Kooperativer Bibliotheksverbund

Berlin Brandenburg

and
and

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    In: Current Neuropharmacology, February 2018, Vol.16(2), pp.117-117
    ISSN: 1570-159X
    Source: Bentham Science (IngentaConnect)
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 2
    Language: English
    In: Current Neuropharmacology, 2011, Vol.9(5), p.1-81
    ISSN: 1570-159X
    E-ISSN: 1875-6190
    Source: Bentham Science Publishers
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 3
    Language: English
    In: Current Neuropharmacology, 2018, Vol.16(2), p.117-117
    Keywords: Article;
    ISSN: 1570-159X
    E-ISSN: 1875-6190
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 4
    Language: English
    In: Current Neuropharmacology, 2019, Vol.17(9), p.861-873
    Description: 〈p〉Three inhibitors of type-B monoamine oxidase (MAOB), selegiline, rasagiline, and safinamide, are used for the treatment of Parkinson’s disease (PD). All three drugs improve motor signs of PD, and are effective in reducing motor fluctuations in patients undergoing long-term L-DOPA treatment. The effect of MAOB inhibitors on non-motor symptoms is not uniform and may not be class-related. Selegiline and rasagiline are irreversible inhibitors forming a covalent bond within the active site of MAOB. In contrast, safinamide is a reversible MAOB inhibitor, and also inhibits voltage- sensitive sodium channels and glutamate release. Safinamide is the prototype of a new generation of multi-active MAOB inhibitors, which includes the antiepileptic drug, zonisamide. Inhibition of MAOB-mediated dopamine metabolism largely accounts for the antiparkinsonian effect of the three drugs. Dopamine metabolism by MAOB generates reactive oxygen species, which contribute to nigro-striatal degeneration. Among all antiparkinsonian agents, MAOB inhibitors are those with the greatest neuroprotective potential because of inhibition of dopamine metabolism, induction of neurotrophic factors, and, in the case of safinamide, inhibition of glutamate release. The recent development of new experimental animal models that more closely mimic the progressive neurodegeneration associated with PD will allow to test the hypothesis that MAOB inhibitors may slow the progression of PD.〈/p〉
    Keywords: Selegiline Rasagiline Safinamide Maob Basal Ganglia Parkinson&Amp;#39;S Disease Glutamate Release.
    ISSN: 1570-159X
    E-ISSN: 1875-6190
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 5
    Language: English
    In: Current Neuropharmacology, 2016, Vol.14(1), p.41-47
    Description: Schizophrenia and Bipolar Disorder are chronic psychiatric disorders, both considered as “major psychosis” they are thought to share some pathogenetic factors involving a dysfunctional 〈i〉gene x environment〈/i〉 interaction. Alterations in the glutamatergic transmission have been suggested to be involved in the pathogenesis of psychosis. Our group developed an epigenetic model of schizophrenia originated by Prenatal Restraint Stress (PRS) paradigm in mice. PRS mice developed some behavioral alterations observed in schizophrenic patients and classic animal models of schizophrenia, i.e. deficits in social interaction, locomotor activity and prepulse inhibition. They also showed specific changes in promoter DNA methylation activity of genes related to schizophrenia such as reelin, BDNF and GAD67, and altered expression and function of mGlu2/3 receptors in the frontal cortex. Interestingly, behavioral and molecular alterations were reversed by treatment with mGlu2/3 agonists. Based on these findings, we speculate that pharmacological modulation of these receptors could have a great impact on early phase treatment of psychosis together with the possibility to modulate specific epigenetic key protein involved in the development of psychosis. 〈/p〉 〈p〉 In this review, we will discuss in more details the specific features of the PRS mice as a suitable epigenetic model for major psychosis. We will then focus on key proteins of chromatin remodeling machinery as potential target for new pharmacological treatment through the activation of metabotropic glutamate receptors. 〈/p〉
    Keywords: Dna Methylation Epigenetics Mglu Receptors Prenatal Stress Psychosis.
    ISSN: 1570-159X
    E-ISSN: 1875-6190
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 6
    Language: English
    In: Current Neuropharmacology, 2017, Vol.15(6), p.918-925
    Description: Background: Spike-wave discharges, underlying absence seizures, are generated within a cortico-thalamo-cortical network that involves the somatosensory cortex, the reticular thalamic nucleus, and the ventrobasal thalamic nuclei. Activation of T-type voltage-sensitive calcium channels (VSCCs) contributes to the pathological oscillatory activity of this network, and some of the first-line drugs used in the treatment of absence epilepsy inhibit T-type calcium channels. The ?2? subunit is a component of high voltage-activated VSCCs (i.e., L-, N-, P/Q-, and R channels) and studies carried out in heterologous expression systems suggest that it may also associate with T channels. The ?2? subunit is also targeted by thrombospondins, which regulate synaptogenesis in the central nervous system. 〈P〉〈/P〉 Objective: To discuss the potential role for the thrombospondin/?2? axis in the pathophysiology of absence epilepsy. 〈P〉〈/P〉 Methods: We searched PubMed articles for the terms “absence epilepsy”, “T-type voltage-sensitive calcium channels”, “?2? subunit”, “ducky mice”, “pregabalin”, “gabapentin”, “thrombospondins”, and included papers focusing this Review's scope. 〈P〉〈/P〉 Results: We moved from the evidence that mice lacking the ?2?-2 subunit show absence seizures and ? 2? ligands (gabapentin and pregabalin) are detrimental in the treatment of absence epilepsy. This suggests that ?2? may be protective against absence epilepsy via a mechanism that does not involve T channels. We discuss the interaction between thrombospondins and ?2? and its potential relevance in the regulation of excitatory synaptic formation in the cortico-thalamo-cortical network. 〈P〉〈/P〉 Conclusion: We speculate on the possibility that the thrombospondin/?2 ? axis is critical for the correct functioning of the cortico-thalamo-cortical network, and that abnormalities in this axis may play a role in the pathophysiology of absence epilepsy.
    Keywords: ?2? Subunit T-Type Voltage-Sensitive Ca≪Sup≫2+≪/Sup≫ Channels Non-T-Type Voltage-Sensitive Ca≪Sup≫2+≪/Sup≫ Channels Ducky Mice Pregabalin Gabapentin Absence Epilepsy Thrombospondins.
    ISSN: 1570-159X
    E-ISSN: 1875-6190
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 7
    Language: English
    In: Current Neuropharmacology, 2006, Vol.4(3), p.173-173
    Description: Although morphine is still the gold-standard for the treatment of pathological pain, the increasing knowledge of the mechanisms that regulate pain threshold breaks the ground for the development of new potent and safe analgesic drugs. Hopefully, these drugs will relieve some forms of pain that are partially resistant to opiates, such as neuropathic pain. This issue of Current Neuropharmacology includes a series of excellent reviews that summarize the current knowledge and the most exciting perspectives on the neurobiology of pain. The opening review by Dr. Marchettini and collaborators is a nice clinical classification of peripheral neuropathies, which are a major source of neuropathic pain. If present, pain associated with peripheral neuropathies is extremely disabling, and its treatment is one of the major challenges in neuroscience. The two following reviews by Dr. Story and Dr. Mc Naughton's group focus on the role of Trp channels in heat sensation and inflammatory pain. One of these channels, named TrpV1, is expressed by neurons of dorsal root ganglia, and responds to heat, protons, inflammatory mediators, and capsaicin. An increased sensitivity of the TrpV1 channel is central to the pathophysiology of heat hyperalgesia in inflammatory pain. The review by the group of Dr. Negri and Dr. Melchiorri describes the role of prokineticins and their receptors in the modulation of pain. Prokineticins are the mammalian homologs of Bv8, a small protein extracted from the frog skin that behaves as a potent hyperalgesic agent. The regulation of pain moves from the periphery to the CNS in the review by Dr. Tao and Dr. Johns, which describes the role of PDZ-domain-containing proteins associated with NMDA receptors in persistent pain. The review by the group of Dr. Maione and Dr. Rossi explores the complex interaction between metabotropic glutamate receptors and cannabinoid receptors in the periaqueductal grey, a region of the brainstem that is critical for the regulation of pain threshold. These two classes of receptors are considered as potential targets for novel analgesic drugs. Along this line, the review by Dr. Chiechio and collaborators describes the mechanism of action of Lacetylcarnitine, a drug that is currently used for the treatment of neuropathic pain. L-Acetylcarnitine up-regulates the expression of a particular metabotropic glutamate receptor subtype, the mGlu2 receptor, which inhibits neurotransmission at the synapse between primary afferent pathways and neurons in the dorsal horns of the spinal cord. Finally, the elegant review by Dr. Manzanares, Dr. Julian, and Dr. Carrascosa describes the multifaceted role of the cannabinoid system in pain transmission, and the potential therapeutic implications for the management of acute and chronic pain. Taken together, the articles included in the issue offer an original view of the molecular and transsynaptic mechanisms underlying inflammatory and neuropathic pain, and are particularly helpful for basic scientists and clinicians interested in the neuropharmacology of pain.
    Keywords: Psychosis;
    ISSN: 1570-159X
    E-ISSN: 1875-6190
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 8
    Language: English
    In: Current Neuropharmacology, 2013, Vol.11(5), p.535-558
    Description: Objectives. To review the role of Wnt pathways in the neurodevelopment of schizophrenia. Methods: Systematic PubMed search, using as keywords all the terms related to the Wnt pathways and crossing them with each of the following areas: normal neurodevelopment and physiology, neurodevelopmental theory of schizophrenia, schizophrenia, and antipsychotic drug action. Results: Neurodevelopmental, behavioural, genetic, and psychopharmacological data point to the possible involvement of Wnt systems, especially the canonical pathway, in the pathophysiology of schizophrenia and in the mechanism of antipsychotic drug action. The molecules most consistently found to be associated with abnormalities or in antipsychotic drug action are Akt1, glycogen synthase kinase3beta, and beta-catenin. However, the extent to which they contribute to the pathophysiology of schizophrenia or to antipsychotic action remains to be established. Conclusions: The study of the involvement of Wnt pathway abnormalities in schizophrenia may help in understanding this multifaceted clinical entity; the development of Wnt-related pharmacological targets must await the collection of more data.
    Keywords: Antipsychotic Drugs; Neurodevelopment; Schizophrenia; Wingless (Wnt) Signalling.
    ISSN: 1570-159X
    E-ISSN: 1875-6190
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 9
    Language: English
    In: Current Neuropharmacology, 2012, Vol.10(3), p.239-253
    Description: Objectives: To review the evidence of the involvement of the Wnt signalling pathway in mood disorders and in the action of drugs used to treat these disorders. 〈p〉〈/p〉 Methods: We performed a careful PubMed search using as keywords all possible terms relevant to the Wnt pathway and crossing them with each of four areas, i.e., developmental effects, behavioural effects, mood disorders, and drugs used in their treatment. Papers were selected on the basis of their content and their data used for discussion. 〈p〉〈/p〉 Results: Neurodevelopmental and behavioural data point to the possibility of involvement of the Wnt pathway in the pathophysiology of mood disorders. Clinical and post-mortem data are not sufficient to corroborate a definite role for Wnt alterations in any mood disorder. Combining genetic and pharmacological data, we may state that glycogen synthase kinase is the key molecule in bipolar disorder, as it is connected with many other signalling pathways that were shown to be involved in mood disorders, while Wnt molecules in the hippocampus appear to be mainly involved in depressive disorders. 〈p〉〈/p〉 Conclusions: Altered Wnt signalling may play a role in the pathophysiology of mood disorders, although not a central one. It is premature to draw conclusions regarding the possible usefulness of Wnt manipulations in the treatment of mood disorders. 〈p〉〈/p〉
    Keywords: Wingless (Wnt) Signalling ; Mood Disorders ; Bipolar Disorder ; Major Depression ; Antidepressant Drugs ; Mood Stabilising Agents ; Antipsychotic Drugs
    ISSN: 1570-159X
    E-ISSN: 1875-6190
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. Further information can be found on the KOBV privacy pages