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  • Journal of neurochemistry
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  • 1
    In: Journal of Neurochemistry, June 2013, Vol.125(5), pp.649-656
    Description: The αδ subunit of voltage‐sensitive calcium channels (s) is the molecular target of pregabalin and gabapentin, two drugs marked for the treatment of focal epilepsy, neuropathic pain, and anxiety disorders. Expression of the αδ subunit is up‐regulated in the dorsal horns of the spinal cord in models of neuropathic pain, suggesting that plastic changes in the αδ subunit are associated with pathological states. Here, we examined the expression of the αδ‐1 subunit in the amygdala, hippocampus, and frontal cortex in the trimethyltiazoline () mouse model of innate anxiety. is a volatile molecule present in the feces of the rodent predator, red fox. Mice that show a high defensive behavior during exposure developed anxiety‐like behavior in the following 72 h, as shown by the light–dark test. Anxiety was associated with an increased expression of the αδ‐1 subunit of s in the amygdaloid complex at all times following exposure (4, 24, and 72 h). No changes in the αδ‐1 protein levels were seen in the hippocampus and frontal cortex of mice exposed to . Pregabalin (30 mg/kg, i.p.) reduced anxiety‐like behavior in ‐exposed mice, but not in control mice. These data offer the first demonstration that the αδ‐1 subunit of s undergoes plastic changes in a model of innate anxiety, and supports the use of pregabalin as a disease‐dependent drug in the treatment of anxiety disorders. Changes in αδ subunit expression in anxiety modelThe αδ subunit is the molecular target for pregabalin, which is used in humans for the treatment of anxiety disorders. We found that αδ subunit was up‐regulated in the amygdala in a mouse model of innate anxiety where pregabalin was proved to be effective. These findings suggest that pregabalin acts as ‘disease‐dependent’ drug in the treatment of anxiety.
    Keywords: Αδ‐1 Subunit ; Amygdala ; Innate Anxiety ; Tmt ; Voltage‐Sensitive Calcium Channels
    ISSN: 0022-3042
    E-ISSN: 1471-4159
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  • 2
    In: Journal of Neurochemistry, September 2005, Vol.94(5), pp.1374-1383
    Description: Activity‐dependent Ca influx into neurones and the subsequent changes in gene expression are thought to be important in shaping neuronal development. In this study, we investigated whether an important mediator of neuronal migration, somatostatin (Srif), alongside its receptors, is controlled in this manner in cerebellar granule cells. We show that Ca influx increases the expression of somatostatin mRNA (), while somatostatin receptor 2 () mRNA expression is decreased. Both genes appear to be regulated independently of each other and in a calcineurin‐dependent manner that does not depend on either the ERK1/2 MAP kinase or the cAMP/CREB pathway. Nonetheless, a second pathway is required to induce changes in and expression, since constitutively active calcineurin alone is not sufficient to induce these changes. Furthermore, calcineurin activation reciprocally regulates the expression of brain‐derived neurotrophic factor, , and its receptor , which have also been shown to play a role in neuronal migration. Finally, calcineurin appears to control the expression of the neuronal marker transient axonal glycoprotein 1, , thereby strongly suggesting that calcineurin activation occurs during the late stages of neuronal migration, possibly during synaptogenesis with mossy fibres. We therefore propose that calcineurin might play an important role as a switch between transcriptional programs during neuronal development.
    Keywords: Calcium ; Calcineurin ; Cerebellar Granule Cells ; Development ; Somatostatin ; Somatostatin Receptor 2
    ISSN: 0022-3042
    E-ISSN: 1471-4159
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  • 3
    In: Journal of Neurochemistry, September 1989, Vol.53(3), pp.724-727
    Description: Glycine potentiates stimulation of inositol phospholipid hydrolysis by glutamate and ‐methyl‐D‐aspartate, but not by quisqualate or carbamylcholine, in primary cultures of cerebellar granule cells. This potentiation occurs in the absence of extracellular Mg, but is more evident when stimulation of inositol phospholipid hydrolysis by ‐methyl‐D‐aspartate is measured in the presence of 1 m Mg. The action of glycine is not antagonized by strychnine. These results suggest that glycine acts as a positive modulator of signal transduction at a specific class of ‐methyl‐D‐aspartate‐sensitive glutamate receptors coupled to inositol phospholipid hydrolysis in cerebellar granule cells.
    Keywords: Glycine ; Iv‐Methyl‐D‐Aspartate ; Glutamate ; Inositol Phospholipid Hydrolysis ; Magnesium Ion
    ISSN: 0022-3042
    E-ISSN: 1471-4159
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  • 4
    In: Journal of Neurochemistry, July 2008, Vol.106(2), pp.551-559
    Description: Trophic deprivation contributes to astrocyte damage that occurs in acute and chronic neurodegenerative disorders. Unraveling the underlying mechanisms may pave way to novel cytoprotective strategies. Cultured mouse astrocytes responded to trophic deprivation with a large and transient increase in the expression of p21, which was secondary to an enhanced formation of reactive oxygen species (ROS) detected by cytofluorimetric analysis after preloading with 2′,7′‐dichlorofluorescein diacetate. The increase in p21 levels was largely attenuated by the reducing agent, ‐acetylcysteine, which was proven to reduce ROS formation in astrocytes subjected to serum deprivation. We extended the analysis to the Ha‐Ras isoform, which has been implicated in mechanisms of cytotoxicity. We found that serum deprivation enhanced the expression and activity of Ha‐Ras without changing Ha‐Ras mRNA levels. The increase in Ha‐Ras levels was sensitive to the protein synthesis inhibitor, cycloheximide, suggesting that serum deprivation increases translation of preformed Ha‐Ras mRNA. The late decline in Ha‐Ras levels observed after 60 min was prevented by the proteasome inhibitor, MG132, as well as by the selective mitogen‐activated protein kinase (MAPK) inhibitor, PD98059. Serum deprivation led to the activation of the MAPK pathway in cultured astrocytes, as shown by an increase in phosphorylated extracellular signal‐regulated kinase 1/2 levels after 5 and 30 min. Finally, using the siRNA technology, we found that an acute knock‐down of Ha‐Ras was protective against astrocyte damage induced by serum deprivation. We conclude that cultured astrocytes respond to trophic deprivation with an increased expression in Ha‐Ras, which is limited by the concomitant activation of the MAPK pathway, but is nevertheless involved in the pathophysiology of cell damage.
    Keywords: Cultured Astrocytes ; Mitogen‐Activated Protein Kinase Pathway ; Ras Protein ; Trophic Deprivation
    ISSN: 0022-3042
    E-ISSN: 1471-4159
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  • 5
    In: Journal of Neurochemistry, March 2008, Vol.104(6), pp.1588-1598
    Description: To purchase or authenticate to the full-text of this article, please visit this link: http://dx.doi.org/10.1111/j.1471-4159.2007.05111.x Keywords: calcium/protein kinase C pathway; PC12 cells; proliferation; [beta]-catenin pathway; Wnt1; Wnt7a Abstract: Abstract We examined the effect of Wnt1 and Wnt7a on cell proliferation using undifferentiated PC12 cells, which originate from the neural crest and are widely employed as a neuronal cell model. Heterologous expression of Wnt1 enhanced [3.sup.H]thymidine incorporation and expression of cyclin D1 and cylin E in PC12 cells. Opposite effects were observed in PC12 cells expressing Wnt7a. Searching for the mechanisms underlying the opposite effects of Wnt1 and Wnt7a on PC12 cell proliferation, we examined the activation of the canonical [beta]-catenin/T-cell-lymphoid enhancer-binding protein transcription factor pathway and the 'calcium pathway' by co-transfecting the cells with a reporter gene controlled by either T-cell-lymphoid enhancer-binding protein transcription factor or the calcium-activated transcription factor, NFAT. Wnt1 and Wnt7a activated both pathways, but to a different extent. While Wnt1 preferentially activated the calcium pathway, Wnt7a mainly activated the canonical pathway. Pharmacological inhibition of protein kinase C, which is a component of the calcium pathway, abrogated the increase in cell proliferation induced by Wnt1 without affecting the antiproliferative action of Wnt7a. The action of Wnt7a was instead occluded by lithium ions, which mimic the activation of the canonical pathway, and was largely reduced by Dickkopf-1, which acts as an inhibitor of the canonical pathway. In addition, expression of a constitutively active mutant of [beta]-catenin potently activated the canonical Wnt pathway and reduced [3.sup.H]thymidine incorporation. These data challenge the view that the canonical Wnt pathway invariably supports cell growth and suggest that, at least in PC12 cells, cell proliferation is regulated by the balance between the calcium/protein kinase C pathway and the canonical pathway. Author Affiliation: (*)Department of Human Physiology and Pharmacology, University of Rome La Sapienza, Rome, Italy ([dagger])Department of Experimental Medicine, University of Rome La Sapienza, Rome, Italy ([double dagger])Sienabiotech s.p.a., Siena, Italy (s.)I. N. M. Neuromed, Pozzilli, Italy Article History: Received August 1, 2007; revised manuscript received October 2, 2007; accepted October 22, 2007. Article note: Address correspondence and reprint requests to Ferdinando Nicoletti, MD, Department of Human Physiology and Pharmacology, P.le Aldo Moro, 5, Roma 00185, Italy. E-mail: ferdinandonicoletti@hotmail.com
    Keywords: Calcium/Protein Kinase C Pathway ; Pc12 Cells ; Proliferation ; Β‐Catenin Pathway ; Wnt1 ; Wnt7a
    ISSN: 0022-3042
    E-ISSN: 1471-4159
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  • 6
    In: Journal of Neurochemistry, April 1985, Vol.44(4), pp.1217-1220
    Description: Repeated (once a day for 8 days) but not single administration of estradiol benzoate (10 μg/kg, s.c.) induced a sevenfold increase in anterior pituitary γ‐aminobutyric acid (GABA) concentration in male rats. GABA concentration also increased in the median eminence whereas no changes or decreases were observed in other brain regions including hypothalamic arcuate nucleus, lateral septum, hippocampus, caudate nucleus, and substantia nigra. Eight‐day estradiol benzoate injection also enhanced the max of median eminence glutamate decarboxylase activity without affecting the of the enzyme for glutamic acid. Taken together, these results suggest that repeated administration of estradiol benzoate increases the activity of the tubero‐infundibular GABAergic system in male rats.
    Keywords: Estradiol Benzoate ; Anterior Pituitary ; Median Eminence ; Gaba ; Glutamate Decarboxylase
    ISSN: 0022-3042
    E-ISSN: 1471-4159
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  • 7
    In: Journal of Neurochemistry, July 2006, Vol.98(1), pp.1-10
    Description: There is increasing evidence that Eph receptors and their transmembrane ligands, named ephrins, interact with glutamate receptors in both developing and adult neurons. EphB receptors interact with proteins that regulate the membrane trafficking of α‐amino‐3‐hydroxy‐5‐methylisoxazole‐4‐propionate (AMPA) receptor subunits, and both ephrins and EphB receptors have been found to co‐localize with ‐methyl‐‐aspartate (NMDA) receptors and to positively modulate NMDA receptor function. Moreover, pharmacologic activation of ephrin‐Bs amplifies group‐I metabotropic glutamate receptor signaling through mechanisms that involve NMDA receptors. The interaction with ionotropic or metabotropic glutamate receptors provides a substrate for the emerging role of ephrins and Eph receptors in the regulation of activity‐dependent forms of synaptic plasticity, such as long‐term potentiation and long‐term depression, which are established electrophysiologic models of associative learning. In addition, these interactions explain the involvement of ephrins/Eph receptors in the regulation of pain threshold and epileptogenesis, as well as their potential implication in processes of neuronal degeneration. This may stimulate the search for new drugs that might modulate excitatory synaptic transmission by interacting with the ephrin/Eph receptor system.
    Keywords: Ephrins ; Epileptogenesis Neurodegeneration ; Glutamate Receptors ; Pain ; Synaptic Plasticity
    ISSN: 0022-3042
    E-ISSN: 1471-4159
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  • 8
    In: Journal of Neurochemistry, October 2006, Vol.99(1), pp.299-307
    Description: We have shown that endogenous activation of type 5 metabotropic glutamate (mGlu5) receptors supports the maintenance of a pluripotent, undifferentiated state in D3 mouse embryonic stem cells cultured in the presence of leukaemia inhibitory factor (LIF). Here, we examined the interaction between LIF and mGlu5 receptors using as a read‐out the immediate early gene, . The selective mGlu5 receptor antagonist, 2‐methyl‐6‐(phenylenthynyl)pyridine (MPEP; 1 μ), reduced the increase in c‐Myc protein levels induced by LIF by enhancing c‐Myc ubiquitination. A reduction in c‐Myc levels was also observed following small interfering RNA‐mediated mGlu5 receptor gene silencing. MPEP reduced glycogen synthase kinase‐3β phosphorylation on Ser9, but increased phosphorylation of the phosphatidylinositol‐3‐kinase (PI‐3‐K) substrate, AKT. In our hands, activated PI‐3‐K reduced the stability of c‐Myc, because (i) the PI‐3‐K inhibitor, LY294002, prevented the reduction in c‐Myc levels induced by MPEP; and (ii) over‐expression of AKT promoted c‐Myc ubiquitination. All effects of MPEP were mimicked by protein kinase C (PKC) inhibitors and reversed by the PKC activator, tetradecanoylphorbol‐13‐acetate. We conclude that endogenous activation of mGlu5 receptors sustains the increase in c‐Myc induced by LIF in embryonic stem cells by inhibiting both glycogen synthase kinase‐3β and PI‐3‐K, both effects resulting from the activation of PKC.
    Keywords: C‐Myc ; Embryonic Stem Cells ; Leukaemia Inhibitory Factor ; Protein Kinase C ; Self‐Renewal ; Type 5 Metabotropic Glutamate Receptors
    ISSN: 0022-3042
    E-ISSN: 1471-4159
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  • 9
    In: Journal of Neurochemistry, July 2003, Vol.86(2), pp.413-421
    Description: The psychostimulant methamphetamine (MA) is toxic to nigro‐striatal dopaminergic terminals in both experimental animals and humans. In mice, three consecutive injections of MA (5 mg/kg, i.p. with 2 h of interval) induced a massive degeneration of the nigro‐striatal pathway, as reflected by a 50% reduction in the striatal levels of dopamine (DA) and 3,4‐dihydroxyphenylacetic acid (DOPAC), by a substantial reduction in striatal tyrosine hydroxylase and high‐affinity DA transporter immunostaining, and by the development of reactive gliosis. MA‐induced nigro‐striatal degeneration was largely attenuated in mice lacking α1b‐adrenergic receptors (ARs). MA‐stimulated striatal DA release (measured by microdialysis in freely moving animals) and locomotor activity were also reduced in α1b‐AR knockout mice. Pharmacological blockade of α‐adrenergic receptors with prazosin also protected wild‐type mice against MA toxicity. These results suggests that α1b‐ARs may play a role in the toxicity of MA on nigro‐striatal DA neurons.
    Keywords: Α1‐Adrenergic Receptor Antagonists ; Methamphetamine Neurotoxicity ; Parkinson'S Disease
    ISSN: 0022-3042
    E-ISSN: 1471-4159
    Source: John Wiley & Sons, Inc.
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  • 10
    Language: English
    In: Journal of neurochemistry, July 2003, Vol.86(2), pp.413-21
    Description: The psychostimulant methamphetamine (MA) is toxic to nigro-striatal dopaminergic terminals in both experimental animals and humans. In mice, three consecutive injections of MA (5 mg/kg, i.p. with 2 h of interval) induced a massive degeneration of the nigro-striatal pathway, as reflected by a 50% reduction in the striatal levels of dopamine (DA) and 3,4-dihydroxyphenylacetic acid (DOPAC), by a substantial reduction in striatal tyrosine hydroxylase and high-affinity DA transporter immunostaining, and by the development of reactive gliosis. MA-induced nigro-striatal degeneration was largely attenuated in mice lacking alpha1b-adrenergic receptors (ARs). MA-stimulated striatal DA release (measured by microdialysis in freely moving animals) and locomotor activity were also reduced in alpha1b-AR knockout mice. Pharmacological blockade of alpha-adrenergic receptors with prazosin also protected wild-type mice against MA toxicity. These results suggests that alpha1b-ARs may play a role in the toxicity of MA on nigro-striatal DA neurons.
    Keywords: Membrane Glycoproteins ; Nerve Tissue Proteins ; Central Nervous System Stimulants -- Toxicity ; Corpus Striatum -- Drug Effects ; Methamphetamine -- Toxicity ; Receptors, Adrenergic, Alpha-1 -- Deficiency
    ISSN: 0022-3042
    E-ISSN: 14714159
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