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Dive into the research topics where Raymond F. Suckow is active.

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Featured researches published by Raymond F. Suckow.


Schizophrenia Research | 2010

High dose D-serine in the treatment of schizophrenia

Joshua T. Kantrowitz; Anil K. Malhotra; Barbara A. Cornblatt; Gail Silipo; Andrea Balla; Raymond F. Suckow; Cyril D'Souza; John R. Saksa; Scott W. Woods; Daniel C. Javitt

BACKGROUND D-serine is an allosteric modulator of the brain N-methyl-d-aspartate (NMDA) receptor and a potential novel treatment of schizophrenia. Double-blind studies have been performed at 30 mg/kg/day (approximately 2 g/day) with encouraging results, but no formal dose escalation studies have been performed. We describe the first evaluation of the efficacy and safety of d-serine at doses >30 mg/kg/day; a 4-week, open-label trial of adjunctive D-serine (30, 60 or 120 mg/kg/day). METHODS 42 antipsychotic-stabilized patients with schizophrenia or schizoaffective disorder participated. PANSS was obtained bi-weekly and neuropsychological (MATRICS) was obtained pre- and post medication phase. The pharmacokinetics/pharmacodynamics (PK/PD), and safety of doses> or =30 mg/kg was also evaluated. RESULTS Significant improvement in symptoms and neuropsychological measures was noted across doses. On the PANSS, improvement was observed for positive (p=0.006;d=0.46), negative (p<0.001;d=0.68), general (p=0.001;d=0.53), and total (p<0.0001;d=0.74) symptoms. On MATRICS, while only non-significant improvement was noted at 30 mg/kg, highly significant, large effect size improvement was noted on the composite score (p<0.01;d=1.0) for doses> or =60 mg/kg, leading to a significant dose-by-time interaction (p<0.01). In PK analyses, significant dose-dependent increases in plasma D-serine levels were seen during the study, predictive of significantly increased brain levels. Furthermore, increases in plasma levels correlated with improved symptomatic and neuropsychological function. DISCUSSION These findings support double-blind investigation of D-serine at doses> or =60 mg/kg/d, and suggest effectiveness in treatment of both persistent symptoms and neurocognitive dysfunction.


Psychiatry Research-neuroimaging | 1991

Effects of chronic fluoxetine treatment on behavioral and neuroendocrine responses to meta-chloro-phenylpiperazine in obsessive-compulsive disorder

Eric Hollander; Concetta M. DeCaria; Robert Gully; Anca Nitescu; Raymond F. Suckow; Jack M. Gorman; Donald F. Klein; Michael R. Liebowitz

To investigate the effect of fluoxetine on serotonergic sensitivity in obsessive-compulsive disorder (OCD), the partial serotonin agonist metachlorophenylpiperazine (mCPP) was compared to placebo under double-blind conditions in six patients with OCD before and during treatment with fluoxetine. Readministration of oral mCPP (0.5 mg/kg) after at least 12 weeks of fluoxetine treatment did not increase obsessive-compulsive (OC) symptoms, in contrast to exacerbation of OC symptoms produced by mCPP before treatment. Chronic fluoxetine treatment resulted in a significant increase in prolactin and cortisol response to mCPP. This may be accounted for, however, by substantially increased plasma mCPP levels during fluoxetine treatment. Chronic fluoxetine treatment diminished the behavioral sensitivity to mCPP and did not diminish, but may have partially normalized, the neuroendocrine response to mCPP in patients with OCD. These adaptive homeostatic effects may reflect fluoxetines antiobsessional mechanism.


Molecular Psychiatry | 2013

Relationship of resting brain hyperconnectivity and schizophrenia-like symptoms produced by the NMDA receptor antagonist ketamine in humans.

Naomi Driesen; Gregory McCarthy; Zubin Bhagwagar; Michael H. Bloch; V.D. Calhoun; Deepak Cyril D'Souza; Ralitza Gueorguieva; George He; Raymond F. Suckow; Alan Anticevic; Peter T. Morgan; John H. Krystal

N-methyl-D-aspartate glutamate receptor (NMDA-R) antagonists produce schizophrenia-like positive and negative symptoms in healthy human subjects. Preclinical research suggests that NMDA-R antagonists interfere with the function of gamma-aminobutyric acid (GABA) neurons and alter the brain oscillations. These changes have been hypothesized to contribute to psychosis. In this investigation, we evaluated the hypothesis that the NMDA-R antagonist ketamine produces alterations in cortical functional connectivity during rest that are related to symptoms. We administered ketamine to a primary sample of 22 subjects and to an additional, partially overlapping, sample of 12 subjects. Symptoms before and after the experimental session were rated with the Positive and Negative Syndrome Scale (PANSS). In the primary sample, functional connectivity was measured via functional magnetic resonance imaging almost immediately after infusion began. In the additional sample, this assessment was repeated after 45 min of continuous ketamine infusion. Global, enhanced functional connectivity was observed at both timepoints, and this hyperconnectivity was related to symptoms in a region-specific manner. This study supports the hypothesis that pathological increases in resting brain functional connectivity contribute to the emergence of positive and negative symptoms associated with schizophrenia.


Psychopharmacology | 1990

Effects ofm-chlorophenylpiperazine in normal subjects: a dose-response study

R.S. Kahn; Scott Wetzler; Gregory M. Asnis; Mitchel A. Kling; Raymond F. Suckow; H. M. van Praag

Abstractm-Chlorophenylpiperazine (MCPP), a direct 5HT receptor agonist, was administered orally to 20 normal subjects in two doses (0.25 and 0.5 mg/kg) in a placebo-controlled design. Behavioral responses; ACTH, cortisol, prolactin and MCPP blood level; temperature and pulse rate were measured over a 210-min period after administration of tablets. Non-linear dose-response relationships between MCPP and ACTH, cortisol and prolactin response were found. On the higher dose, a significant increase in the number of physical symptoms was also noted and three subjects (15%) had a panic attack, while one subject (5%) had a panic attack on the lower dose. No effects on other behavioral variables, pulse rate and temperature were found using either dose. These findings attest to the usefulness of MCPP as a challenge agent to assess 5HT receptor hypersensitivity when given at a low oral dose (i.e. around 0.25 mg/kg), and to assess 5HT receptor hyposensitivity when given at higher oral doses (i.e. around 0.5 mg/kg).


Journal of Molecular Neuroscience | 1999

Expression of aspartoacylase activity in cultured rat macroglial cells is limited to oligodendrocytes

Morris H. Baslow; Raymond F. Suckow; Victor Sapirstein; Basalingappa L. Hungund

N-acetyl-l-aspartate (NAA) is an important osmolyte in the vertebrate brain and eye, and its cyclical metabolism is accomplished in two separate compartments. In the brain, NAA is synthesized primarily in neurons, and after its regulated release, NAA is hydrolyzed by aspartoacylase, which is present in a glial-associated compartment. However, the precise nature of this hydrolytic compartment has remained obscure. It has been proposed that one role of aspartoacylase in the central nervous system (CNS) is as part of a molecular water pump (MWP) that uses the NAA intercompartmental cycle to remove nerve cell metabolic water against a water gradient and that oligodendrocytes comprise the second compartment in this metabolic sequence. The absence of aspartoacylase activity in Canavan disease (CD), a rare early onset genetic spongiform leukodystrophy, is associated with CNS edema, intramyelinic swelling and a progressive loss of oligdendrocytes. In order to evaluate the MWP hypothesis and its possible relationship to the etiology of CD further, both oligodendrocytes and astrocytes obtained from neonatal rat brain were grown in culture and tested for the presence of aspartoacylase activity. The results of this study show for the first time that aspartoacylase activity is expressed only in oligodendrocytes. The meaning of this observation in understanding the function of the NAA metabolic cycle is discussed.


Neuropsychopharmacology | 2013

The impact of NMDA receptor blockade on human working memory-related prefrontal function and connectivity

Naomi Driesen; Gregory McCarthy; Zubin Bhagwagar; Michael H. Bloch; V.D. Calhoun; Deepak Cyril D'Souza; Ralitza Gueorguieva; George He; Hoi-Chung Leung; Alan Anticevic; Raymond F. Suckow; Peter T. Morgan; John H. Krystal

Preclinical research suggests that N-methyl-D-aspartate glutamate receptors (NMDA-Rs) have a crucial role in working memory (WM). In this study, we investigated the role of NMDA-Rs in the brain activation and connectivity that subserve WM. Because of its importance in WM, the lateral prefrontal cortex, particularly the dorsolateral prefrontal cortex and its connections, were the focus of analyses. Healthy participants (n=22) participated in a single functional magnetic resonance imaging session. They received saline and then the NMDA-R antagonist ketamine while performing a spatial WM task. Time-course analysis was used to compare lateral prefrontal activation during saline and ketamine administration. Seed-based functional connectivity analysis was used to compare dorsolateral prefrontal connectivity during the two conditions and global-based connectivity was used to test for laterality in these effects. Ketamine reduced accuracy on the spatial WM task and brain activation during the encoding and early maintenance (EEM) period of task trials. Decrements in task-related activation during EEM were related to performance deficits. Ketamine reduced connectivity in the DPFC network bilaterally, and region-specific reductions in connectivity were related to performance. These results support the hypothesis that NMDA-Rs are critical for WM. The knowledge gained may be helpful in understanding disorders that might involve glutamatergic deficits such as schizophrenia and developing better treatments.


Journal of Chromatography B: Biomedical Sciences and Applications | 1999

Sensitive and selective liquid chromatographic assay of memantine in plasma with fluorescence detection after pre-column derivatization.

Raymond F. Suckow; Ming F. Zhang; Eric D. Collins; Marian W. Fischman; Thomas B. Cooper

A procedure was developed for the determination of memantine in plasma using liquid chromatography with fluorescence detection. Following a liquid-liquid extraction from 1 ml of plasma containing the internal standard amantadine, the extract was derivatized at room temperature with dansyl chloride, and the highly fluorescent derivatives were chromatographed with a reversed-phase C18 column and a mobile phase of phosphate buffer and acetonitrile. Dansylated memantine and amantadine were eluted in less than 13 min with no interference from endogenous material. The calibration curve was linear over the concentration range of 3-400 ng/ml with inter- and intra-assay imprecision (C.V.) of less than 10%. The limit of quantitation was 3 ng/ml, and no major antidepressant, neuroleptic or their respective metabolites interfered with the quantitation of memantine. This method could also be applied to the quantitation of amantadine.


Biomedical Chromatography | 1997

Enantiomeric determination of the phenylmorpholinol metabolite of bupropion in human plasma using coupled achiral-chiral liquid chromatography.

Raymond F. Suckow; Ming F. Zhang; Thomas B. Cooper

A coupled achiral-chiral stationary phase liquid chromatographic technique was developed to separate and quantitate the enantiomers of the phenylmorpholinol metabolite (2) of the antidepressant bupropion (1) in human plasma. At the retention time of 2, a switching valve loaded a portion of the eluting compound onto a protein-bonded chiral stationary phase which resolved 2 into the (+) and (-) stereoisomers using an aqueous mobile phase of potassium phosphate (pH = 6.25) and 5% 2-propanol. All eluting compounds were monitored using UV detection at 214 nm, and no plasma endogenous material or other commonly used psychotropic drugs were found to interfere. Within-day and between-day variation were less than 6% over the expected concentration range, and a limit of quantitation of about 125 ng/mL of 2 was observed. Steady-state plasma samples from 17 patients receiving 1 were found to contain the (-) enantiomer to the extent of about 96% of total 2. The potential clinical implications of these results are not known since all previous pharmacological studies were carried out with the racemic 2.


Journal of Pharmacology and Experimental Therapeutics | 2010

Sex-Specific Effects of Chronic Fluoxetine Treatment on Neuroplasticity and Pharmacokinetics in Mice

Georgia E. Hodes; Tiffany E. Hill-Smith; Raymond F. Suckow; Thomas B. Cooper; Irwin Lucki

Neurogenesis is a mechanism through which antidepressants may produce therapeutic effects. There is a dearth of information regarding the effects of antidepressants on neurogenesis and neurotrophin mobilization in females. This study examined sex differences in the alteration of cell proliferation and survival in multiple regions of the brain. Additional experiments examined brain-derived neurotrophic factor (BDNF) levels and pharmacokinetics of fluoxetine to determine whether they mediate sex differences. MRL/MpJ mice were treated with fluoxetine (5 and 10 mg/kg b.i.d.) for 21 days and received injections of 5-bromo-2′-deoxyuridine (200 mg/kg) to measure DNA synthesis. In the hippocampus, fluoxetine increased cell proliferation at both doses; females treated with 10 mg/kg produced more new cells than males. Fluoxetine did not alter survival in males, but 10 mg/kg reduced survival in females. In the frontal cortex, fluoxetine increased cell proliferation and survival in males treated with 10 mg/kg. In the cerebellum and amygdala, 10 mg/kg fluoxetine increased cell proliferation in both sexes but did not alter the incorporation of the new cells. Fluoxetine increased BDNF levels in the hippocampus of both sexes. BDNF levels correlated with cell proliferation in males but not females. Brain and plasma levels indicated that females metabolized fluoxetine faster than males and produced more of the metabolite norfluoxetine. These data suggest that fluoxetine acts on multiple areas of the brain to increase cell proliferation, and the pattern of activation differs between males and females. Sex-specific effects of fluoxetine on neurotrophin mobilization and pharmacokinetics may contribute to these differences in neural plasticity.


Clinical Pharmacology & Therapeutics | 1985

Tricyclic antidepressant and metabolite levels in chronic renal failure.

Jeffrey A. Lieberman; Thomas B. Cooper; Raymond F. Suckow; Herbert Steinberg; Michael Borenstein; Ronald Brenner; John M. Kane

Serial blood samples were drawn from 12 patients undergoing hemodialysis who were receiving tricyclic antidepressants (TCAs). Samples were drawn before, during, and after a dialysis session (two to 17 sessions per subject). Samples were analyzed by HPLC before and after hydrolysis with β‐glucuronidase/sulfatase to determine the conjugated and nonconjugated metabolites. Analysis of these data in comparison with those of controls with depression and normal renal function showed that: (1) at steady state, tertiary and secondary amine TCA levels did not differ; (2) levels of the hydroxylated metabolites had greater variability and were somewhat higher at steady state; (3) levels of the conjugated hydroxylated compounds were markedly elevated, reaching 500% to 1500% normal; (4) the time to reach a steady‐state level appeared to be slightly increased; and (5) elimination t½s of unconjugated and conjugated drug forms were longer in our patients with normal renal function than those reported in the literature. Levels of the tertiary, secondary, and hydroxylated metabolites were not changed by dialysis, whereas there were substantial decrements in glucuronidated metabolite levels. These findings demonstrate increased concentrations of conjugated drug forms and suggest an abnormal distribution or delayed elimination of unconjugated and conjugated metabolites. These observations may shed some light on the apparent hypersensitivity of these patients to TCA side effects, particularly because glucuronides may exert peripheral pharmacologic effects.

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Catherine L. Clelland

Columbia University Medical Center

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Concetta M. DeCaria

Icahn School of Medicine at Mount Sinai

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