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  • 1
    Language: English
    In: Neuropharmacology, March, 2013, Vol.66, p.24(7)
    Description: To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.neuropharm.2012.05.005 Byline: Luisa Iacovelli (a), Ferdinando Nicoletti (a)(c), Antonio De Blasi (b) Abstract: The purpose of the present article is to review our actual knowledge on the desensitization of metabotropic glutamate receptors based on the literature available so far, with the attempt to emphasize all converging data and to give a possible explanation to those evidences that still remain controversial. 1. We review our knowledge on the regulation of mGlu receptors based on the available literature 2. We report converging data and we comment on issues that still remain controversial. This article is part of a Special Issue entitled 'Metabotropic Glutamate Receptors'. Author Affiliation: (a) Dept. of Physiology and Pharmacology "V. Erspamer", University of Rome "Sapienza", P.le Aldo Moro 5, 00185 Rome, Italy (b) Dept. of Molecular Medicine, University of Rome "Sapienza", Rome, Italy (c) I.N.M. Neuromed, Pozzilli, Italy Article History: Received 29 February 2012; Revised 6 May 2012; Accepted 8 May 2012
    Keywords: Amino Acids -- Physiological Aspects ; Glutamate -- Physiological Aspects
    ISSN: 0028-3908
    Source: Cengage Learning, Inc.
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  • 2
    Language: English
    In: Neuropharmacology, March 2013, Vol.66, pp.24-30
    Description: The purpose of the present article is to review our actual knowledge on the desensitization of metabotropic glutamate receptors based on the literature available so far, with the attempt to emphasize all converging data and to give a possible explanation to those evidences that still remain controversial. 1. We review our knowledge on the regulation of mGlu receptors based on the available literature 2. We report converging data and we comment on issues that still remain controversial. This article is part of a Special Issue entitled ‘Metabotropic Glutamate Receptors’. ► We review our knowledge on the desensitization of mGlu receptors. ► We focus both on converging data and on issues that still remain controversial. ► GRK2 regulates mGlu1 receptor by a phosphorylation-independent mechanism. ► The mGlu2 (but not the mGlu3) receptor is resistant to homologous desensitization.
    Keywords: Metabotropic Glutamate Receptors ; Receptor Desensitization ; Grks ; Arrestins ; Pharmacy, Therapeutics, & Pharmacology
    ISSN: 0028-3908
    E-ISSN: 1873-7064
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  • 3
    Language: English
    In: Neuropharmacology, 15 March 2017, Vol.115, pp.1-3
    Description: To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.neuropharm.2016.09.029 Byline: Graham L. Collingridge Author Affiliation: Department of Physiology, University of Toronto, Mount Sinai Hospital, Toronto, Canada Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, Canada Centre for Synaptic Plasticity, School of Physiology, Pharmacology and Neuroscience, University of Bristol, Bristol, UK Article History: Accepted 29 September 2016
    Keywords: Pharmacy, Therapeutics, & Pharmacology
    ISSN: 0028-3908
    E-ISSN: 1873-7064
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  • 4
    Language: English
    In: Neuropharmacology, 15 March 2017, Vol.115, pp.180-192
    Description: Metabotropic glutamate (mGlu) receptor ligands are under clinical development for the treatment of CNS disorders with high social and economic burden, such as schizophrenia, major depressive disorder (MDD), and Parkinson’s disease (PD), and are promising drug candidates for the treatment of Alzheimer’s disease (AD). So far, clinical studies have shown symptomatic effects of mGlu receptor ligands, but it is unknown whether these drugs act as disease modifiers or, at the opposite end, they accelerate disease progression by enhancing neurodegeneration. This is a fundamental issue in the treatment of PD and AD, and is also an emerging theme in the treatment of schizophrenia and MDD, in which neurodegeneration is also present and contribute to disease progression. Moving from data and preclinical studies, we discuss the potential impact of drugs targeting mGlu2, mGlu3, mGlu4 and mGlu5 receptor ligands on active neurodegeneration associated with AD, PD, schizophrenia, and MDD. We wish to highlight that our final comments on the best drug candidates are not influenced by commercial interests or by previous or ongoing collaborations with drug companies. This article is part of the Special Issue entitled ‘Metabotropic Glutamate Receptors, 5 years on’.
    Keywords: Metabotropic Glutamate Receptors ; Schizophrenia ; Major Depressive Disorders ; Alzhiemer’s Disease ; Parkinson’s Disease ; Neurodegeneration ; Pharmacy, Therapeutics, & Pharmacology
    ISSN: 0028-3908
    E-ISSN: 1873-7064
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  • 5
    Language: English
    In: Neuropharmacology, March 2013, Vol.66, pp.143-150
    Description: Synaptic transmission is essential for early development of the central nervous system. However, the mechanisms that regulate early synaptic transmission in the cerebral cortex are unclear. PKMζ is a kinase essential for the maintenance of LTP. We show for the first time that inhibition of PKMζ produces a profound depression of basal synaptic transmission in neonatal, but not adult, rat perirhinal cortex. This suggests that synapses in early development are in a constitutive LTP-like state. Furthermore, basal synaptic transmission in immature, but not mature, perirhinal cortex relies on persistent activity of metabotropic glutamate (mGlu) receptor, PI3Kinase and mammalian target of rapamycin (mTOR). Thus early in development, cortical synapses exist in an LTP-like state maintained by tonically active mGlu receptor-, mTOR- and PKMζ- dependent cascades. These results provide new understanding of the molecular mechanisms that control synapses during development and may aid our understanding of developmental disorders such as autism and schizophrenia. This article is part of a Special Issue entitled ‘Metabotropic Glutamate Receptors’. ► Synapses are in a constitutive LTP-like state in the developing perirhinal cortex. ► PKMζ inhibition reduces synaptic transmission in the developing perirhinal cortex. ► Group-I mGlu receptors support the LTP-like state in the perirhinal cortex. ► PKMζ, PI3Kinase and mTOR are down stream of group-I mGlu receptors.
    Keywords: Ltp ; Pkmζ ; Group I Mglu Receptor ; Cerebral Cortex ; Development ; Mtor ; Protein Translation ; Pharmacy, Therapeutics, & Pharmacology
    ISSN: 0028-3908
    E-ISSN: 1873-7064
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  • 6
    Language: English
    In: Neuropharmacology, August 2015, Vol.95, pp.50-58
    Description: Neuroadaptive changes involving the indirect pathway of the basal ganglia motor circuit occur in the early phases of parkinsonism. The precise identification of these changes may shed new light into the pathophysiology of parkinsonism and better define the time window of pharmacological intervention. We examined some of these changes in mice challenged with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), or with the dopamine receptor blocker, haloperidol. These two models clearly diverge from Parkinson's disease (PD); however, they allow an accurate time-dependent analysis of neuroadaptive changes occurring in the striatum. Acute haloperidol injection caused a significant increase in the transcripts of mGlu4 receptors, CB1 receptors and preproenkephalin-A at 2 and 24 h, and a reduction in the transcripts of mGlu5 and A receptors at 2 h. At least changes in the expression of mGlu4 receptors might be interpreted as compensatory because haloperidol-induced catalepsy was enhanced in mGlu4 mice. Mice injected with 30 mg/kg of MPTP also showed an increase in the transcripts of mGlu4 receptors, CB1 receptors, and preproenkephalin-A at 3 d, and a reduction of the transcript of A receptors at 1 d in the striatum. Genetic deletion of mGlu4 receptors altered the functional response to MPTP, assessed by counting c-Fos neurons in the external globus pallidus and ventromedial thalamic nucleus. These findings offer the first evidence that changes in the expression of mGlu4 and mGlu5 receptors occur in acute models of parkinsonisms, and lay the groundwork for the study of these changes in models that better recapitulate the temporal profile of nigrostriatal dysfunction associated with PD.
    Keywords: Metabotropic Glutamate Receptors ; Haloperidol ; Mptp ; Parkinsonism ; Indirect Pathway ; Pharmacy, Therapeutics, & Pharmacology
    ISSN: 0028-3908
    E-ISSN: 1873-7064
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  • 7
    Language: English
    In: Neuropharmacology, January 2017, Vol.112, pp.365-372
    Description: Cinnabarinic and xanthurenic acids are kynurenine metabolites generated by oxidative dimerization of 3-hydroxyanthranilic acid and transamination of 3-hydroxykynurenine, respectively. Recent evidence suggests that both compounds can affect brain function and neurotransmission and interact with metabotropic glutamate (mGlu) receptors. Cinnabarinic acid behaves as an orthosteric agonist of mGlu4 receptors, whereas some of the and effects produced by xanthurenic acid appear to be mediated by the activation of mGlu2 and mGlu3 receptors. Cinnabarinic acid could play an important role in mechanisms of neuroinflammation acting as a linking bridge between the immune system and the CNS. Xanthurenic acid has potential implications in the pathophysiology of schizophrenia and is a promising candidate as a peripheral biomarker of the disorder. The action of cinnabarinic acid and xanthurenic acid may extend beyond the regulation of mGlu receptors and may involve several diverse molecular targets, such as the aryl hydrocarbon receptor for cinnabarinic acid and vesicular glutamate transporters for xanthurenic acid. The growing interest on these two metabolites of the kynurenine pathway may unravel new aspects in the complex interaction between tryptophan metabolism and brain function, and lead to the discovery of new potential targets for the treatment of neurological and psychiatric disorders. This article is part of the Special Issue entitled ‘The Kynurenine Pathway in Health and Disease’.
    Keywords: Cinnabarinic Acid ; Xanthurenic Acid ; Metabotropic Glutamate Receptors ; Neuroinflammation ; Schizophrenia ; Pharmacy, Therapeutics, & Pharmacology
    ISSN: 0028-3908
    E-ISSN: 1873-7064
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  • 8
    Language: English
    In: Neuropharmacology, May 2013, Vol.68, pp.184-194
    Description: Human studies suggest that a variety of prenatal stressors are related to high risk for cognitive and behavioral abnormalities associated with psychiatric illness ( ). Recently, a downregulation in the expression of GABAergic genes (i.e., glutamic acid decarboxylase 67 and reelin) associated with DNA methyltransferase (DNMT) overexpression in GABAergic neurons has been regarded as a characteristic phenotypic component of the neuropathology of psychotic disorders ( ). Here, we characterized mice exposed to prenatal restraint stress (PRS) in order to study neurochemical and behavioral abnormalities related to development of schizophrenia in the adult. Offspring born from non-stressed mothers (control mice) showed high levels of DNMT1 and 3a mRNA expression in the frontal cortex at birth, but these levels progressively decreased at post-natal days (PND) 7, 14, and 60. Offspring born from stressed mothers (PRS mice) showed increased levels of DNMTs compared to controls at all time-points studied including at birth and at PND 60. Using GAD67-GFP transgenic mice, we established that, in both control and PRS mice, high levels of DNMT1 and 3a were preferentially expressed in GABAergic neurons of frontal cortex and hippocampus. Importantly, the overexpression of DNMT in GABAergic neurons was associated with a decrease in reelin and GAD67 expression in PRS mice in early and adult life. PRS mice also showed an increased binding of DNMT1 and MeCP2, and an increase in 5-methylcytosine and 5-hydroxymethylcytosine in specific CpG-rich regions of the reelin and GAD67 promoters. Thus, the epigenetic changes in PRS mice are similar to changes observed in the post-mortem brains of psychiatric patients. Behaviorally, adult PRS mice showed hyperactivity and deficits in social interaction, prepulse inhibition, and fear conditioning that were corrected by administration of valproic acid (a histone deacetylase inhibitor) or clozapine (an atypical antipsychotic with DNA-demethylation activity). Taken together, these data show that prenatal stress in mice induces abnormalities in the DNA methylation network and in behaviors indicative of a schizophrenia-like phenotype. Thus, PRS mice may be a valid model for the investigation of new drugs for schizophrenia treatment targeting DNA methylation. This article is part of the Special Issue entitled ‘Neurodevelopmental Disorders’. ► Prenatal restraint stress (PRS) in mice as a model of schizophrenia. ► Epigenetic alterations of DNMT1 and 3a, reelin and GAD67 in PRS mice. ► DNMT1 and 3a were preferentially expressed in GABAergic interneurons. ► Schizophrenia-like behavioral abnormalities in adult PRS mice.
    Keywords: Schizophrenia ; DNA Methyltransferase ; Prenatal Stress ; Epigenetic ; Antipsychotic ; Valproic Acid ; Pharmacy, Therapeutics, & Pharmacology
    ISSN: 0028-3908
    E-ISSN: 1873-7064
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  • 9
    Language: English
    In: Neuropharmacology, 15 March 2017, Vol.115, pp.51-59
    Description: The neuronal K /Cl symporter, KCC2, shapes synaptic responses mediated by Cl -permeant GABA receptors. Moving from the evidence that excitatory neurotransmission drives changes in KCC2 expression in cerebellar neurons, we studied the regulation of KCC2 expression by group-I metabotropic glutamate (mGlu) receptors in the cerebellum of adult mice. Mice lacking mGlu5 receptors showed a large reduction in cerebellar KCC2 protein levels and a loss of KCC2 immunoreactivity in Purkinje cells. Similar changes were seen in mice treated with the mGlu5 receptor antagonist, MPEP, whereas treatment with the mGlu5 receptor positive allosteric modulator (PAM), VU0360172, increased KCC2 expression. In contrast, pharmacological inhibition of mGlu1 receptors with JNJ16259685 enhanced cerebellar KCC2 protein levels and KCC2 immunoreactivity in Purkinje cells, whereas treatment with the mGlu1 receptor PAM, RO0711401, reduced KCC2 expression. To examine whether the reduction in KCC2 expression caused by the absence or the inhibition of mGlu5 receptors could affect GABAergic transmission, we performed electrophysiological and behavioral studies. Recording of extracellular action potentials in Purkinje cells showed that the inhibitory effect of the GABA receptor agonist, muscimol, was lost in cerebellar slices prepared from mGlu5 mice or from mice treated systemically with MPEP, in line with the reduction in KCC2 expression. Similarly, motor impairment caused by the GABA receptor PAM, diazepam, was attenuated in mice pre-treated with MPEP. These findings disclose a novel function of mGlu5 receptors in the cerebellum and suggest that mGlu5 receptor ligands might influence GABAergic transmission in the cerebellum and affect motor responses to GABA-mimetic drugs. This article is part of the Special Issue entitled ‘Metabotropic Glutamate Receptors, 5 years on’.
    Keywords: Cerebellum ; Purkinje Cells ; Kcc2 ; Mglu1 Receptor ; Mglu5 Receptors ; Pharmacy, Therapeutics, & Pharmacology
    ISSN: 0028-3908
    E-ISSN: 1873-7064
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  • 10
    Language: English
    In: Neuropharmacology, June 2010, Vol.58(7), pp.1078-1084
    Description: Abuse of anabolic androgenic steroids (AASs) is frequently associated with changes in mood, including depression. However, the nature of this association is still largely unexplored. As a model of AAS abuse, we used male adult rats injected for 4 weeks with either nandrolone or stanozolol at daily doses (5 mg/kg, s.c.) that are considered equivalent to those abused by humans on a milligram per kilogram of body weight basis. AAS treatment reduced levels of brain-derived neurotrophic factor in the hippocampus and prefrontal cortex, reduced the expression of low-affinity glucocorticoid receptors in the hippocampus, and increased morning trough basal plasma corticosterone levels. All these changes have been related to the pathophysiology of major depressive disorder. Accordingly, rats treated with nandrolone or stanozolol showed an increased immobility time in the forced swim test, which is widely used for the screening of antidepressant drugs. All effects produced by AASs were prevented by co-administration with the classical antidepressant, chlorimipramine. The evidence that supraphysiological doses of AASs induce changes indicative of a depressive state in normal rats, raises the concern that AAS abuse in humans may cause depression regardless of exposure to stress or other risk factors.
    Keywords: Anabolic Androgenic Steroids ; Bdnf ; Corticosteroid Receptors ; Chlorimipramine ; Corticosterone ; Depression ; Pharmacy, Therapeutics, & Pharmacology
    ISSN: 0028-3908
    E-ISSN: 1873-7064
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