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Jay D Amsterdam - One of the best experts on this subject based on the ideXlab platform.
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Gepirone, a selective serotonin (5HT1A) Partial Agonist in the treatment of major depression.
Progress in Neuro-psychopharmacology & Biological Psychiatry, 1992Co-Authors: Jay D AmsterdamAbstract:1. 1. The present study assessed the potential antidepressant action of gepirone hydrochloride, an azapirone serotonin (5-HT1A) Partial Agonist in patients with major depression. 2. 2. Overall, gepirone demonstrated a significant antidepressant activity within the entire patient group (p
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Gepirone, a selective serotonin (5HT1A) Partial Agonist in the treatment of major depression.
Progress in neuro-psychopharmacology & biological psychiatry, 1992Co-Authors: Jay D AmsterdamAbstract:Abstract 1. 1. The present study assessed the potential antidepressant action of gepirone hydrochloride, an azapirone serotonin (5-HT1A) Partial Agonist in patients with major depression. 2. 2. Overall, gepirone demonstrated a significant antidepressant activity within the entire patient group (p 3. 3. Similarly, patients who were more severely ill at the pretreatment period had less improvement compared to those with more modest illness severity (p 4. 4. These observations compliment those of prior studies suggesting antidepressant activity for gepirone. 5. 5. However, a consistent efficacy comparable to conventional neuronal reuptake inhibitor antidepressants remains to be established in patients with more severe depression characterized by melancholic features.
Françoise Chesney - One of the best experts on this subject based on the ideXlab platform.
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SSR180711, a Novel Selective α7 Nicotinic Receptor Partial Agonist: (1) Binding and Functional Profile
Neuropsychopharmacology, 2007Co-Authors: Bruno Biton, Olivier E Bergis, Frédéric Galli, Alain Nedelec, Alistair W Lochead, Samir Jegham, Danielle Godet, Christophe Lanneau, Raphaël Santamaria, Françoise ChesneyAbstract:In this paper, we report on the pharmacological and functional profile of SSR180711 (1,4-Diazabicyclo[3.2.2]nonane-4-carboxylic acid, 4-bromophenyl ester), a new selective α 7 acetylcholine nicotinic receptor (n-AChRs) Partial Agonist. SSR180711 displays high affinity for rat and human α 7 n-AChRs ( K _i of 22±4 and 14±1 nM, respectively). Ex vivo ^3[H] α -bungarotoxin binding experiments demonstrate that SSR180711 rapidly penetrates into the brain (ID_50=8 mg/kg p.o.). In functional studies performed with human α 7 n-AChRs expressed in Xenopus oocytes or GH4C1 cells, the compound shows Partial Agonist effects (intrinsic activity=51 and 36%, EC_50=4.4 and 0.9 μM, respectively). In rat cultured hippocampal neurons, SSR180711 induced large GABA-mediated inhibitory postsynaptic currents and small α -bungarotoxin sensitive currents through the activation of presynaptic and somato-dendritic α 7 n-AChRs, respectively. In mouse hippocampal slices, the compound increased the amplitude of both glutamatergic (EPSCs) and GABAergic (IPSCs) postsynaptic currents evoked in CA1 pyramidal cells. In rat and mouse hippocampal slices, a concentration of 0.3 μM of SSR180711 increased long-term potentiation (LTP) in the CA1 field. Null mutation of the α 7 n-AChR gene totally abolished SSR180711-induced modulation of EPSCs, IPSCs and LTP in mice. Intravenous administration of SSR180711 strongly increased the firing rate of single ventral pallidum neurons, extracellularly recorded in anesthetized rats. In microdialysis experiments, administration of the compound (3–10 mg/kg i.p.) dose-dependently increased extracellular acetylcholine (ACh) levels in the hippocampus and prefrontal cortex of freely moving rats. Together, these results demonstrate that SSR180711 is a selective and Partial Agonist at human, rat and mouse α 7 n-AChRs, increasing glutamatergic neurotransmission, ACh release and LTP in the hippocampus.
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SSR180711, a Novel Selective α7 Nicotinic Receptor Partial Agonist: (1) Binding and Functional Profile
Neuropsychopharmacology, 2007Co-Authors: Bruno Biton, Olivier E Bergis, Frédéric Galli, Alain Nedelec, Alistair W Lochead, Samir Jegham, Danielle Godet, Christophe Lanneau, Raphaël Santamaria, Françoise ChesneyAbstract:In this paper, we report on the pharmacological and functional profile of SSR180711 (1,4-Diazabicyclo[3.2.2]nonane-4-carboxylic acid, 4-bromophenyl ester), a new selective α 7 acetylcholine nicotinic receptor (n-AChRs) Partial Agonist. SSR180711 displays high affinity for rat and human α 7 n-AChRs ( K _i of 22±4 and 14±1 nM, respectively). Ex vivo ^3[H] α -bungarotoxin binding experiments demonstrate that SSR180711 rapidly penetrates into the brain (ID_50=8 mg/kg p.o.). In functional studies performed with human α 7 n-AChRs expressed in Xenopus oocytes or GH4C1 cells, the compound shows Partial Agonist effects (intrinsic activity=51 and 36%, EC_50=4.4 and 0.9 μM, respectively). In rat cultured hippocampal neurons, SSR180711 induced large GABA-mediated inhibitory postsynaptic currents and small α -bungarotoxin sensitive currents through the activation of presynaptic and somato-dendritic α 7 n-AChRs, respectively. In mouse hippocampal slices, the compound increased the amplitude of both glutamatergic (EPSCs) and GABAergic (IPSCs) postsynaptic currents evoked in CA1 pyramidal cells. In rat and mouse hippocampal slices, a concentration of 0.3 μM of SSR180711 increased long-term potentiation (LTP) in the CA1 field. Null mutation of the α 7 n-AChR gene totally abolished SSR180711-induced modulation of EPSCs, IPSCs and LTP in mice. Intravenous administration of SSR180711 strongly increased the firing rate of single ventral pallidum neurons, extracellularly recorded in anesthetized rats. In microdialysis experiments, administration of the compound (3–10 mg/kg i.p.) dose-dependently increased extracellular acetylcholine (ACh) levels in the hippocampus and prefrontal cortex of freely moving rats. Together, these results demonstrate that SSR180711 is a selective and Partial Agonist at human, rat and mouse α 7 n-AChRs, increasing glutamatergic neurotransmission, ACh release and LTP in the hippocampus.
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ssr180711 a novel selective α 7 nicotinic receptor Partial Agonist 1 binding and functional profile
Neuropsychopharmacology, 2007Co-Authors: Bruno Biton, Olivier E Bergis, Frédéric Galli, Alain Nedelec, Alistair W Lochead, Samir Jegham, Danielle Godet, Christophe Lanneau, Raphaël Santamaria, Françoise ChesneyAbstract:In this paper, we report on the pharmacological and functional profile of SSR180711 (1,4-Diazabicyclo[3.2.2]nonane-4-carboxylic acid, 4-bromophenyl ester), a new selective α7 acetylcholine nicotinic receptor (n-AChRs) Partial Agonist. SSR180711 displays high affinity for rat and human α7 n-AChRs (Ki of 22±4 and 14±1 nM, respectively). Ex vivo 3[H]α-bungarotoxin binding experiments demonstrate that SSR180711 rapidly penetrates into the brain (ID50=8 mg/kg p.o.). In functional studies performed with human α7 n-AChRs expressed in Xenopus oocytes or GH4C1 cells, the compound shows Partial Agonist effects (intrinsic activity=51 and 36%, EC50=4.4 and 0.9 μM, respectively). In rat cultured hippocampal neurons, SSR180711 induced large GABA-mediated inhibitory postsynaptic currents and small α-bungarotoxin sensitive currents through the activation of presynaptic and somato-dendritic α7 n-AChRs, respectively. In mouse hippocampal slices, the compound increased the amplitude of both glutamatergic (EPSCs) and GABAergic (IPSCs) postsynaptic currents evoked in CA1 pyramidal cells. In rat and mouse hippocampal slices, a concentration of 0.3 μM of SSR180711 increased long-term potentiation (LTP) in the CA1 field. Null mutation of the α7 n-AChR gene totally abolished SSR180711-induced modulation of EPSCs, IPSCs and LTP in mice. Intravenous administration of SSR180711 strongly increased the firing rate of single ventral pallidum neurons, extracellularly recorded in anesthetized rats. In microdialysis experiments, administration of the compound (3–10 mg/kg i.p.) dose-dependently increased extracellular acetylcholine (ACh) levels in the hippocampus and prefrontal cortex of freely moving rats. Together, these results demonstrate that SSR180711 is a selective and Partial Agonist at human, rat and mouse α7 n-AChRs, increasing glutamatergic neurotransmission, ACh release and LTP in the hippocampus.
Bruno Biton - One of the best experts on this subject based on the ideXlab platform.
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SSR180711, a Novel Selective α7 Nicotinic Receptor Partial Agonist: (1) Binding and Functional Profile
Neuropsychopharmacology, 2007Co-Authors: Bruno Biton, Olivier E Bergis, Frédéric Galli, Alain Nedelec, Alistair W Lochead, Samir Jegham, Danielle Godet, Christophe Lanneau, Raphaël Santamaria, Françoise ChesneyAbstract:In this paper, we report on the pharmacological and functional profile of SSR180711 (1,4-Diazabicyclo[3.2.2]nonane-4-carboxylic acid, 4-bromophenyl ester), a new selective α 7 acetylcholine nicotinic receptor (n-AChRs) Partial Agonist. SSR180711 displays high affinity for rat and human α 7 n-AChRs ( K _i of 22±4 and 14±1 nM, respectively). Ex vivo ^3[H] α -bungarotoxin binding experiments demonstrate that SSR180711 rapidly penetrates into the brain (ID_50=8 mg/kg p.o.). In functional studies performed with human α 7 n-AChRs expressed in Xenopus oocytes or GH4C1 cells, the compound shows Partial Agonist effects (intrinsic activity=51 and 36%, EC_50=4.4 and 0.9 μM, respectively). In rat cultured hippocampal neurons, SSR180711 induced large GABA-mediated inhibitory postsynaptic currents and small α -bungarotoxin sensitive currents through the activation of presynaptic and somato-dendritic α 7 n-AChRs, respectively. In mouse hippocampal slices, the compound increased the amplitude of both glutamatergic (EPSCs) and GABAergic (IPSCs) postsynaptic currents evoked in CA1 pyramidal cells. In rat and mouse hippocampal slices, a concentration of 0.3 μM of SSR180711 increased long-term potentiation (LTP) in the CA1 field. Null mutation of the α 7 n-AChR gene totally abolished SSR180711-induced modulation of EPSCs, IPSCs and LTP in mice. Intravenous administration of SSR180711 strongly increased the firing rate of single ventral pallidum neurons, extracellularly recorded in anesthetized rats. In microdialysis experiments, administration of the compound (3–10 mg/kg i.p.) dose-dependently increased extracellular acetylcholine (ACh) levels in the hippocampus and prefrontal cortex of freely moving rats. Together, these results demonstrate that SSR180711 is a selective and Partial Agonist at human, rat and mouse α 7 n-AChRs, increasing glutamatergic neurotransmission, ACh release and LTP in the hippocampus.
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SSR180711, a Novel Selective α7 Nicotinic Receptor Partial Agonist: (1) Binding and Functional Profile
Neuropsychopharmacology, 2007Co-Authors: Bruno Biton, Olivier E Bergis, Frédéric Galli, Alain Nedelec, Alistair W Lochead, Samir Jegham, Danielle Godet, Christophe Lanneau, Raphaël Santamaria, Françoise ChesneyAbstract:In this paper, we report on the pharmacological and functional profile of SSR180711 (1,4-Diazabicyclo[3.2.2]nonane-4-carboxylic acid, 4-bromophenyl ester), a new selective α 7 acetylcholine nicotinic receptor (n-AChRs) Partial Agonist. SSR180711 displays high affinity for rat and human α 7 n-AChRs ( K _i of 22±4 and 14±1 nM, respectively). Ex vivo ^3[H] α -bungarotoxin binding experiments demonstrate that SSR180711 rapidly penetrates into the brain (ID_50=8 mg/kg p.o.). In functional studies performed with human α 7 n-AChRs expressed in Xenopus oocytes or GH4C1 cells, the compound shows Partial Agonist effects (intrinsic activity=51 and 36%, EC_50=4.4 and 0.9 μM, respectively). In rat cultured hippocampal neurons, SSR180711 induced large GABA-mediated inhibitory postsynaptic currents and small α -bungarotoxin sensitive currents through the activation of presynaptic and somato-dendritic α 7 n-AChRs, respectively. In mouse hippocampal slices, the compound increased the amplitude of both glutamatergic (EPSCs) and GABAergic (IPSCs) postsynaptic currents evoked in CA1 pyramidal cells. In rat and mouse hippocampal slices, a concentration of 0.3 μM of SSR180711 increased long-term potentiation (LTP) in the CA1 field. Null mutation of the α 7 n-AChR gene totally abolished SSR180711-induced modulation of EPSCs, IPSCs and LTP in mice. Intravenous administration of SSR180711 strongly increased the firing rate of single ventral pallidum neurons, extracellularly recorded in anesthetized rats. In microdialysis experiments, administration of the compound (3–10 mg/kg i.p.) dose-dependently increased extracellular acetylcholine (ACh) levels in the hippocampus and prefrontal cortex of freely moving rats. Together, these results demonstrate that SSR180711 is a selective and Partial Agonist at human, rat and mouse α 7 n-AChRs, increasing glutamatergic neurotransmission, ACh release and LTP in the hippocampus.
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ssr180711 a novel selective α 7 nicotinic receptor Partial Agonist 1 binding and functional profile
Neuropsychopharmacology, 2007Co-Authors: Bruno Biton, Olivier E Bergis, Frédéric Galli, Alain Nedelec, Alistair W Lochead, Samir Jegham, Danielle Godet, Christophe Lanneau, Raphaël Santamaria, Françoise ChesneyAbstract:In this paper, we report on the pharmacological and functional profile of SSR180711 (1,4-Diazabicyclo[3.2.2]nonane-4-carboxylic acid, 4-bromophenyl ester), a new selective α7 acetylcholine nicotinic receptor (n-AChRs) Partial Agonist. SSR180711 displays high affinity for rat and human α7 n-AChRs (Ki of 22±4 and 14±1 nM, respectively). Ex vivo 3[H]α-bungarotoxin binding experiments demonstrate that SSR180711 rapidly penetrates into the brain (ID50=8 mg/kg p.o.). In functional studies performed with human α7 n-AChRs expressed in Xenopus oocytes or GH4C1 cells, the compound shows Partial Agonist effects (intrinsic activity=51 and 36%, EC50=4.4 and 0.9 μM, respectively). In rat cultured hippocampal neurons, SSR180711 induced large GABA-mediated inhibitory postsynaptic currents and small α-bungarotoxin sensitive currents through the activation of presynaptic and somato-dendritic α7 n-AChRs, respectively. In mouse hippocampal slices, the compound increased the amplitude of both glutamatergic (EPSCs) and GABAergic (IPSCs) postsynaptic currents evoked in CA1 pyramidal cells. In rat and mouse hippocampal slices, a concentration of 0.3 μM of SSR180711 increased long-term potentiation (LTP) in the CA1 field. Null mutation of the α7 n-AChR gene totally abolished SSR180711-induced modulation of EPSCs, IPSCs and LTP in mice. Intravenous administration of SSR180711 strongly increased the firing rate of single ventral pallidum neurons, extracellularly recorded in anesthetized rats. In microdialysis experiments, administration of the compound (3–10 mg/kg i.p.) dose-dependently increased extracellular acetylcholine (ACh) levels in the hippocampus and prefrontal cortex of freely moving rats. Together, these results demonstrate that SSR180711 is a selective and Partial Agonist at human, rat and mouse α7 n-AChRs, increasing glutamatergic neurotransmission, ACh release and LTP in the hippocampus.
Andy N Mead - One of the best experts on this subject based on the ideXlab platform.
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the α4β2 nicotinic acetylcholine receptor Partial Agonist varenicline inhibits both nicotine self administration following repeated dosing and reinstatement of nicotine seeking in rats
Psychopharmacology, 2010Co-Authors: Eoin C Oconnor, Hans Rollema, Dale Parker, Andy N MeadAbstract:Introduction The α4β2 nicotinic acetylcholine receptor Partial Agonist varenicline has greater efficacy than other pharmacotherapeutic aids for smoking cessation. This presents an opportunity to evaluate the predictive validity of rat models of nicotine taking and relapse. The aim of this study was to evaluate the ability of varenicline to attenuate nicotine self-administration and relapse, as modelled by the reinstatement model of nicotine relapse in rats.
Hans Rollema - One of the best experts on this subject based on the ideXlab platform.
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the α4β2 nicotinic acetylcholine receptor Partial Agonist varenicline inhibits both nicotine self administration following repeated dosing and reinstatement of nicotine seeking in rats
Psychopharmacology, 2010Co-Authors: Eoin C Oconnor, Hans Rollema, Dale Parker, Andy N MeadAbstract:Introduction The α4β2 nicotinic acetylcholine receptor Partial Agonist varenicline has greater efficacy than other pharmacotherapeutic aids for smoking cessation. This presents an opportunity to evaluate the predictive validity of rat models of nicotine taking and relapse. The aim of this study was to evaluate the ability of varenicline to attenuate nicotine self-administration and relapse, as modelled by the reinstatement model of nicotine relapse in rats.
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pharmacological profile of the α4β2 nicotinic acetylcholine receptor Partial Agonist varenicline an effective smoking cessation aid
Neuropharmacology, 2007Co-Authors: Hans Rollema, Leslie K Chambers, John Glowa, Raymond S Hurst, Charles C Rovetti, Robert J Mather, Robert S Mansbach, Lorraine A Lebel, Yi Lu, Steven Bradley SandsAbstract:The preclinical pharmacology of the α4β2 nicotinic acetylcholine receptor (nAChR) Partial Agonist varenicline, a novel smoking cessation agent is described. Varenicline binds with subnanomolar affinity only to α4β2 nAChRs and in vitro functional patch clamp studies in HEK cells expressing nAChRs show that varenicline is a Partial Agonist with 45% of nicotine's maximal efficacy at α4β2 nAChRs. In neurochemical models varenicline has significantly lower (40–60%) efficacy than nicotine in stimulating [3H]-dopamine release from rat brain slices in vitro and in increasing dopamine release from rat nucleus accumbens in vivo, while it is more potent than nicotine. In addition, when combined with nicotine, varenicline effectively attenuates the nicotine-induced dopamine release to the level of the effect of varenicline alone, consistent with Partial agonism. Finally, varenicline reduces nicotine self-administration in rats and supports lower self-administration break points than nicotine. These data suggest that varenicline can reproduce to some extent the subjective effects of smoking by Partially activating α4β2 nAChRs, while preventing full activation of these receptors by nicotine. Based on these findings, varenicline was advanced into clinical development and recently shown to be an effective and safe aid for smoking cessation treatment.