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  • 1
    Electronic Resource
    Electronic Resource
    SB 242084: A Selective 5-HT2C Receptor Antagonist (2000)
    Oxford, UK : Blackwell Publishing Ltd
    CNS drug reviews 6 (2000), S. 0 
    Details
    ISSN: 1527-3458
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: SB 242084 is the most potent and selective 5-HT2C receptor antagonist thus far available. Thus, SB 242084 has high affinity for the cloned human 5-HT2C receptor with a pKi of 9.0, a much lower affinity for the human cloned 5-HT2B (pKi 7.0) and 5-HT2A (pKi 6.8) receptors, and low affinity for other 5-HT, dopamine, and adrenergic receptors. In the 5-HT-stimulated PI hydrolysis model of 5-HT2C receptor function, SB 242084 was found to be a competitive antagonist with a pKB of 9.3. A series of in vivo studies have shown that SB 242084 is a very effective antagonist of behavioral responses mediated by 5-HT2C receptors such as penile erections, and the hypophagic and hypolocomotor effect of mCPP in rats. In addition, this compound has anxiolytic-like properties. Moreover, SB 242084 increases the basal activity of dopaminergic neurons in the VTA and the in vivo DA release in the nucleus accumbens, and it is capable of blocking the inhibitory effects of mCPP and RO 60-0175 on mesolimbic dopaminergic activity. These data are consistent with the evidence that 5-HT2C receptors exert an inhibitory control upon the mesolimbic dopaminergic system.Taken togheter, the available data on SB 242084 might have implication for the possible use of this compound in the treatment of anxiety, depression, and the negative symptoms of schizophrenia.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1527-3458.2000.tb00147.x
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  • 2
    Electronic Resource
    Electronic Resource
    Activation of Glutamate Receptors Stimulates the Formation of Nitrite in Synaptosomes from Rat Cerebellum (1994)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 62 (1994), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Synaptosomes from rat cerebellum were used to investigate the involvement of different glutamate receptor subtypes in the control of the synthesis of nitric oxide (NO), measured as its breakdown product nitrite (NO2-). Synaptosomes incubated in the presence of NAD|PH and l-arginine produced measurable levels of NO2-, which were reduced by addition of Nω-nitro-l-arginine methyl ester, an inhibitor of nitric oxide synthase. The selective ionotropic glutamate receptor agonist N-methyl-d-aspartate (NMDA) induced a pronounced increase in NO2-formation, which was prevented by Nω-nitro-l-arginine methyl ester and by the specific NMDA receptor antagonist Dl-2-amino-5-phosphonovaleric acid (AP-5). The NMDA-induced increase in NO2-formation was blocked by chelation of extracellular Ca2+ with EGTA. Both l-glutamate and the selective agonist for the metabotropic glutamate receptors (β)-1-aminocyclopentane-trans-1,3-dicarboxylic acid raised NO2-production, which retumed to control levels after addition of Nω-nitro-l-arginine methyl ester. The selective glutamate ionotropic receptor agonist (R,S)-α-amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid did not cause any change in NO2 formation. The stimulatory effect of l-glutamate was blocked by the metabotropic glutamate receptor antagonist Dl-2-amino-4-phosphonobutyric acid but was unaffected by the selective NMDA receptor blocker AP-5. Removal of extracellular Ca2+ by EGTA did not affect the action of l-glutamate; whereas W-7, an inhibitor of calmodulin, and dantrolene, a compound that blocks the mobilization of Ca2+ from intracellular stores, abolished the effect of l-glutamate on NO2-formation. It is suggested that stimulation of ionotropic NMDA receptors activates NO metabolism by causing an influx of Ca2+ from the extracellular space, whereas activation of metabotropic receptors by l-glutamate provokes a mobilization of Ca2+ from intracellular stores, which stimulates nitric oxide synthase activity by forning Ca2+/calmodulin complexes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.1994.62062205.x
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  • 3
    Electronic Resource
    Electronic Resource
    Selective stimulation of serotonin2C receptors blocks the enhancement of striatal and accumbal dopamine release induced by nicotine administration (2004)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 89 (2004), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The effects of acute and repeated nicotine administration on the extracellular levels of dopamine (DA) in the corpus striatum and the nucleus accumbens were studied in conscious, freely moving rats by in vivo microdialysis. Acute intraperitoneal (i.p.) injection of nicotine (1 mg/kg) increased DA outflow both in the corpus striatum and the nucleus accumbens. Repeated daily injection of nicotine (1 mg/kg, i.p.) for 10 consecutive days caused a significant increase in basal DA outflow both in the corpus striatum and the nucleus accumbens. Acute challenge with nicotine (1 mg/kg, i.p.) in animals treated repeatedly with this drug enhanced DA extracellular levels in both brain areas. However, the effect of nicotine was potentiated in the nucleus accumbens, but not in the corpus striatum. To test the hypothesis that stimulation of 5-HT (5-hydroxytryptamine, serotonin)2C receptors could affect nicotine-induced DA release, the selective 5-HT2C receptor agonist RO 60–0175 was used. Pretreatment with RO 60–0175 (1 and 3 mg/kg, i.p.) dose-dependently prevented the enhancement in DA release elicited by acute nicotine in the corpus striatum, but was devoid of any significant effect in the nucleus accumbens. RO 60–0175 (1 and 3 mg/kg, i.p.) dose-dependently reduced the stimulatory effect on striatal and accumbal DA release induced by an acute challenge with nicotine (1 mg/kg, i.p.) in rats treated repeatedly with this alkaloid. However, only the effect of 3 mg/kg RO 60–0175 reached statistical significance. The inhibitory effect of RO 60–0175 on DA release induced by nicotine in the corpus striatum and the nucleus accumbens was completely prevented by SB 242084 (0.5 mg/kg, i.p.) and SB 243213 (0.5 mg/kg, i.p.), two selective antagonists of 5-HT2C receptors. It is concluded that selective activation of 5-HT2C receptors can block the stimulatory action of nicotine on central DA function, an effect that might be relevant for the reported antiaddictive properties of RO 60–0175.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.2004.02337.x
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  • 4
    Electronic Resource
    Electronic Resource
    Neurochemical and electrophysiological evidence that 5-HT4 receptors exert a state-dependent facilitatory control in vivo on nigrostriatal, but not mesoaccumbal, dopaminergic function (2001)
    Oxford, UK : Blackwell Science Ltd
    European journal of neuroscience 13 (2001), S. 0 
    Details
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: In this study we investigated, using in vivo microdialysis and single unit recordings, the role of serotonin4 (5-HT4) receptors in the control of nigrostriatal and mesoaccumbal dopaminergic (DA) pathway activity. In freely moving rats, the 5-HT4 antagonist GR 125487 (1 mg/kg, i.p.), without effect on its own, significantly reduced the enhancement of striatal DA outflow induced by 0.01 (−35%) and 0.1 (−66%), but not 1 mg/kg, s.c. haloperidol (HAL). Intrastriatal infusion of GR 125487 (1 µm) had no influence on basal DA outflow, but attenuated (−49%) the effect of 0.01 mg/kg HAL. Systemic administration of GR 125487 modified neither basal nor 0.01 mg/kg HAL-stimulated accumbal DA outflow. In halothane-anaesthetized rats, 1 or 10 mg/kg GR 125487, without effect by itself, failed to modify the changes in accumbal and striatal DA outflow elicited by electrical stimulation (300 µA, 1 ms, 20 Hz, 15 min) of the dorsal raphe nucleus. Finally, GR 125487 (444 µg/kg, i.v.), whilst not affecting basal firing of DA neurons within either the substantia nigra or the ventral tegmental area, reduced HAL-stimulated (1–300 µg/kg, i.v.) impulse flow of nigrostriatal DA neurons only. These results indicate that 5-HT4 receptors exert a facilitatory control on both striatal DA release and nigral DA neuron impulse flow only when nigrostriatal DA transmission is under activated conditions. Furthermore, they indicate that the striatum constitutes a major site for the expression of the control exerted by 5-HT4 receptors on DA release. In contrast, 5-HT4 receptors have no influence on mesoaccumbal DA activity in either basal or activated conditions.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.0953-816x.2000.01453.x
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  • 5
    Electronic Resource
    Electronic Resource
    Studies on the separate roles of forebrain and spinal serotonin in morphine analgesia (1986)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 332 (1986), S. 208-212 
    Details
    ISSN: 1432-1912
    Keywords: Forebrain 5-HT ; Spinal 5-HT ; Morphine ; Analgesia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 5,7-Dihydroxytryptamine (5,7-DHT) injections in the ventromedial tegmentum (VMT) at the level of nucleus interpeduncularis or in the ventral raphe area (VR) of the medulla oblongata were used to study the separate roles of forebrain and spinal 5-HT in the antinociceptive effect of morphine in rats. 5,7-DHT injections in the VMT, which caused marked, selective depletion of forebrain 5-HT, did not modify the effect of morphine in the hot plate and tail immersion tests. Direct injection of 5,7-DHT into the nucleus raphe medianus also failed to modify the effect of morphine in the two tests used to measure nociceptive responses. The effect of morphine was significantly reduced 30 min after injection to rats depleted of spinal 5-HT by 5,7-DHT injected in the VR but the areas under the curves between vehicle and 5,7-DHT treated animals were not significantly different. The data show that the integrity of 5-HT neurons in the forebrain is not necessary for the antinociceptive effect of morphine and a substantial amount of this effect is still present in rats with marked depletion of spinal 5-HT.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00504855
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