localita Camerelle, 86077, Pozzilli, Italy (d) Department of Human Physiology and Pharmacology, University of Rome La Sapienza, 00185 Rome, Italy (e) Department of Experimental and Clinical Pharmacology, University of Catania, 95125, Catania, Italy Article History: Accepted 9 October 2009
    Keywords: Depression (Mood disorder) -- Risk Factors ; Depression (Mood disorder) -- Development And Progression ; Alzheimer's Disease -- Risk Factors ; Alzheimer's Disease -- Development And Progression ; Peptide Hormones ; Transforming Growth Factors ; Brain
    ISSN: 0014-2999
    Source: Cengage Learning, Inc.
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  • 7
    Language: English
    In: Diabetologia, 2014, Vol.57(5), pp.980-990
    Description: Byline: Ivana Nikolic (1), Tamara Saksida (1), Katia Mangano (2), Milica Vujicic (1), Ivana Stojanovic (1), Ferdinando Nicoletti (2), Stanislava Stosic-Grujicic (1) Keywords: Beta cell apoptosis; Carbon monoxide-releasing molecule-A1; Cytokines; Type 1 diabetes Abstract: Aims/hypothesis Recent studies have identified carbon monoxide (CO) as a potential therapeutic molecule for the treatment of autoimmune diseases owing to its anti-inflammatory and anti-apoptotic properties. We explored the efficacy and the mechanisms of action of the CO-releasing molecule (CORM)-A1 in preclinical models of type 1 diabetes. Methods The impact of CORM-A1 on diabetes development was evaluated in models of spontaneous diabetes in NOD mice and in diabetes induced in C57BL/6 mice by multiple low-dose streptozotocin (MLDS). Ex vivo analysis was performed to determine the impact of CORM-A1 both on T helper (Th) cell and macrophage differentiation and on their production of soluble mediators in peripheral tissues and in infiltrates of pancreatic islets. The potential effect of CORM-A1 on cytokine-induced apoptosis in pancreatic islets or beta cells was evaluated in vitro. Results CORM-A1 conferred protection from diabetes in MLDS-induced mice and reduced diabetes incidence in NOD mice as confirmed by preserved insulin secretion and improved histological signs of the disease. In MLDS-challenged mice, CORM-A1 attenuated Th1, Th17, and M1 macrophage response and facilitated Th2 cell differentiation. In addition, CORM-A1 treatment in NOD mice upregulated the regulatory arm of the immune response (M2 macrophages and FoxP3.sup.+ regulatory T cells). Importantly, CORM-A1 interfered with in vitro cytokine-induced beta cell apoptosis through the reduction of cytochrome c and caspase 3 levels. Conclusions/interpretation The ability of CORM-A1 to protect mice from developing type 1 diabetes provides a valuable proof of concept for the potential exploitation of controlled CO delivery in clinical settings for the treatment of autoimmune diabetes. Author Affiliation: (1) Department of Immunology, Institute for Biological Research 'Sinisa Stankovic', University of Belgrade, Bul. Despota Stefana 142, 11060, Belgrade, Serbia (2) Department of Biomedical Sciences, School of Medicine, University of Catania, Via Androne 83, 95124, Catania, Italy Article History: Registration Date: 10/01/2014 Received Date: 19/07/2013 Accepted Date: 18/12/2013 Online Date: 02/02/2014 Article note: Electronic supplementary material The online version of this article (doi: 10.1007/s00125-014-3170-7) contains peer-reviewed but unedited supplementary material, which is available to authorised users.
    Keywords: Beta cell apoptosis ; Carbon monoxide-releasing molecule-A1 ; Cytokines ; Type 1 diabetes
    ISSN: 0012-186X
    E-ISSN: 1432-0428
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  • 8
    Language: English
    In: Proceedings of the National Academy of Sciences of the United States of America, 19 March 2013, Vol.110(12), pp.4804-4809
    Description: Epigenetic mechanisms are involved in the pathophysiology of depressive disorders and are unique potential targets for therapeutic intervention. The acetylating agent L-acetylcarnitine (LAC), a welltolerated drug, behaves as an antidepressant by the epigenetic regulation of type 2 metabotropic glutamate (mGlu2) receptors. It caused a rapid and long-lasting antidepressant effect in Flinders Sensitive Line rats and in mice exposed to chronic unpredictable stress, which, respectively, model genetic and environmentally induced depression. In both models, LAC increased levels of acetylated H3K27 bound to the Grm2 promoter and also increased acetylation of NF-KB-p65 subunit, thereby enhancing the transcription of Grm2 gene encoding for the mGlu2 receptor in hippocampus and prefrontal cortex. Importantly, LAC reduced the immobility time in the forced swim test and increased sucrose preference as early as 3 d of treatment, whereas 14 d of treatment were needed for the antidepressant effect of chlorimipramine. Moreover, there was no tolerance to the action of LAC, and the antidepressant effect was still seen 2 wk after drug withdrawal. Conversely, NF-κB inhibition prevented the increase in mGlu2 expression induced by LAC, whereas the use of a histone deacetylase inhibitor supported the epigenetic control of mGlu2 expression. Finally, LAC had no effect on mGlu2 knockout mice exposed to chronic unpredictable stress, and a single injection of the mGlu2/3 receptor antagonist LY341495 partially blocked LAC action. The rapid and long-lasting antidepressant action of LAC strongly suggests a unique approach to examine the epigenetic hypothesis of depressive disorders in humans, paving the way for more efficient antidepressants with faster onset of action.
    ISSN: 00278424
    Source: Archival Journals (JSTOR)
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  • 9
    Language: English
    In: Proceedings of the National Academy of Sciences of the United States of America, 19 March 2013, Vol.110(12), pp.4804-9
    Description: Epigenetic mechanisms are involved in the pathophysiology of depressive disorders and are unique potential targets for therapeutic intervention. The acetylating agent L-acetylcarnitine (LAC), a well-tolerated drug, behaves as an antidepressant by the epigenetic regulation of type 2 metabotropic glutamate (mGlu2) receptors. It caused a rapid and long-lasting antidepressant effect in Flinders Sensitive Line rats and in mice exposed to chronic unpredictable stress, which, respectively, model genetic and environmentally induced depression. In both models, LAC increased levels of acetylated H3K27 bound to the Grm2 promoter and also increased acetylation of NF-ĸB-p65 subunit, thereby enhancing the transcription of Grm2 gene encoding for the mGlu2 receptor in hippocampus and prefrontal cortex. Importantly, LAC reduced the immobility time in the forced swim test and increased sucrose preference as early as 3 d of treatment, whereas 14 d of treatment were needed for the antidepressant effect of chlorimipramine. Moreover, there was no tolerance to the action of LAC, and the antidepressant effect was still seen 2 wk after drug withdrawal. Conversely, NF-ĸB inhibition prevented the increase in mGlu2 expression induced by LAC, whereas the use of a histone deacetylase inhibitor supported the epigenetic control of mGlu2 expression. Finally, LAC had no effect on mGlu2 knockout mice exposed to chronic unpredictable stress, and a single injection of the mGlu2/3 receptor antagonist LY341495 partially blocked LAC action. The rapid and long-lasting antidepressant action of LAC strongly suggests a unique approach to examine the epigenetic hypothesis of depressive disorders in humans, paving the way for more efficient antidepressants with faster onset of action.
    Keywords: Acetylcarnitine -- Pharmacology ; Antidepressive Agents -- Pharmacology ; Epigenesis, Genetic -- Drug Effects ; Hippocampus -- Metabolism ; Nerve Tissue Proteins -- Biosynthesis ; Prefrontal Cortex -- Metabolism ; Receptors, Metabotropic Glutamate -- Biosynthesis
    ISSN: 00278424
    E-ISSN: 1091-6490
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  • 10
    Language: English
    In: Cell Chemical Biology, 18 August 2016, Vol.23(8), pp.887-888
    Description: In this issue of , the elegant manuscript by describes a negative allosteric modulator (NAM) of mGlu4 metabotropic glutamate receptors with in vivo activity. This compound is rapidly and reversibly inactivated by light and represents a powerful pharmacological tool for the study of mGlu4 receptors in their native environment. In this issue of , the elegant manuscript by Rovira et al. (2016) describes a negative allosteric modulator (NAM) of mGlu4 metabotropic glutamate receptors with in vivo activity. This compound is rapidly and reversibly inactivated by light and represents a powerful pharmacological tool for the study of mGlu4 receptors in their native environment.
    Keywords: Anatomy & Physiology
    ISSN: 2451-9456
    E-ISSN: 24519448
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