K E Isenberg

Georgia Health Sciences University, Augusta, GA, United States

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Publications (61)276.39 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: OBJECTIVE: To determine whether starting antidepressant medication at the start of electroconvulsive therapy (ECT) reduces post-ECT relapse and to determine whether continuation pharmacotherapy with nortriptyline (NT) and lithium (Li) differs in efficacy or adverse effects from continuation pharmacotherapy with venlafaxine (VEN) and Li. METHODS: During an acute ECT phase, 319 patients were randomized to treatment with moderate dosage bilateral ECT or high-dosage right unilateral ECT. They were also randomized to concurrent treatment with placebo, NT, or VEN. Of 181 patients to meet post-ECT remission criteria, 122 (67.4%) participated in a second continuation pharmacotherapy phase. Patients earlier randomized to NT or VEN continued on the antidepressant, whereas patients earlier randomized to placebo were now randomized to NT or VEN. Lithium was added for all patients who were followed until relapse or 6 months. RESULTS: Starting an antidepressant medication at the beginning of the ECT course did not affect the rate or timing of relapse relative to starting pharmacotherapy after ECT completion. The combination of NT and Li did not differ from VEN and Li in any relapse or adverse effect measure. Older age was strongly associated with lower relapse risk, whereas the type of ECT administered in the acute phase and medication resistance were not predictive. Across sites, 50% of the patients relapsed, 33.6% continued in remission 6 months after ECT, and 16.4% dropped out. CONCLUSIONS: Starting an antidepressant medication during ECT does not affect relapse, and there are concerns about administering Li during an acute ECT course. Nortriptyline and VEN were equally effective in prolonging remission, although relapse rates after ECT are substantial despite intensive pharmacology. As opposed to the usual abrupt cessation of ECT, the impact of an ECT taper should be evaluated.
    The journal of ECT 01/2013; · 1.19 Impact Factor
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    ABSTRACT: BACKGROUND: Health-related quality of life (HRQOL) is diminished in depressed adult outpatients and especially impaired among depressed patients referred for ECT. We compare pretreatment HRQOL in ECT and non-ECT depressed patients from two large samples, and examined whether sustained remission in depressive symptoms after ECT is associated with normalization of HRQOL. METHODS: HRQOL was measured with the Medical Outcomes Study Short Form 36 (SF36) before ECT and 6 months after ECT in an effectiveness (n=286) and an efficacy (n=243) clinical trial. RESULTS: ECT patients had very low baseline SF36 scores. With one exception, SF36 subscale scores in both trials were significantly lower than those of depressed outpatients. A minority of patients in both trials entered and sustained remission over the 24 week timeframe. Among sustained remitters, average SF36 scores were no different from normative scores of the general adult population, except that in the effectiveness study ECT patients reported less Bodily Pain (p<0.05) and better Mental Health (p<0.05), while in the efficacy study ECT patients reported more difficulty with Role-Emotional (p<0.01). LIMITATIONS: Only a modest number of patients were observed in sustained remission. CONCLUSIONS: HRQOL is very poor in patients referred for ECT. Depressed patients who experience sustained remission after ECT, however, can expect improvement in their quality of life that leaves many in a position indistinguishable from the general adult population.
    Journal of Affective Disorders 11/2012; · 3.76 Impact Factor
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    ABSTRACT: : To examine the determinants of health-related quality of life (HRQOL) immediately after a clinical trial of electroconvulsive therapy (ECT) for major depression and then again after 24 weeks of a continuation pharmacotherapy in a clinical trial comparing nortriptyline (NT) plus lithium (Li) versus venlafaxine (VEN) plus Li. : During acute ECT, 184 patients randomized to treatment with moderate-dosage bilateral (BL) ECT or high-dosage right unilateral (RUL) ECT completed the Medical Outcomes Study Short Form-36 (SF-36) as a measure of HRQOL before and immediately after ECT. They were also randomized to concurrent treatment with placebo, NT, or VEN. Seventy-four of these met remission criteria and agreed to be further randomized to 24 more weeks of VEN + Li versus NT + Li for relapse prevention and completed a final SF-36. Cognitive testing was also completed. : Scores from SF-36 were low before ECT, and the SF-36 subscales reflecting mental health were particularly low. Right unilateral electrode placement was associated with better SF-36 scores immediately after ECT, even after controlling for improvement in depression. Medication assignment during ECT (VEN, NT, or placebo) was not related to immediate HRQOL outcome, and cognitive performance was not related to immediate HRQOL. Remission immediately after ECT was associated with robust improvement in SF-36 scores compared with those who did not remit. Remission status remained a strong predictor of HRQOL 24 weeks after ECT, and sustained remitters showed additional gains in HRQOL 24 weeks after ECT. Electrode placement and medication assignment were not predictors at 24 weeks. : Using state-of-the-art delivery of acute ECT and continuation antidepressant medication, HRQOL improves remarkably after ECT, and this improvement shows further gains with those persons who sustain remission. Health-related QOL is superior with RUL versus BL ECT in the immediate post-ECT period, but at 24-weeks HRQOL has absent or inconsistent relationship with mode of ECT delivery or type of continuation antidepressant pharmacotherapy.
    The journal of ECT 01/2011; 27(2):97-102. · 1.19 Impact Factor
  • Biological psychiatry 11/2009; 67(2):e15-7. · 8.93 Impact Factor
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    ABSTRACT: Medication resistance is the leading indication for use of electroconvulsive therapy (ECT) in major depression. The practice of stopping antidepressant medications prior to ECT derived from studies in the 1960s and 1970s in nonresistant samples. There is also continuing controversy regarding the relative efficacy and adverse effects of right unilateral and bilateral ECT. To test the hypotheses that, compared with placebo, concomitant treatment with nortriptline or venlafaxine during the ECT course enhances short-term efficacy without a meaningful effect on adverse effects and reduces the rate of post-ECT relapse, and to test the hypotheses that high-dose, right-sided, unilateral ECT is equivalent in efficacy to moderate-dosage bilateral ECT and retains advantages with respect to cognitive adverse effects. Prospective, randomized, triple-masked, placebo-controlled study conducted from 2001 through 2005. Three university-based hospitals. Of approximately 750 consecutive patients referred for ECT, 319 with a major depressive episode consented, were randomized to pharmacological or ECT treatment conditions, and received at least 1 ECT treatment. Scores on the Hamilton Rating Scale for Depression, remission rate following completion of ECT, and selective measures of cognitive adverse effects. Treatment with nortriptyline enhanced the efficacy and reduced the cognitive adverse effects of ECT relative to placebo. Venlafaxine resulted in a weaker degree of improvement and tended to worsen cognitive adverse effects. High-dosage right unilateral ECT did not differ or was superior to bilateral ECT in efficacy and resulted in less severe amnesia. The efficacy of ECT is substantially increased by the addition of an antidepressant medication, but such medications may differ in whether they reduce or increase cognitive adverse effects. High-dose, right-sided, unilateral ECT is at least equivalent to moderate-dosage bilateral ECT in efficacy, but retains advantages with respect to cognitive adverse effects.
    Archives of general psychiatry 08/2009; 66(7):729-37. · 12.26 Impact Factor
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    ABSTRACT: This report describes the results of an open-label extension study of active trans-cranial magnetic stimulation (TMS) in medication-resistant patients with major depressive disorder who did not benefit from an initial course of therapy in a previously reported 6-week, randomized controlled study of active versus sham TMS. Patients with DSM-IV-defined major depressive disorder were actively enrolled in the study from February 2004 through September 2005 and treated with left prefrontal TMS administered 5 times per week at 10 pulses per second, at 120% of motor threshold, for a total of 3000 pulses/session. The primary outcome was the baseline to endpoint change score on the Montgomery-Asberg Depression Rating Scale (MADRS). In those patients who received sham in the preceding randomized controlled trial (N = 85), the mean reduction in MADRS scores after 6 weeks of open-label active TMS was -17.0 (95% CI = -14.0 to -19.9). Further, at 6 weeks, 36 (42.4%) of these patients achieved response on the MADRS, and 17 patients (20.0%) remitted (MADRS score < 10). For those patients who received and did not respond to active TMS in the preceding randomized controlled trial (N = 73), the mean reduction in MADRS scores was -12.5 (95% CI = -9.7 to -15.4), and response and remission rates were 26.0% and 11.0%, respectively, after 6 weeks of additional open-label TMS treatment. This open-label study provides further evidence that TMS is a safe and effective treatment of major depressive disorder. Furthermore, continued active TMS provided additional benefit to some patients who failed to respond to 4 weeks of treatment, suggesting that longer courses of treatment may confer additional therapeutic benefit. clinicaltrials.gov Identifier: NCT00104611.
    The Journal of Clinical Psychiatry 03/2008; 69(3):441-51. · 5.81 Impact Factor
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    ABSTRACT: We tested whether transcranial magnetic stimulation (TMS) over the left dorsolateral prefrontal cortex (DLPFC) is effective and safe in the acute treatment of major depression. In a double-blind, multisite study, 301 medication-free patients with major depression who had not benefited from prior treatment were randomized to active (n = 155) or sham TMS (n = 146) conditions. Sessions were conducted five times per week with TMS at 10 pulses/sec, 120% of motor threshold, 3000 pulses/session, for 4-6 weeks. Primary outcome was the symptom score change as assessed at week 4 with the Montgomery-Asberg Depression Rating Scale (MADRS). Secondary outcomes included changes on the 17- and 24-item Hamilton Depression Rating Scale (HAMD) and response and remission rates with the MADRS and HAMD. Active TMS was significantly superior to sham TMS on the MADRS at week 4 (with a post hoc correction for inequality in symptom severity between groups at baseline), as well as on the HAMD17 and HAMD24 scales at weeks 4 and 6. Response rates were significantly higher with active TMS on all three scales at weeks 4 and 6. Remission rates were approximately twofold higher with active TMS at week 6 and significant on the MADRS and HAMD24 scales (but not the HAMD17 scale). Active TMS was well tolerated with a low dropout rate for adverse events (4.5%) that were generally mild and limited to transient scalp discomfort or pain. Transcranial magnetic stimulation was effective in treating major depression with minimal side effects reported. It offers clinicians a novel alternative for the treatment of this disorder.
    Biological Psychiatry 01/2008; 62(11):1208-16. · 9.25 Impact Factor
  • Keith E. Isenberg, Keith Garcia
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    ABSTRACT: The disorders under consideration are the result of identifiable conditions. Historically, an arbitrary distinction has been made between “organic” conditions, associated with a presumably clear pathological basis, and “functional” conditions, or psychiatric disorders that lacked obvious disease processes. Delirium, however, is a disorder of cognitive dysfunction that lacks a well-understood pathophysiology despite unequivocal association with multiple and various medical conditions. More generally, delirium and dementia are frequently complicated by psychopathology (for example, delusions or changes in mood) traditionally associated with so-called functional disorders (schizophrenia and affective disorders, respectively). The organic/functional distinction obscured the propensity of medical conditions (e.g., thyroid dysfunction) to present with psychiatric symptoms that resolved after effective treatment of the nonpsychiatric condition. The nosological conventions of the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM-IV-TR) (1) allow recognition of syndromes of disseminated cognitive dysfunction, such as delirium and dementia, as well as the psychopathology that is the product of various and multiple medical conditions without obscuring the need to consider these entities in the differential diagnosis of “functional” symptomatology. Regardless of the evolution of diagnostic convention, the illnesses described in this chapter can present to the psychiatrist as a “mental” condition or present to other medical specialists as “medical” conditions.
    12/2007: pages 17-37;
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    ABSTRACT: An abstract is unavailable. This article is available as HTML full text and PDF.
    Journal of Ect 02/2007; 23(1):56. · 1.69 Impact Factor
  • Keith E Isenberg, Charles F Zorumski
    Journal of Ect 01/2007; 22(4):233-4. · 1.69 Impact Factor
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    ABSTRACT: Glucose transporters play a critical role in mammalian brain energy metabolism because glucose is the principal brain energy source and these transporters promote glucose movement into neural cells. When glucose is unavailable, fructose can serve as an alternative energy source. Using real-time polymerase chain reaction and actin as a reference mRNA, we investigated the impact of fructose feeding on rat brain and other tissue mRNA expression of glucose transporter 5 which has high affinity for fructose. Brain mRNA levels of glucose transporter 5 increased 1.5-fold in 35-day old rats after 7 days of fructose feeding compared with controls, whereas it increased 2.5-fold in jejunum. Semi-quantitative analysis of protein expression by immunofluorescence of glucose transporter 5 in rat hippocampi indicated a 2.4-fold increase. We demonstrated the specificity of fructose feeding on glucose transporter 5 expression by showing that the expression of the neuronal glucose transporter 3 and insulin-regulated glucose transporter 4 were unaffected. In addition, the expression of glucose transporter 5 increased in fructose fed older adult rats (8-months and 12-months old) when compared with controls. These results suggest that short-term fructose feeding increases the expression of glucose transporter 5 in both young and aging adult rats. Increased brain expression of glucose transporter 5 is likely to be important in the role of fructose as an alternative energy source.
    Neuroscience 08/2006; 140(3):889-95. · 3.12 Impact Factor
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    ABSTRACT: We investigated conditions that promote basal and activity-dependent neuronal apoptosis in postnatal rat hippocampal cultures. Low-density mixed cultures of astrocytes and neurons exhibited lower sensitivity than high-density cultures to basal neuronal death and activity-sensitive neuronal death, induced with glutamate receptor blockers, sodium channel blockers, or calcium channel blockers. Although elevations of [Ca(2+)](i) protect neurons from apoptosis, low-density microcultures and mass cultures exhibited only minor differences in resting [Ca(2+)](i) and Ca(2+) current density, suggesting that these variables are unlikely to explain differences in susceptibility. Astrocytes, rather than neurons, were implicated in the neuronal loss. Several candidate molecules implicated in other astrocyte-dependent neurotoxicity models were excluded, but heat inactivation experiments suggested that a heat-labile factor is critically involved. In sum, our results suggest the surprising result that astrocytes can be negative modulators of neuronal survival during development and when the immature nervous system is challenged with drugs that dampen electrical excitability.
    Neuroscience 02/2005; 131(2):349-58. · 3.12 Impact Factor
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    ABSTRACT: Repetitive transcranial magnetic stimulation (rTMS) is a promising relatively non-invasive alternative for the treatment of depression. The purpose of this study was to compare the apparent effectiveness of high frequency (20 Hertz) rTMS applied over the left dorsolateral prefrontal cortex (DLPFC) with that of low frequency (1 Hz) rTMS applied over the right DLPFC METHODS: Twenty-eight antidepressant-free adults with major depressive (n = 25) or bipolar (n = 3) disorder (not on mood stabilizers) in a current major depression (Hamilton Rating Scale for Depression [HAM-D-21] > or = 18; Mean = 24.5, SD = 5.51) were treated (14 right, 14 left) for 4 weeks. Overall paired t-tests revealed a significant reduction in mean HAM-D-21, Beck Depression Inventory (BDI-II), and Clinical Global Impression of Change (CGIC) scores at the end of treatment for both groups (high frequency left DLPFC and low frequency right DLPFC). The treatment response rate found (32%) was typical of other response rates reported in the literature (6,30). One-month follow-up data was obtained from 50% of participants. At 1-month follow-up no significant differences were noted as compared to patients' performance at last treatment visit, indicating moderate robustness of rTMS treatment over time. Furthermore, magnetic stimulation did not substantially alter patient memory over the course of treatment. rTMS given at low frequency over the right frontal cortex appears to be as effective treatment of refractory depression as high frequency treatment over the left frontal cortex.
    Annals of Clinical Psychiatry 01/2005; 17(3):153-9. · 1.54 Impact Factor
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    ABSTRACT: Fetal alcohol exposure causes severe neuropsychiatric problems, but mechanisms of the ethanol-associated changes in central nervous system development are unclear. In vivo, ethanol's interaction with N-methyl-D-aspartate (NMDA) and gamma-aminobutyric acid type A (GABA(A)) receptors may cause increased apoptosis in the immature forebrain. We examined whether ethanol affects survival of neonatal hippocampal neurons in primary cultures. A 6-day ethanol exposure killed hippocampal neurons with an LD50 of approximately 25 mM. Elevated extracellular potassium or insulin-related growth factor 1 inhibited cell loss. Although potentiation of GABA(A) receptors or complete block of NMDA receptors also kills hippocampal neurons, pharmacological studies suggest that ethanol's interaction with GABA(A) and NMDA receptors is not sufficient to explain ethanol's effects on neuronal survival. Ca(2+) influx in response to depolarization was depressed >50% by chronic ethanol treatment. We suggest that chronic ethanol may promote neuronal loss through a mechanism affecting Ca(2+) influx in addition to effects on postsynaptic GABA and glutamate receptors.
    Neurobiology of Disease 08/2002; 10(3):396-409. · 5.62 Impact Factor
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    ABSTRACT: Neuroactive steroids rapidly modulate gamma-aminobutyric acid (GABA) and glutamate receptors. GABA-enhancing steroids have potential clinical utility as anesthetics, hypnotics, anticonvulsants and anxiolytics. Furthermore, GABAergic neurosteroids may participate in regulating mood and the effects of alcohol on the nervous system, suggesting a potential role in major psychiatric disorders. Neuroactive steroids that alter the function of glutamate receptors could be useful for treating neurodegenerative disorders, and as cognitive enhancers. Recent progress in developing water-soluble steroids and steroids with enhanced oral efficacy foster optimism that certain neuroactive steroids will be developed for clinical use.
    IDrugs: the investigational drugs journal 10/2000; 3(9):1053-63. · 2.33 Impact Factor
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    ABSTRACT: Neurotransmitters can have both toxic and trophic functions in addition to their role in neural signaling. Surprisingly, chronic blockade of GABA(A) receptor activity for 5-8 d in vitro enhanced survival of hippocampal neurons, suggesting that GABA(A) receptor overactivation may be neurotoxic. Potentiating GABA(A) receptor activity by chronic treatment with the endogenous neurosteroid (3alpha,5alpha)-3-hydroxypregnan-20-one caused massive cell loss over 1 week in culture. Other potentiators of GABA(A) receptors, including benzodiazepines, mimicked the cell loss, suggesting that potentiating endogenous GABA activity is sufficient to produce neuronal death. Neurosteroid-treated neurons had lower resting intracellular calcium levels than control cells and produced smaller calcium rises in response to depolarizing challenges. Manipulating intracellular calcium levels with chronic elevated extracellular potassium or with the calcium channel agonist Bay K 8644 protected neurons. The results may have implications for the mechanisms of programmed cell death in the developing CNS as well as implications for the long-term consequences of chronic GABAmimetic drug use during development.
    Journal of Neuroscience 06/2000; 20(9):3147-56. · 6.91 Impact Factor
  • Journal of Ect 04/2000; 16(1):68-70. · 1.69 Impact Factor
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    ABSTRACT: Although inhibitors of glutamate transport prolong synaptic currents at many glutamate synapses, the cause of the current prolongation is unclear. Transport inhibitors may prolong synaptic currents by simply interfering with synaptic glutamate binding to transporters, by inhibiting substrate translocation, or by promoting accumulation of ambient glutamate, which may act cooperatively at receptors with synaptic glutamate. We show that reversal of the membrane potential of astrocytes surrounding the synapse prolongs synaptic currents but does not decrease the apparent affinity of transporters or significantly alter glutamate-dependent kinetics of macroscopic transporter currents in excised membrane patches. Positive membrane potentials do not affect binding of a nontransported glutamate analog, nor do positive membrane potentials alter the number of transporters available to bind analog. We also test the hypothesis that glutamate accumulation during uptake inhibition by transporter substrates is the direct cause of synaptic current prolongations. Transporter substrates elevate ambient glutamate near synapses by fostering reverse transport of endogenous glutamate. However, increases in ambient glutamate cannot account for the prolongations of synaptic currents, because a nonsubstrate transport inhibitor does not foster reverse uptake yet it prolongs synaptic currents. Moreover, exogenous glutamate does not mimic synaptic current prolongations induced by substrate inhibitors. These results provide strong support for a major role of substrate translocation in determining the time course of the glutamate concentration transient at excitatory synapses.
    Journal of Neuroscience 12/1999; 19(21):9242-51. · 6.91 Impact Factor
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    ABSTRACT: 3beta-hydroxysteroid dehydrogenase/steroid delta5-->4-isomerase (3beta-HSD/isomerase) was expressed by baculovirus in Spodoptera fungiperda (Sf9) insect cells from cDNA sequences encoding human wild-type I (placental) and the human type I mutants - H261R, Y253F and Y253,254F. Western blots of SDS-polyacrylamide gels showed that the baculovirus-infected Sf9 cells expressed the immunoreactive wild-type, H261R, Y253F or Y253,254F protein that co-migrated with purified placental 3beta-HSD/isomerase (monomeric Mr=42,000 Da). The wild-type, H261R and Y253F enzymes were each purified as a single, homogeneous protein from a suspension of the Sf9 cells (5.01). In kinetic studies with purified enzyme, the H261R mutant enzyme had no 3beta-HSD activity, whereas the Km and Vmax values of the isomerase substrate were similar to the values obtained with the wild-type and native enzymes. The Vmax (88 nmol/min/mg) for the conversion of 5-androstene-3,17-dione to androstenedione by the Y253F isomerase activity was 7.0-fold less than the mean Vmax (620 nmol/min/mg) measured for the isomerase activity of the wild-type and native placental enzymes. In microsomal preparations, isomerase activity was completely abolished in the Y253,254F mutant enzyme, but Y253,254F had 45% of the 3beta-HSD activity of the wild-type enzyme. In contrast, the purified Y253F, wild-type and native enzymes had similar Vmax values for substrate oxidation by the 3beta-HSD activity. The 3beta-HSD activities of the Y253F, Y253,254F and wild-type enzymes reduced NAD+ with similar kinetic values. Although NADH activated the isomerase activities of the H261R and wild-type enzymes with similar kinetics, the activation of the isomerase activity of H261R by NAD+ was dramatically decreased. Based on these kinetic measurements, His261 appears to be a critical amino acid residue for the 3beta-HSD activity, and Tyr253 or Tyr254 participates in the isomerase activity of human type I (placental) enzyme.
    The Journal of Steroid Biochemistry and Molecular Biology 10/1998; 66(5-6):327-34. · 3.98 Impact Factor
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    ABSTRACT: To address the question of the relative contributions of glial and neuronal glutamate transport in the vertebrate CNS, we studied the distribution of forebrain glutamate transporters in rat hippocampal microcultures, a preparation in which physiological functions of glutamate transporters have been well characterized. Two of the three transporters, GLAST (EAAT1) and EAAC1 (EAAT3), are localized to microculture glia and neurons, respectively, as expected. However, we find strong immunoreactivity for the third glutamate transporter GLT-1 (EAAT2), a putatively glial transporter, in microculture neurons and in a small subset of microculture glia. Indistinguishable immunohistochemical staining patterns for GLT-1 were obtained with antibodies directed against both the N terminal and C terminal of the GLT-1 protein. Double-labeling experiments suggest that neuronal GLT-1 protein is primarily localized to the dendrites of excitatory neurons. Neuronal electrogenic transport currents in response to D-aspartate applications were occluded by the selective GLT-1 inhibitor dihydrokainate. In contrast, glia exhibited a larger transporter current density than did neurons, and the glial transport current was less sensitive to dihydrokainate. Neuronal transport currents were potentiated less than were glial currents when the chaotropic anion thiocyanate was substituted for gluconate in the whole-cell recording pipette, consistent with the previously reported lower anion permeability of EAAC1 and GLT-1 compared with that of GLAST. After microculture glia were rendered nonviable, excitatory autaptic currents (EACs) were prolonged in the presence of dihydrokainate, suggesting that neuronal GLT-1 is capable of participating in the clearance of synaptically released glutamate. Our results suggest that the initially proposed characterization of GLT-1 as a purely glial transporter is too simplistic and that under certain conditions functional GLT-1 protein can be expressed in brain neurons. The study suggests that changes in GLT-1 levels that occur with pathology or experimental manipulations cannot be assumed to be glial.
    Journal of Neuroscience 07/1998; 18(12):4490-9. · 6.91 Impact Factor

Publication Stats

1k Citations
276.39 Total Impact Points

Institutions

  • 2012
    • Georgia Health Sciences University
      • Department of Psychiatry & Health Behavior
      Augusta, GA, United States
    • Washington School of Psychiatry
      Washington, Washington, D.C., United States
  • 2011
    • Wake Forest University
      Winston-Salem, North Carolina, United States
  • 2008–2009
    • University of Pennsylvania
      • Department of Psychiatry
      Philadelphia, PA, United States
  • 1989–2008
    • Washington University in St. Louis
      • Department of Psychiatry
      San Luis, Missouri, United States
    • University of Alabama at Birmingham
      Birmingham, Alabama, United States
  • 1991–1995
    • University of Washington Seattle
      • Department of Neurology
      Seattle, WA, United States
  • 1993
    • St. Louis College of Pharmacy
      • Department of Pharmacy Practice
      Saint Louis, MO, United States
  • 1990–1993
    • University of Vienna
      Wien, Vienna, Austria
  • 1992
    • University of Maryland, Baltimore
      Baltimore, Maryland, United States