The Experts below are selected from a list of 1032 Experts worldwide ranked by ideXlab platform

Marco A. Riva - One of the best experts on this subject based on the ideXlab platform.

  • Dopaminergic D2 receptor activation modulates FGF-2 gene expression in rat prefrontal cortex and hippocampus
    Journal of Neuroscience Research, 2003
    Co-Authors: Fabio Fumagalli, Giorgio Racagni, Francesco Bedogni, Maria Elisabetta Maragnoli, Massimo Gennarelli, Jorge Perez, Marco A. Riva
    Abstract:

    We have investigated the role of dopaminergic receptors in modulation of basic fibroblast growth factor (FGF-2) expression in rat prefrontal cortex and hippocampus, two brain regions important for cognition. We found that FGF-2 expression is upregulated by quinpirole, a D2 agonist, in prefrontal cortex and to a lesser extent in hippocampus. This modulation was specific for dopamine D2 receptors because no effect was observed when the dopamine D1 and D3 agonists, SKF38393 and 7-OH-DPAT, respectively, were administered. Our findings show that activation of dopaminergic D2 receptors modulates FGF-2 expression in rat prefrontal cortex and hippocampus. Our data highlight the complex modulation of FGF-2 expression in limbic areas pointing to this Trophic Molecule as a putative target of drugs used against acute and chronic neurodegenerative diseases such as Parkinson's disease. © 2003 Wiley-Liss, Inc.

  • Stimulatory role of dopamine on fibroblast growth factor-2 expression in rat striatum
    Journal of Neurochemistry, 2001
    Co-Authors: Mila Roceri, Raffaella Molteni, Giorgio Racagni, Fabio Fumagalli, Massimo Gennarelli, Giovanni Umberto Corsini, Roberto Maggio, Marco A. Riva
    Abstract:

    We have previously shown that systemic injection of (-)nicotine produces a selective up-regulation of fibroblast growth factor (FGF)-2 mRNA levels in rat striatum. Because (-)nicotine can increase striatal release of dopamine and glutamate, in the present study we have investigated the contribution of these neurotransmitters in the modulation of FGF-2 expression. We found that coinjection of dopaminergic D1 (SCH23390) or D2 (haloperidol) receptor antagonists prevents nicotine-induced elevation of FGF-2 expression. However, injection of the NMDA receptor antagonist MK-801 produced a significant increment of FGF-2 mRNA and protein levels in rat striatum similar to the effect produced by (-)nicotine alone. Interestingly this effect of MK-801 could also be prevented by D1 or D2 receptor antagonists, suggesting that an elevation of dopamine levels may be required for the regulation of the Trophic Molecule. Accordingly we found that the non-selective dopaminergic agonist apomorphine can similarly increase striatal FGF-2 mRNA levels. Despite the observation that both D1 and D2 receptors appear to contribute to the modulation of FGF-2 expression, only a direct activation of D2 receptors, through quinpirole administration, was able to mimic the effect of apomorphine. On the basis of FGF-2 neuroTrophic activity, these results suggest that direct or indirect activation of dopaminergic system can be neuroprotective and might reduce cell vulnerability in degenerative disorders.

  • Selective modulation of fibroblast growth factor-2 expression in the rat brain by the atypical antipsychotic clozapine.
    Neuropharmacology, 1999
    Co-Authors: Marco A. Riva, Raffaella Molteni, Fabio Tascedda, A. Massironi, Giorgio Racagni
    Abstract:

    In the present paper we investigated, in the rat brain, the expression of basic fibroblast growth factor (FGF-2) in response to the atypical antipsychotic clozapine. We found that acute or chronic administration of this compound produced a selective increase of FGF-2 mRNA and protein in the striatum. Although acute injection of clozapine did increase FGF-2 expression in parietal cortex and nucleus accumbens we found that, following repeated administration, the induction of the Trophic Molecule was taking place only at striatal level. The analysis of other antipsychotic drugs did not provide conclusive evidence for the molecular mechanisms involved in clozapine-induced elevation of FGF-2. In fact, chronic administration of classical neuroleptics, haloperidol and chlorpromazine, did not alter the expression of FGF-2. Furthermore the novel drugs quetiapine and olanzapine, despite some similarities in their receptor profiles, were similarly ineffective. Hence these data suggest that, among antipsychotic drugs, the induction of FGF-2 is unique to clozapine. On the basis of the neuroprotective activity of this Trophic Molecule, our data might be relevant for the potential use of clozapine in tardive dyskinesia and parkinsonism, which develop during long term administration of classical neuroleptic drugs.

V Silani - One of the best experts on this subject based on the ideXlab platform.

  • Detection of beta-nerve growth factor mRNA in the human fetal brain.
    Brain research, 1990
    Co-Authors: A Pizzuti, G Borsani, A Falini, E I Rugarli, A Sidoli, F E Baralle, G Scarlato, V Silani
    Abstract:

    Nerve growth factor (NGF) is a Trophic Molecule recently demonstrated to interact with different structures in the central nervous system. The expression of the beta-NGF mRNA from human fetal cortices at the 15-16th week of gestational age has been demonstrated and quantitated by polymerase chain reaction amplification of the specific cDNA. beta-NGF mRNA expression in the human brain coincides with the period of active differentiation and synaptogenesis, suggesting that the Trophic agent plays a role in the cerebral development.

  • Detection of β-nerve growth factor mRNA in the human fetal brain
    Brain Research, 1990
    Co-Authors: A Pizzuti, G Borsani, A Falini, E I Rugarli, A Sidoli, F E Baralle, G Scarlato, V Silani
    Abstract:

    Nerve growth factor (NGF) is a Trophic Molecule recently demonstrated to interact with different structures in the central nervous system. The expression of the beta-NGF mRNA from human fetal cortices at the 15-16th week of gestational age has been demonstrated and quantitated by polymerase chain reaction amplification of the specific cDNA. beta-NGF mRNA expression in the human brain coincides with the period of active differentiation and synaptogenesis, suggesting that the Trophic agent plays a role in the cerebral development.

Giorgio Racagni - One of the best experts on this subject based on the ideXlab platform.

  • Dopaminergic D2 receptor activation modulates FGF-2 gene expression in rat prefrontal cortex and hippocampus
    Journal of Neuroscience Research, 2003
    Co-Authors: Fabio Fumagalli, Giorgio Racagni, Francesco Bedogni, Maria Elisabetta Maragnoli, Massimo Gennarelli, Jorge Perez, Marco A. Riva
    Abstract:

    We have investigated the role of dopaminergic receptors in modulation of basic fibroblast growth factor (FGF-2) expression in rat prefrontal cortex and hippocampus, two brain regions important for cognition. We found that FGF-2 expression is upregulated by quinpirole, a D2 agonist, in prefrontal cortex and to a lesser extent in hippocampus. This modulation was specific for dopamine D2 receptors because no effect was observed when the dopamine D1 and D3 agonists, SKF38393 and 7-OH-DPAT, respectively, were administered. Our findings show that activation of dopaminergic D2 receptors modulates FGF-2 expression in rat prefrontal cortex and hippocampus. Our data highlight the complex modulation of FGF-2 expression in limbic areas pointing to this Trophic Molecule as a putative target of drugs used against acute and chronic neurodegenerative diseases such as Parkinson's disease. © 2003 Wiley-Liss, Inc.

  • Stimulatory role of dopamine on fibroblast growth factor-2 expression in rat striatum
    Journal of Neurochemistry, 2001
    Co-Authors: Mila Roceri, Raffaella Molteni, Giorgio Racagni, Fabio Fumagalli, Massimo Gennarelli, Giovanni Umberto Corsini, Roberto Maggio, Marco A. Riva
    Abstract:

    We have previously shown that systemic injection of (-)nicotine produces a selective up-regulation of fibroblast growth factor (FGF)-2 mRNA levels in rat striatum. Because (-)nicotine can increase striatal release of dopamine and glutamate, in the present study we have investigated the contribution of these neurotransmitters in the modulation of FGF-2 expression. We found that coinjection of dopaminergic D1 (SCH23390) or D2 (haloperidol) receptor antagonists prevents nicotine-induced elevation of FGF-2 expression. However, injection of the NMDA receptor antagonist MK-801 produced a significant increment of FGF-2 mRNA and protein levels in rat striatum similar to the effect produced by (-)nicotine alone. Interestingly this effect of MK-801 could also be prevented by D1 or D2 receptor antagonists, suggesting that an elevation of dopamine levels may be required for the regulation of the Trophic Molecule. Accordingly we found that the non-selective dopaminergic agonist apomorphine can similarly increase striatal FGF-2 mRNA levels. Despite the observation that both D1 and D2 receptors appear to contribute to the modulation of FGF-2 expression, only a direct activation of D2 receptors, through quinpirole administration, was able to mimic the effect of apomorphine. On the basis of FGF-2 neuroTrophic activity, these results suggest that direct or indirect activation of dopaminergic system can be neuroprotective and might reduce cell vulnerability in degenerative disorders.

  • Selective modulation of fibroblast growth factor-2 expression in the rat brain by the atypical antipsychotic clozapine.
    Neuropharmacology, 1999
    Co-Authors: Marco A. Riva, Raffaella Molteni, Fabio Tascedda, A. Massironi, Giorgio Racagni
    Abstract:

    In the present paper we investigated, in the rat brain, the expression of basic fibroblast growth factor (FGF-2) in response to the atypical antipsychotic clozapine. We found that acute or chronic administration of this compound produced a selective increase of FGF-2 mRNA and protein in the striatum. Although acute injection of clozapine did increase FGF-2 expression in parietal cortex and nucleus accumbens we found that, following repeated administration, the induction of the Trophic Molecule was taking place only at striatal level. The analysis of other antipsychotic drugs did not provide conclusive evidence for the molecular mechanisms involved in clozapine-induced elevation of FGF-2. In fact, chronic administration of classical neuroleptics, haloperidol and chlorpromazine, did not alter the expression of FGF-2. Furthermore the novel drugs quetiapine and olanzapine, despite some similarities in their receptor profiles, were similarly ineffective. Hence these data suggest that, among antipsychotic drugs, the induction of FGF-2 is unique to clozapine. On the basis of the neuroprotective activity of this Trophic Molecule, our data might be relevant for the potential use of clozapine in tardive dyskinesia and parkinsonism, which develop during long term administration of classical neuroleptic drugs.

Kazuyo Yamauchi - One of the best experts on this subject based on the ideXlab platform.

  • low density lipoprotein receptor related protein 1 lrp1 dependent cell signaling promotes neuroTrophic activity in embryonic sensory neurons
    PLOS ONE, 2013
    Co-Authors: Kazuyo Yamauchi, Tomonori Yamauchi, Elisabetta Mantuano, Kenichi Murakami, Kenneth Henry, Kazuhisa Takahashi, Wendy M Campana
    Abstract:

    Developing sensory neurons require neuroTrophic support for survival, neurite outgrowth and myelination. The low-density lipoprotein receptor-related protein-1 (LRP1) transactivates Trk receptors and thereby functions as a putative neurotrophin. Herein, we show that LRP1 is abundantly expressed in developing dorsal root ganglia (DRG) and that LRP1-dependent cell signaling supports survival, neurite extension and receptivity to Schwann cells even in the absence of neurotrophins. Cultured embryonic DRG neurons (E15) were treated with previously characterized LRP1 ligands, LRP1-receptor binding domain of α2-macroglobulin (RBD), hemopexin domain of MMP-9 (PEX) or controls (GST) for two weeks. These structurally diverse LRP1 ligands significantly activated and sustained extracellular signal-regulated kinases (ERK1/2) 5-fold (p 2 weeks in vitro, to an extent equaling NGF, a finding associated with canonical signaling mechanisms and blockade of caspase-3 cleavage. LRP1 ligand-induced survival and sprouting were blocked by co-incubation with the LRP1 antagonist, receptor associated protein (RAP), whereas RAP had no effect on NGF-induced activity. Site directed mutagenesis of the LRP1 ligand, RBD, in which Lys1370 and Lys1374 are converted to alanine to preclude LRP1 binding, were ineffective in promoting cell signaling, survival or inducing neurite extension in primary sensory neurons, confirming LRP1 specificity. Furthermore, LRP1-induced neurite sprouting was mediated by Src-family kinase (SFK) activation, suggesting transactivation of Trk receptors. Co-cultures of primary embryonic neurons and Schwann cells showed that LRP1 agonists promoted axonal receptivity to myelination to Schwann cells. Collectively, these findings identify LRP1 as a novel and perhaps essential Trophic Molecule for sensory neuronal survival and development.

Bryan Kolb - One of the best experts on this subject based on the ideXlab platform.

  • Differential expression of basic fibroblast growth factor-2 in the developing rat brain.
    Neuroscience, 2006
    Co-Authors: Marie H. Monfils, Ira Driscoll, N.r. Melvin, Bryan Kolb
    Abstract:

    Basic fibroblast growth factor-2 is a Trophic Molecule involved in a number of functions within the CNS, including the regulation of CNS responses to injury. Prior studies suggest that rats recover differently from injury inflicted to different regions and at different ages throughout development, and that basic fibroblast growth factor-2 may, at least in part, underlie this phenomenon. In the present study, we describe the distribution of basic fibroblast growth factor-2 at postnatal days 0, 2, 6, 10, 12, 14, 18, 21 and 30 in the indusium griseum, the external capsule, the hippocampus, the medial prefrontal cortex, the motor cortex, the rostral migratory stream, and the subventricular zone. Our results suggest a differential temporal and spatial expression of basic fibroblast growth factor-2 throughout development, which may explain the differential recovery observed from cortical lesions inflicted at different time points after birth.