licostinel and 1-hydroxy-3-amino-2-pyrrolidone

licostinel has been researched along with 1-hydroxy-3-amino-2-pyrrolidone* in 3 studies

Reviews

1 review(s) available for licostinel and 1-hydroxy-3-amino-2-pyrrolidone

Article	Year
The glycine site on the NMDA receptor: structure-activity relationships and therapeutic potential. Journal of medicinal chemistry, 1994, Nov-25, Volume: 37, Issue:24 Topics: Animals; Anti-Anxiety Agents; Antipsychotic Agents; Binding Sites; Cognition; Glycine; Humans; Kynurenic Acid; Neuroprotective Agents; Pyrrolidinones; Receptors, N-Methyl-D-Aspartate; Structure-Activity Relationship	1994

Other Studies

2 other study(ies) available for licostinel and 1-hydroxy-3-amino-2-pyrrolidone

Article	Year
The effect of (R)-HA966 or ACEA 1021 on dexfenfluramine or (S)-MDMA-induced changes in temperature, activity, and neurotoxicity. Pharmacology, biochemistry, and behavior, 2001, Volume: 68, Issue:3 The glycine site-specific N-methyl-D-aspartate (NMDA) antagonist 5-nitro-6,7-dichloro-2,3-quinoxalinedione (ACEA 1021, 4x30 mg/kg, i.p.) given 30 min before dexfenfluramine (4x15 mg/kg, i.p., every 2 h) was unable to prevent dexfenfluramine-induced depletion of 5-hydroxytryptamine (5-HT), 5-hydroxyindoleacetic acid (5-HIAA) content, and 5-HT transporter (5-HTT) density. Another glycine site-specific NMDA antagonist, R(+)-3-aminohydroxypyrrolidin-2-one [(R)-HA 966] (2x30 mg/kg, ip), given 30 min before dexfenfluramine (2x10 mg/kg, ip, 2 hourly) was also unable to prevent regional depletion of 5-HT, 5-HIAA, and 5-HTT density. However, ACEA 1021 (4x30 mg/kg, i.p.) given 30 min before (S)-3,4-methylenedioxymethamphetamine (MDMA, 4x10 mg/kg, 2 hourly, ip) attenuated the regional depletion of dopamine (DA), dihydroxyphenylacetic acid (DOPAC), 5-HT, 5-HIAA content, and 5-HTT density. ACEA 1021 combined with (S)-MDMA also prevented (S)-MDMA-induced hyperthermia without causing hypothermia or preventing an (S)-MDMA-induced increase in locomotor activity. Topics: Animals; Autoradiography; Body Temperature; Brain Chemistry; Carrier Proteins; Chromatography, High Pressure Liquid; Dexfenfluramine; Dose-Response Relationship, Drug; Excitatory Amino Acid Antagonists; Male; Membrane Glycoproteins; Membrane Transport Proteins; Motor Activity; N-Methyl-3,4-methylenedioxyamphetamine; Nerve Tissue Proteins; Neurotoxicity Syndromes; Pyrrolidinones; Quinoxalines; Rats; Rats, Wistar; Receptors, N-Methyl-D-Aspartate; Serotonin; Serotonin Plasma Membrane Transport Proteins; Serotonin Receptor Agonists; Stereoisomerism; Telemetry	2001
Strychnine-insensitive glycine site antagonists attenuate a cardiac arrest-induced movement disorder. European journal of pharmacology, 1995, Mar-06, Volume: 275, Issue:2 Male Sprague-Dawley rats underwent experimentally induced cardiac arrest and resuscitation, subsequently exhibiting involuntary jerking movements (myoclonus) with salient features similar to the human form of the disorder. The novel strychnine-insensitive glycine site antagonists ACEA-1011 (5-chloro-7-trifluoromethyl-1,2,3,4-tetrahydroquinoxaline-2,3,-dio ne) and ACEA-1021 (5-nitro-6,7-dichloro-quinoxalinedione) significantly attenuated the myoclonus in cardiac-arrested rats. (+)-HA-966, (+/-)-HA-966 (3-amino-1-hydroxy-2-pyrrolidinone), and felbamate (2-phenyl-1,3-propanediol dicarbamate) were also effective. Although the drugs vary in their selectivity for strychnine-insensitive glycine sites, they all possess antagonist activity at these sites. Vehicle injections (saline, dimethyl sulfoxide, water) were without effect and no obvious side effects were observed with any of the ligands tested in this study. Since hyperexcitability in the central nervous system is thought to underlie myoclonus, the attenuation of excitatory amino acid neurotransmission through antagonism of strychnine-insensitive glycine sites provides a logical mechanism of action for the antimyoclonic effects observed herein. Topics: Animals; Anticonvulsants; Behavior, Animal; Cardiopulmonary Resuscitation; Central Nervous System; Dose-Response Relationship, Drug; Felbamate; Heart Arrest; Male; Myoclonus; Phenylcarbamates; Propylene Glycols; Pyrrolidinones; Quinoxalines; Rats; Rats, Sprague-Dawley; Receptors, Glycine; Stereoisomerism; Strychnine	1995

Article

Year

The effect of (R)-HA966 or ACEA 1021 on dexfenfluramine or (S)-MDMA-induced changes in temperature, activity, and neurotoxicity.

Pharmacology, biochemistry, and behavior, 2001, Volume: 68, Issue:3

The glycine site-specific N-methyl-D-aspartate (NMDA) antagonist 5-nitro-6,7-dichloro-2,3-quinoxalinedione (ACEA 1021, 4x30 mg/kg, i.p.) given 30 min before dexfenfluramine (4x15 mg/kg, i.p., every 2 h) was unable to prevent dexfenfluramine-induced depletion of 5-hydroxytryptamine (5-HT), 5-hydroxyindoleacetic acid (5-HIAA) content, and 5-HT transporter (5-HTT) density. Another glycine site-specific NMDA antagonist, R(+)-3-aminohydroxypyrrolidin-2-one [(R)-HA 966] (2x30 mg/kg, ip), given 30 min before dexfenfluramine (2x10 mg/kg, ip, 2 hourly) was also unable to prevent regional depletion of 5-HT, 5-HIAA, and 5-HTT density. However, ACEA 1021 (4x30 mg/kg, i.p.) given 30 min before (S)-3,4-methylenedioxymethamphetamine (MDMA, 4x10 mg/kg, 2 hourly, ip) attenuated the regional depletion of dopamine (DA), dihydroxyphenylacetic acid (DOPAC), 5-HT, 5-HIAA content, and 5-HTT density. ACEA 1021 combined with (S)-MDMA also prevented (S)-MDMA-induced hyperthermia without causing hypothermia or preventing an (S)-MDMA-induced increase in locomotor activity.

Topics: Animals; Autoradiography; Body Temperature; Brain Chemistry; Carrier Proteins; Chromatography, High Pressure Liquid; Dexfenfluramine; Dose-Response Relationship, Drug; Excitatory Amino Acid Antagonists; Male; Membrane Glycoproteins; Membrane Transport Proteins; Motor Activity; N-Methyl-3,4-methylenedioxyamphetamine; Nerve Tissue Proteins; Neurotoxicity Syndromes; Pyrrolidinones; Quinoxalines; Rats; Rats, Wistar; Receptors, N-Methyl-D-Aspartate; Serotonin; Serotonin Plasma Membrane Transport Proteins; Serotonin Receptor Agonists; Stereoisomerism; Telemetry

2001

Strychnine-insensitive glycine site antagonists attenuate a cardiac arrest-induced movement disorder.

European journal of pharmacology, 1995, Mar-06, Volume: 275, Issue:2

Male Sprague-Dawley rats underwent experimentally induced cardiac arrest and resuscitation, subsequently exhibiting involuntary jerking movements (myoclonus) with salient features similar to the human form of the disorder. The novel strychnine-insensitive glycine site antagonists ACEA-1011 (5-chloro-7-trifluoromethyl-1,2,3,4-tetrahydroquinoxaline-2,3,-dio ne) and ACEA-1021 (5-nitro-6,7-dichloro-quinoxalinedione) significantly attenuated the myoclonus in cardiac-arrested rats. (+)-HA-966, (+/-)-HA-966 (3-amino-1-hydroxy-2-pyrrolidinone), and felbamate (2-phenyl-1,3-propanediol dicarbamate) were also effective. Although the drugs vary in their selectivity for strychnine-insensitive glycine sites, they all possess antagonist activity at these sites. Vehicle injections (saline, dimethyl sulfoxide, water) were without effect and no obvious side effects were observed with any of the ligands tested in this study. Since hyperexcitability in the central nervous system is thought to underlie myoclonus, the attenuation of excitatory amino acid neurotransmission through antagonism of strychnine-insensitive glycine sites provides a logical mechanism of action for the antimyoclonic effects observed herein.

Topics: Animals; Anticonvulsants; Behavior, Animal; Cardiopulmonary Resuscitation; Central Nervous System; Dose-Response Relationship, Drug; Felbamate; Heart Arrest; Male; Myoclonus; Phenylcarbamates; Propylene Glycols; Pyrrolidinones; Quinoxalines; Rats; Rats, Sprague-Dawley; Receptors, Glycine; Stereoisomerism; Strychnine

1995