ro-60-0175 and 3-(2-carboxypiperazin-4-yl)propyl-1-phosphonic-acid

ro-60-0175 has been researched along with 3-(2-carboxypiperazin-4-yl)propyl-1-phosphonic-acid* in 2 studies

Other Studies

2 other study(ies) available for ro-60-0175 and 3-(2-carboxypiperazin-4-yl)propyl-1-phosphonic-acid

Article	Year
Dorsal-striatal 5-HT₂A and 5-HT₂C receptors control impulsivity and perseverative responding in the 5-choice serial reaction time task. Psychopharmacology, 2012, Volume: 219, Issue:2 Prefrontal cortex (PFC) and dorsal striatum are part of the neural circuit critical for executive attention. The relationship between 5-HT and aspects of attention and executive control is complex depending on experimental conditions and the level of activation of different 5-HT receptors within the nuclei of corticostriatal circuitry.. The present study investigated which 5-HT(2A) and 5-HT(2C) receptors in the dorsomedial-striatum (dm-STR) contribute to executive attention deficit induced by blockade of NMDA receptors in the PFC.. Executive attention was assessed by the five-choice serial reaction time task (5-CSRTT), which provides indices of attention (accuracy) and those of executive control over performance such as premature (an index of impulsivity) and perseverative responding. The effects of targeted infusion in dm-STR of 100 and 300 ng/μl doses of the selective 5-HT(2A) antagonist M100907 and 1 and 3 μg/μl doses of 5-HT(2C) agonist Ro60-0175 was examined in animals injected with 50 ng/μl dose of a competitive NMDA receptor antagonist 3-(R)-2-carboxypiperazin-4-phosphonic acid (CPP) in the mPFC. Blockade of NMDA receptors impaired accuracy as well as executive control as shown by increased premature and perseverative responding. The CPP-induced premature and perseverative over-responding were dose-dependently prevented by both M100907 and Ro60-0175. Both drugs partially removed the CPP-induced accuracy deficit but only at the highest dose tested.. It is suggested that in the dorsal striatum, 5-HT by an action on 5-HT(2A) and 5-HT(2C) receptors may integrate the glutamate corticostriatal inputs critical for different aspects of the 5-CSRT task performance. Topics: Animals; Animals, Outbred Strains; Attention; Choice Behavior; Corpus Striatum; Dose-Response Relationship, Drug; Ethylamines; Fluorobenzenes; Impulsive Behavior; Indoles; Male; Microinjections; Piperazines; Piperidines; Prefrontal Cortex; Rats; Reaction Time; Receptor, Serotonin, 5-HT2A; Receptor, Serotonin, 5-HT2C; Receptors, N-Methyl-D-Aspartate; Serial Learning; Serotonin 5-HT2 Receptor Agonists; Serotonin 5-HT2 Receptor Antagonists	2012
Endogenous serotonin and serotonin2C receptors are involved in the ability of M100907 to suppress cortical glutamate release induced by NMDA receptor blockade. Journal of neurochemistry, 2009, Volume: 108, Issue:2 Blockade of NMDA receptors by intracortical infusion of 3-(R)-2-carboxypiperazin-4-propyl-1-phosphonic acid (CPP) increases glutamate (GLU) and serotonin (5-HT) release in the medial prefrontal cortex and impairs attentional performance in the 5-choice serial reaction time task. These effects are prevented by the 5-HT(2A) receptor antagonist, (R)-(+)-(2,3-dimethoxyphenyl)-1-[2-(4-fluorophenyl)ethyl]-4-piperidine methanol (M100907). We explored the roles of endogenous 5-HT and 5-HT(1A) and 5-HT(2C) receptors in the mechanisms by which M100907 suppresses CPP-induced release of cortical GLU and 5-HT using in vivo microdialysis. CPP raised extracellular GLU and 5-HT by about 250% and 170% respectively. The 5-HT synthesis inhibitor, p-chlorophenylalanine (300 mg/kg), prevented M100907 suppressing CPP-induced GLU release. The effect of M100907 on these rises of GLU and 5-HT and attentional performance deficit was mimicked by the 5-HT(2C) receptor agonist, (S)-2-(6-chloro-5-fluoroindol-1-yl)-1-methylethylamine fumarate, (Ro60-0175, 30 microg/kg) while intra-mPFC (SB242084, 6-chloro-5-methyl-1-[[2-[(2-methyl-3-pyridyl)oxy]-5-pyridyl]carbamoyl]-indoline, 0.1 microM), a 5-HT(2C) receptor antagonist, prevented the effect of M100907 on extracellular GLU. The 5-HT(1A) receptor antagonist, N-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-N-(2-pyridinyl)cyclohexane carboxenide trihydrochloride (100 microM) abolished the effect of M100907 on the CPP-induced 5-HT release. The data show that blockade of 5-HT(2A) receptors is not sufficient to suppress the CPP-induced rise of extracellular GLU and 5-HT and suggest that M100907 suppresses GLU release induced by CPP by enhancing the action of endogenous 5-HT on 5-HT(2C) receptors. Topics: Animals; Behavior, Animal; Cerebral Cortex; Chromatography, High Pressure Liquid; Ethylamines; Excitatory Amino Acid Antagonists; Fluorobenzenes; Glutamic Acid; Indoles; Male; Microdialysis; Piperazines; Piperidines; Rats; Rats, Sprague-Dawley; Receptor, Serotonin, 5-HT2C; Receptors, N-Methyl-D-Aspartate; Serotonin; Serotonin 5-HT2 Receptor Agonists; Serotonin Antagonists; Time Factors	2009

Article

Year

Dorsal-striatal 5-HT₂A and 5-HT₂C receptors control impulsivity and perseverative responding in the 5-choice serial reaction time task.

Psychopharmacology, 2012, Volume: 219, Issue:2

Prefrontal cortex (PFC) and dorsal striatum are part of the neural circuit critical for executive attention. The relationship between 5-HT and aspects of attention and executive control is complex depending on experimental conditions and the level of activation of different 5-HT receptors within the nuclei of corticostriatal circuitry.. The present study investigated which 5-HT(2A) and 5-HT(2C) receptors in the dorsomedial-striatum (dm-STR) contribute to executive attention deficit induced by blockade of NMDA receptors in the PFC.. Executive attention was assessed by the five-choice serial reaction time task (5-CSRTT), which provides indices of attention (accuracy) and those of executive control over performance such as premature (an index of impulsivity) and perseverative responding. The effects of targeted infusion in dm-STR of 100 and 300 ng/μl doses of the selective 5-HT(2A) antagonist M100907 and 1 and 3 μg/μl doses of 5-HT(2C) agonist Ro60-0175 was examined in animals injected with 50 ng/μl dose of a competitive NMDA receptor antagonist 3-(R)-2-carboxypiperazin-4-phosphonic acid (CPP) in the mPFC. Blockade of NMDA receptors impaired accuracy as well as executive control as shown by increased premature and perseverative responding. The CPP-induced premature and perseverative over-responding were dose-dependently prevented by both M100907 and Ro60-0175. Both drugs partially removed the CPP-induced accuracy deficit but only at the highest dose tested.. It is suggested that in the dorsal striatum, 5-HT by an action on 5-HT(2A) and 5-HT(2C) receptors may integrate the glutamate corticostriatal inputs critical for different aspects of the 5-CSRT task performance.

Topics: Animals; Animals, Outbred Strains; Attention; Choice Behavior; Corpus Striatum; Dose-Response Relationship, Drug; Ethylamines; Fluorobenzenes; Impulsive Behavior; Indoles; Male; Microinjections; Piperazines; Piperidines; Prefrontal Cortex; Rats; Reaction Time; Receptor, Serotonin, 5-HT2A; Receptor, Serotonin, 5-HT2C; Receptors, N-Methyl-D-Aspartate; Serial Learning; Serotonin 5-HT2 Receptor Agonists; Serotonin 5-HT2 Receptor Antagonists

2012

Endogenous serotonin and serotonin2C receptors are involved in the ability of M100907 to suppress cortical glutamate release induced by NMDA receptor blockade.

Journal of neurochemistry, 2009, Volume: 108, Issue:2

Blockade of NMDA receptors by intracortical infusion of 3-(R)-2-carboxypiperazin-4-propyl-1-phosphonic acid (CPP) increases glutamate (GLU) and serotonin (5-HT) release in the medial prefrontal cortex and impairs attentional performance in the 5-choice serial reaction time task. These effects are prevented by the 5-HT(2A) receptor antagonist, (R)-(+)-(2,3-dimethoxyphenyl)-1-[2-(4-fluorophenyl)ethyl]-4-piperidine methanol (M100907). We explored the roles of endogenous 5-HT and 5-HT(1A) and 5-HT(2C) receptors in the mechanisms by which M100907 suppresses CPP-induced release of cortical GLU and 5-HT using in vivo microdialysis. CPP raised extracellular GLU and 5-HT by about 250% and 170% respectively. The 5-HT synthesis inhibitor, p-chlorophenylalanine (300 mg/kg), prevented M100907 suppressing CPP-induced GLU release. The effect of M100907 on these rises of GLU and 5-HT and attentional performance deficit was mimicked by the 5-HT(2C) receptor agonist, (S)-2-(6-chloro-5-fluoroindol-1-yl)-1-methylethylamine fumarate, (Ro60-0175, 30 microg/kg) while intra-mPFC (SB242084, 6-chloro-5-methyl-1-[[2-[(2-methyl-3-pyridyl)oxy]-5-pyridyl]carbamoyl]-indoline, 0.1 microM), a 5-HT(2C) receptor antagonist, prevented the effect of M100907 on extracellular GLU. The 5-HT(1A) receptor antagonist, N-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-N-(2-pyridinyl)cyclohexane carboxenide trihydrochloride (100 microM) abolished the effect of M100907 on the CPP-induced 5-HT release. The data show that blockade of 5-HT(2A) receptors is not sufficient to suppress the CPP-induced rise of extracellular GLU and 5-HT and suggest that M100907 suppresses GLU release induced by CPP by enhancing the action of endogenous 5-HT on 5-HT(2C) receptors.

Topics: Animals; Behavior, Animal; Cerebral Cortex; Chromatography, High Pressure Liquid; Ethylamines; Excitatory Amino Acid Antagonists; Fluorobenzenes; Glutamic Acid; Indoles; Male; Microdialysis; Piperazines; Piperidines; Rats; Rats, Sprague-Dawley; Receptor, Serotonin, 5-HT2C; Receptors, N-Methyl-D-Aspartate; Serotonin; Serotonin 5-HT2 Receptor Agonists; Serotonin Antagonists; Time Factors

2009