Biological Psychiatry RSS feed: Current Issue. This international rapid-publication journal is the official journal of the Society of Biological Psychiatry. It covers a broad range of topics in psychiatric neuroscience and therapeutics. Both basic and clinical contributions are encouraged from all disciplines and research areas relevant to the pathophysiology and treatment of major neuropsychiatric disorders. Novel results of original research, in Archival and Brief Report formats, Commentaries, and Correspondence judged to be of high impact to the field are published, particularly those addressing genetic and environmental risk factors, neural circuitry and neurochemistry, and important new therapeutic approaches. Concise Reviews and Editorials that focus on topics of current research and interest are also published rapidly. Visit the web site of the Society of Biological Psychiatry at URL: http://www.sobp.org for details on membership, publications, awards and other society information. Biological Psychiatry is ranked 4th out of 117 Psychiatry titles and 13th out of 230 Neurosciences titles in the 2010 ISI Journal Citations Reports® published by Thomson Reuters. The 2009 Impact Factor score for Biological Psychiatry has increased to 8.926. Biological Psychiatry 's acceptance rate is approximately 15%. The average time from submission to first decision is less than 20 days, with an editorial rejection (reject without peer review) decision issued within 5 days. Accepted articles are published online ahead of print in an average of 35 business days, and articles are published in print 4-6 months after acceptance. http://www.biologicalpsychiatryjournal.com/?rss=yesElsevier Inc.en © 2010 Published by Elsevier Inc. All rights reserved. Biological Psychiatry0006-322368615 September 2010 © 2010 Published by Elsevier Inc. All rights reserved. healthpermissions@elsevier.comhttp://www.biologicalpsychiatryjournal.com/article/PIIS0006322310008097/abstract?rss=yesMukherjee et al. (pages 503-511) found that knock-down of Clock using RNA interference in the ventral tegmental area of adult mice leads to increased dopamine cell activity and a mixed behavioral response that resembles aspects of mania and depression in humans. These results show that manipulation of this single gene, which is involved in generating circadian rhythms in one of the brain's central reward and mood-related regions, has a profound impact on mood-related behavior.A brief summary of the articles appearing in this issue of Biological Psychiatry10.1016/j.biopsych.2010.08.001Biological Psychiatry 68, 6 (2010)2010-09-15Biological Psychiatry2010-09-15686S0006-3223(10)X0016-6499499http://www.biologicalpsychiatryjournal.com/article/PIIS0006322310007651/abstract?rss=yesThe field of biological psychiatry has been hindered by the paucity of animal models of depression and bipolar disorder that are reliable across laboratories, assess constructs with relevance to core symptomatology of these disorders, and include inducing conditions that are based on solid theoretical rationales about the etiologies of these disorders. Two studies published in this issue of Biological Psychiatry used molecular genetic techniques in rodents to reveal previously unidentified mechanisms involved in the neurobiological regulation of mood and affect, moving beyond the traditional targets of current pharmacotherapies. These studies suggest roles for γ-aminobutyric acid (GABA) A receptor and Circadian Locomotor Output Cycles Kaput transcription factor in depression and bipolar disorder. Because malfunctions in such regulatory mechanisms lead to affective symptoms of depression and mania, these findings provide new insights regarding the etiology of mood dysregulation and its potential treatment.Studies in Genetically Modified Mice Suggest Novel Mechanisms of Mood RegulationAthina Markou, Mark A. Geyer10.1016/j.biopsych.2010.07.020Biological Psychiatry 68, 6 (2010)2010-09-15Biological Psychiatry2010-09-15686S0006-3223(10)X0016-6Commentary500502http://www.biologicalpsychiatryjournal.com/article/PIIS0006322310004257/abstract?rss=yesBackground: Circadian rhythm abnormalities are strongly associated with bipolar disorder; however the role of circadian genes in mood regulation is unclear. Previously, we reported that mice with a mutation in the Clock gene (ClockΔ19) display a behavioral profile that is strikingly similar to bipolar patients in the manic state.Methods: Here, we used RNA interference and viral-mediated gene transfer to knock down Clock expression specifically in the ventral tegmental area (VTA) of mice. We then performed a variety of behavioral, molecular, and physiological measures.Results: We found that knockdown of Clock, specifically in the VTA, results in hyperactivity and a reduction in anxiety-related behavior, which is similar to the phenotype of the ClockΔ19 mice. However, VTA-specific knockdown also results in a substantial increase in depression-like behavior, creating an overall mixed manic state. Surprisingly, VTA knockdown of Clock also altered circadian period and amplitude, suggesting a role for Clock in the VTA in the regulation of circadian rhythms. Furthermore, VTA dopaminergic neurons expressing the Clock short hairpin RNA have increased activity compared with control neurons, and this knockdown alters the expression of multiple ion channels and dopamine-related genes in the VTA that could be responsible for the physiological and behavioral changes in these mice.Conclusions: Taken together, these results suggest an important role for Clock in the VTA in the regulation of dopaminergic activity, manic and depressive-like behavior, and circadian rhythms.Knockdown of Clock in the Ventral Tegmental Area Through RNA Interference Results in a Mixed State of Mania and Depression-Like BehaviorShibani Mukherjee, Laurent Coque, Jun-Li Cao, Jaswinder Kumar, Sumana Chakravarty, Aroumougame Asaithamby, Ami Graham, Elizabeth Gordon, John F. Enwright, Ralph J. DiLeone, Shari G. Birnbaum, Donald C. Cooper, Colleen A. McClung10.1016/j.biopsych.2010.04.031Biological Psychiatry 68, 6 (2010)2010-06-30Biological Psychiatry2010-06-30686S0006-3223(10)X0016-6Archival Reports503511http://www.biologicalpsychiatryjournal.com/article/PIIS0006322310004099/abstract?rss=yesBackground: The γ-aminobutyric acid (GABA) Type A receptor deficits that are induced by global or forebrain-specific heterozygous inactivation of the γ2 subunit gene in mouse embryos result in behavior indicative of trait anxiety and depressive states. By contrast, a comparable deficit that is delayed to adolescence is without these behavioral consequences. Here we characterized γ2-deficient mice with respect to hypothalamic-pituitary-adrenal (HPA) axis abnormalities and antidepressant drug responses.Methods: We analyzed the behavioral responses of γ2+/− mice to desipramine and fluoxetine in novelty suppressed feeding, forced swim, tail suspension, and sucrose consumption tests as well as GABAA receptor deficit- and antidepressant drug treatment-induced alterations in serum corticosterone.Results: Baseline corticosterone concentrations in adult γ2-deficient mice were elevated independent of whether the genetic lesion was induced during embryogenesis or delayed to adolescence. However, the manifestation of anxious-depressive behavior in different γ2-deficient mouse lines was correlated with early onset HPA axis hyperactivity during postnatal development. Chronic but not subchronic treatment of γ2+/− mice with fluoxetine or desipramine normalized anxiety-like behavior in the novelty suppressed feeding test. Moreover, desipramine had antidepressant-like effects in that it normalized HPA axis function and depression-related behavior of γ2+/− mice in the forced swim, tail suspension, and sucrose consumption tests. By contrast, fluoxetine was ineffective as an antidepressant and failed to normalize HPA axis function.Conclusions: Developmental deficits in GABAergic inhibition in the forebrain cause behavioral and endocrine abnormalities and selective antidepressant drug responsiveness indicative of anxious-depressive disorders such as melancholic depression, which are frequently characterized by HPA axis hyperactivity and greater efficacy of desipramine versus fluoxetine.γ-Aminobutyric Acid-Type A Receptor Deficits Cause Hypothalamic-Pituitary-Adrenal Axis Hyperactivity and Antidepressant Drug Sensitivity Reminiscent of Melancholic Forms of DepressionQiuying Shen, Rachnanjali Lal, Beth A. Luellen, John C. Earnheart, Anne Milasincic Andrews, Bernhard Luscher10.1016/j.biopsych.2010.04.024Biological Psychiatry 68, 6 (2010)2010-06-28Biological Psychiatry2010-06-28686S0006-3223(10)X0016-6Archival Reports512520http://www.biologicalpsychiatryjournal.com/article/PIIS0006322310004087/abstract?rss=yesBackground: Despite recent interest in glycogen synthase kinase-3β (GSK-3β) as a target for the treatment of mood disorders, there has been very little work related to these illnesses on the upstream signaling molecules that regulate this kinase as well as downstream targets.Methods: With a focused microarray approach we examined the influence of different classes of antidepressants on Wnt signaling that controls GSK-3β activity as well as the transcription factors that contribute to the actions of GSK-3β.Results: The results demonstrate that Wnt2 is a common target of different classes of antidepressants and also show differential regulation of Wnt-GSK-3β signaling genes. Increased expression and function of Wnt2 was confirmed by secondary measures. Moreover, with a viral vector approach we demonstrate that increased expression of Wnt2 in the hippocampus is sufficient to produce antidepressant-like behavioral actions in well-established models of depression and treatment response.Conclusions: These findings demonstrate that Wnt2 expression and signaling is a common target of antidepressants and that increased Wnt2 is sufficient to produce antidepressant effects.Wnt2 Expression and Signaling Is Increased by Different Classes of Antidepressant TreatmentsHideki Okamoto, Bhavya Voleti, Mounira Banasr, Maysa Sarhan, Vanja Duric, Matthew J. Girgenti, Ralph J. DiLeone, Samuel S. Newton, Ronald S. Duman10.1016/j.biopsych.2010.04.023Biological Psychiatry 68, 6 (2010)2010-06-07Biological Psychiatry2010-06-07686S0006-3223(10)X0016-6Archival Reports521527http://www.biologicalpsychiatryjournal.com/article/PIIS0006322310004233/abstract?rss=yesBackground: The protein p11 (also called S100A10) is downregulated in human and rodent depressive-like states. Considerable experimental evidence also implicates p11 in the mechanism of action of antidepressant drugs and electroconvulsive seizures, in part due to its interaction with specific serotonin receptors. Brain-derived neurotrophic factor (BDNF) has been linked to the therapeutic activity of antidepressants in rodent models and humans. In the current study, we investigated whether BDNF regulates p11 in vitro and in vivo.Methods: We utilized primary neuronal cultures, in vivo analyses of transgenic mice, and behavioral techniques to assess the effects of BDNF on p11.Results: Results indicate that BDNF stimulates p11 expression through tropomyosin-related kinase B (trkB) receptors and via the mitogen-activated protein kinase signaling pathway. Brain-derived neurotrophic factor-induced changes in p11 in vivo correlate with changes in ligand binding to the 5-hydroxytryptamine receptor 1B, the subcellular localization of which is known to be regulated by p11. Behavioral studies demonstrate that p11 knockout mice are insensitive to the antidepressant actions of BDNF.Conclusions: Taken together, our data demonstrate that p11 levels are regulated by BDNF in vitro and in vivo and that the antidepressant-like effect of BDNF in two well-established behavioral models requires p11. These data support a role for p11 in the antidepressant activity of neurotrophins.A Role for p11 in the Antidepressant Action of Brain-Derived Neurotrophic FactorJennifer L. Warner-Schmidt, Emily Y. Chen, Xiaoqun Zhang, John J. Marshall, Alexei Morozov, Per Svenningsson, Paul Greengard10.1016/j.biopsych.2010.04.029Biological Psychiatry 68, 6 (2010)2010-06-30Biological Psychiatry2010-06-30686S0006-3223(10)X0016-6Archival Reports528535http://www.biologicalpsychiatryjournal.com/article/PIIS0006322310004282/abstract?rss=yesBackground: The serotonin transporter gene-linked polymorphic region (5-HTTLPR) has been proposed as a predictor of antidepressant response. Insertion or deletion of a 44-base pair-long region gives rise to short “S” and long “L” forms of the promoter region, the “S” form being associated with reduced serotonin transporter expression.Methods: A systematic review and meta-analysis was performed to clarify the effect of 5-HTTLPR on antidepressant response and remission rates. Data were obtained from 28 studies with 5408 participants. Three genotype comparisons were tested—SS versus (SL or LL), (SS or SL) versus LL, and SS versus LL.Results: There was no statistically significant effect on antidepressant response. Compared with L carriers, there was an apparent effect of the SS genotype on remission rate (relative risk: .88; 95% confidence interval: .79–.98; p = .02). However, after trim and fill correction for missing data, the effect disappeared (relative risk: .92; 95% confidence interval: .81–1.05; p = .23), indicating that the initial significant effect was likely the result of publication bias. No significant effect on remission rate was seen for SS versus LL and SS/SL versus LL. Substantial unexplained heterogeneity of effect sizes was observed between studies, pointing to additional interacting factors contributing to an association in some cases.Conclusions: The 5-HTTLPR biallelic short/long polymorphism by itself does not seem to usefully predict antidepressant response.Antidepressant Response and the Serotonin Transporter Gene-Linked Polymorphic RegionMatthew J. Taylor, Srijan Sen, Zubin Bhagwagar10.1016/j.biopsych.2010.04.034Biological Psychiatry 68, 6 (2010)2010-07-23Biological Psychiatry2010-07-23686S0006-3223(10)X0016-6Archival Reports536543http://www.biologicalpsychiatryjournal.com/article/PIIS0006322310005251/abstract?rss=yesBackground: The neuroplasticity hypothesis of depression proposes that a dysfunction of neural plasticity—the basic ability of living organisms to adapt their neural function and structure to external and internal cues—might represent a final common pathway underlying the biological and clinical characteristics of the disorder. This study examined learning and memory as correlates of long-term synaptic plasticity in humans to further test the neuroplasticity hypothesis of depression.Methods: Learning in three tasks, for which memory consolidation has been shown to depend on local synaptic refinement in areas of interest (hippocampus-dependent declarative word-pair learning, amygdala-dependent fear conditioning, and primary-cortex-dependent visual texture discrimination), was assessed in 23 inpatients who met International Classification of Disease, 10th Revision, criteria for severe unipolar depression and 35 nondepressed comparison subjects.Results: Depressed subjects showed a significant deficit in declarative memory consolidation and enhanced fear acquisition as indicated by skin conductance responses to conditioned stimuli, in comparison with nondepressed subjects. Depressed subjects demonstrated impaired visual discrimination at baseline, not allowing for valid group comparisons of gradual improvement, the plasticity-dependent phase of the task.Conclusions: The results of the study are consistent with the neuroplasticity hypothesis of depression, showing decreased synaptic plasticity in a dorsal executive network that comprises the hippocampus and elevated synaptic plasticity in a ventral emotional network that includes the amygdala in depression. Evaluation of further techniques aimed at modulating synaptic plasticity might prove useful for developing novel treatments for major depressive disorder.Learning as a Model for Neural Plasticity in Major DepressionChristoph Nissen, Johannes Holz, Jens Blechert, Bernd Feige, Dieter Riemann, Ulrich Voderholzer, Claus Normann10.1016/j.biopsych.2010.05.026Biological Psychiatry 68, 6 (2010)2010-07-26Biological Psychiatry2010-07-26686S0006-3223(10)X0016-6Archival Reports544552http://www.biologicalpsychiatryjournal.com/article/PIIS0006322310004191/abstract?rss=yesBackground: The hippocampus is likely involved in mood disorders, but in vivo evidence for the role of anatomically distinct hippocampal subregions is lacking. Multiple sclerosis, an inflammatory disease of the central nervous system, is linked to a high prevalence of depression as well as hippocampal damage and may thus provide important insight into the pathologic correlates of medical depression. We examined the role of subregional hippocampal volume for depression in relapsing-remitting multiple sclerosis.Methods: Anatomically defined hippocampal subregional volumes (cornu ammonis 1–3 [CA1–CA3] and the dentate gyrus [CA23DG], subiculum, entorhinal cortex) were measured using a high-resolution T2-weighted magnetic resonance imaging sequence in 29 relapsing-remitting multiple sclerosis patients and 20 matched healthy control subjects. Diurnal salivary cortisol was assessed at awakening, 4 pm, and 9 pm on 2 consecutive days. Subjects also completed the Beck Depression Inventory.Results: Multiple sclerosis patients showed smaller hippocampal volumes compared with control subjects, particularly in the CA1 and subiculum subregions. In addition, multiple sclerosis patients with depressive symptoms (Beck Depression Inventory score >13) also showed smaller CA23DG volumes and higher cortisol levels. Within the multiple sclerosis group, CA23DG volume was correlated with depressive symptoms and cortisol levels. There were no associations with number of previous steroid treatments, global atrophy, or disease duration.Conclusions: This report provides in vivo evidence for selective association of smaller CA23DG subregional volumes in the hippocampus with cortisol hypersecretion and depressive symptoms in multiple sclerosis.Smaller Cornu Ammonis 2–3/Dentate Gyrus Volumes and Elevated Cortisol in Multiple Sclerosis Patients with Depressive SymptomsStefan M. Gold, Kyle C. Kern, Mary-Frances O'Connor, Michael J. Montag, Aileen Kim, Ye S. Yoo, Barbara S. Giesser, Nancy L. Sicotte10.1016/j.biopsych.2010.04.025Biological Psychiatry 68, 6 (2010)2010-06-21Biological Psychiatry2010-06-21686S0006-3223(10)X0016-6Archival Reports553559http://www.biologicalpsychiatryjournal.com/article/PIIS0006322310004300/abstract?rss=yesObjectives: The absence of pathophysiologically relevant diagnostic markers of bipolar disorder (BD) leads to its frequent misdiagnosis as unipolar depression (UD). We aimed to determine whether whole brain white matter connectivity differentiated BD from UD depression.Methods: We employed a three-way analysis of covariance, covarying for age, to examine whole brain fractional anisotropy (FA), and corresponding longitudinal and radial diffusivity, in currently depressed adults: 15 with BD-type I (mean age 36.3 years, SD 12.0 years), 16 with recurrent UD (mean age 32.3 years, SD 10.0 years), and 24 healthy control adults (HC) (mean age 29.5 years, SD 9.43 years). Depressed groups did not differ in depression severity, age of illness onset, and illness duration.Results: There was a main effect of group in left superior and inferior longitudinal fasciculi (SLF and ILF) (all F ≥ 9.8; p ≤ .05, corrected). Whole brain post hoc analyses (all t ≥ 4.2; p ≤ .05, corrected) revealed decreased FA in left SLF in BD, versus UD adults in inferior temporal cortex and, versus HC, in primary sensory cortex (associated with increased radial and decreased longitudinal diffusivity, respectively); and decreased FA in left ILF in UD adults versus HC. A main effect of group in right uncinate fasciculus (in orbitofrontal cortex) just failed to meet significance in all participants but was present in women. Post hoc analyses revealed decreased right uncinate fasciculus FA in all and in women, BD versus HC.Conclusions: White matter FA in left occipitotemporal and primary sensory regions supporting visuospatial and sensory processing differentiates BD from UD depression. Abnormally reduced FA in right fronto-temporal regions supporting mood regulation, might underlie predisposition to depression in BD. These measures might help differentiate pathophysiologic processes of BD versus UD depression.Right Orbitofrontal Corticolimbic and Left Corticocortical White Matter Connectivity Differentiate Bipolar and Unipolar DepressionAmelia Versace, Jorge R.C. Almeida, Karina Quevedo, Wesley K. Thompson, Robert A. Terwilliger, Stefanie Hassel, David J. Kupfer, Mary L. Phillips10.1016/j.biopsych.2010.04.036Biological Psychiatry 68, 6 (2010)2010-07-02Biological Psychiatry2010-07-02686S0006-3223(10)X0016-6Archival Reports560567http://www.biologicalpsychiatryjournal.com/article/PIIS0006322310005986/abstract?rss=yesBackground: Electroconvulsive therapy (ECT) is the most acutely effective treatment for depression, but is limited by cognitive side effects. However, research on their persistence, severity, and pattern is inconsistent. We aimed to quantify ECT-associated cognitive changes, specify their pattern, and determine progression.Methods: MEDLINE, EMBASE, PsycArticles, PsychINFO, PsychLIT, and reference lists were systematically searched through January 2009. We included all independent, within-subjects design studies of depressed patients receiving ECT where cognition was assessed using standardized tests. Main outcome was change in performance after ECT relative to pretreatment scores with respect to delay between finishing ECT and cognitive testing. We explored potential moderators' influence, e.g., electrode placement, stimulus waveform.Results: Twenty-four cognitive variables (84 studies, 2981 patients) were meta-analyzed. No standardized retrograde amnesia tests were identified. Significant decreases in cognitive performance were observed 0 to 3 days after ECT in 72% of variables: effect sizes (ES) ranging from −1.10 (95% confidence interval [CI], −1.53 to −.67) to −.21 (95% CI, −.40 to .01). Four to 15 days post-ECT, all but one CI included zero or showed positive ES. No negative ES were observed after 15 days, with 57% of variables showing positive ES, ranging from .35 (95% CI, .07–.63) to .75 (95% CI, .43–1.08). Moderators did not influence cognitive outcomes after 3 days post-ECT.Conclusions: Cognitive abnormalities associated with ECT are mainly limited to the first 3 days posttreatment. Pretreatment functioning levels are subsequently recovered. After 15 days, processing speed, working memory, anterograde memory, and some aspects of executive function improve beyond baseline levels.Objective Cognitive Performance Associated with Electroconvulsive Therapy for Depression: A Systematic Review and Meta-AnalysisMaria Semkovska, Declan M. McLoughlin10.1016/j.biopsych.2010.06.009Biological Psychiatry 68, 6 (2010)2010-08-02Biological Psychiatry2010-08-02686S0006-3223(10)X0016-6Archival Reports568577http://www.biologicalpsychiatryjournal.com/article/PIIS0006322310005780/abstract?rss=yesBackground: Genome-wide association studies are a powerful tool for unravelling the genetic background of complex disorders such as major depression.Methods: We conducted a genome-wide association study of 604 patients with major depression and 1364 population based control subjects. The top hundred findings were followed up in a replication sample of 409 patients and 541 control subjects.Results: Two SNPs showed nominally significant association in both the genome-wide association study and the replication samples: 1) rs9943849 (pcombined = 3.24E-6) located upstream of the carboxypeptidase M (CPM) gene and 2) rs7713917 (pcombined = 1.48E-6), located in a putative regulatory region of HOMER1. Further evidence for HOMER1 was obtained through gene-wide analysis while conditioning on the genotypes of rs7713917 (pcombined = 4.12E-3). Homer1 knockout mice display behavioral traits that are paradigmatic of depression, and transcriptional variants of Homer1 result in the dysregulation of cortical-limbic circuitry. This is consistent with the findings of our subsequent human imaging genetics study, which revealed that variation in single nucleotide polymorphism rs7713917 had a significant influence on prefrontal activity during executive cognition and anticipation of reward.Conclusion: Our findings, combined with evidence from preclinical and animal studies, suggest that HOMER1 plays a role in the etiology of major depression and that the genetic variation affects depression via the dysregulation of cognitive and motivational processes.Genome-Wide Association-, Replication-, and Neuroimaging Study Implicates HOMER1 in the Etiology of Major DepressionMarcella Rietschel, Manuel Mattheisen, Josef Frank, Jens Treutlein, Franziska Degenhardt, René Breuer, Michael Steffens, Daniela Mier, Christine Esslinger, Henrik Walter, Peter Kirsch, Susanne Erk, Knut Schnell, Stefan Herms, H.-Erich Wichmann, Stefan Schreiber, Karl-Heinz Jöckel, Jana Strohmaier, Darina Roeske, Britta Haenisch, Magdalena Gross, Susanne Hoefels, Susanne Lucae, Elisabeth B. Binder, Thomas F. Wienker, Thomas G. Schulze, Christine Schmäl, Andreas Zimmer, Dilafruz Juraeva, Benedikt Brors, Thomas Bettecken, Andreas Meyer-Lindenberg, Bertram Müller-Myhsok, Wolfgang Maier, Markus M. Nöthen, Sven Cichon10.1016/j.biopsych.2010.05.038Biological Psychiatry 68, 6 (2010)2010-08-02Biological Psychiatry2010-08-02686S0006-3223(10)X0016-6Archival Reports578585http://www.biologicalpsychiatryjournal.com/article/PIIS0006322310005779/abstract?rss=yesBackground: Genetic variation in CACNA1C has been repeatedly shown to increase risk for psychiatric disorders, with the strongest evidence for involvement in bipolar disorder. To elucidate the mechanisms by which such effects on psychiatric disease are brought about by genetic factors, we investigated the influence of CACNA1C polymorphisms on brain structure.Methods: In 585 healthy volunteers, for whom magnetic resonance imaging data at 1.5 T (n = 282) or 3 T (n = 304) were available, we tested 193 single nucleotide polymorphisms (SNPs) in or near CACNA1C for association with FSL FIRST–segmented subcortical brain structures and hippocampus as well as SPM5-derived total brain volume and global gray and white matter volume using PLINK.Results: A study-wide significant association of SNPs in intron 3 of the CACNA1C gene was found for brainstem volume (lowest p value = 3.62E-05) and was confirmed by voxel-based morphometry. An effect on gray matter volume of the bipolar disorder–associated SNP rs1006737, as reported earlier in a sample of 77 healthy adults, could not be confirmed.Conclusions: Genetic variation in the pleiotropic psychiatric disease gene CACNA1C is associated with brainstem volume. Modulation of this structure, with its central control over motor, cognitive, affective, and arousal functions, constitutes an interesting novel potential mode of action of psychiatric risk factors.Genetic Variation in CACNA1C, a Gene Associated with Bipolar Disorder, Influences Brainstem Rather than Gray Matter Volume in Healthy IndividualsBarbara Franke, Alejandro Arias Vasquez, Joris A. Veltman, Han G. Brunner, Mark Rijpkema, Guillén Fernández10.1016/j.biopsych.2010.05.037Biological Psychiatry 68, 6 (2010)2010-07-20Biological Psychiatry2010-07-20686S0006-3223(10)X0016-6Brief Report586588http://www.biologicalpsychiatryjournal.com/article/PIIS0006322310007675/abstract?rss=yesOur goal is to rapidly disseminate information to our readers. Pre-publication abstracts of accepted articles are posted on our website weekly, and upon availability of a corrected proof, full articles are immediately posted and citable. Articles posted since the last issue are listed below. Interested readers are encouraged to contact authors directly for information prior to publication and to read the associated article in its entirety upon publication.The following Biological Psychiatry articles in press are now available in full text at http://www.sobp.org/journal10.1016/j.biopsych.2010.07.022Biological Psychiatry 68, 6 (2010)2010-09-15Biological Psychiatry2010-09-15686S0006-3223(10)X0016-6On the Internet589589http://www.biologicalpsychiatryjournal.com/article/PIIS0006322310005792/abstract?rss=yesTelomeres are lengths of repetitive DNA that cap the ends of chromosomes. They protect the ends of the chromosome and shorten with each cell division. Short leukocyte telomere length has been related to a number of age-related diseases (). In addition, shorter telomere length has been associated with environmental factors such as smoking and lack of exercise (). In a recent issue of Biological Psychiatry, Tyrka et al. () published a report suggesting a link between maltreatment in childhood and telomere shortening in 31 subjects. Individuals who had suffered maltreatment had telomere length .70 ± .24 compared with 1.02 ± .52 in individuals who had not been abused.No Correlation Between Childhood Maltreatment and Telomere LengthDaniel Glass, Leopold Parts, David Knowles, Abraham Aviv, Tim D. Spector10.1016/j.biopsych.2010.02.026Biological Psychiatry 68, 6 (2010)2010-08-02Biological Psychiatry2010-08-02686S0006-3223(10)X0016-6Correspondencee21e22http://www.biologicalpsychiatryjournal.com/article/PIIS0006322310005809/abstract?rss=yesGlass et al (). have not replicated our preliminary finding of shorter telomeres in adults reporting a history of childhood maltreatment. Unfortunately, their analysis is not comparable with the design of our study, and the number of affected subjects in our preliminary study and in the analysis by Glass et al. is too small to draw robust conclusions regarding the effect of childhood maltreatment on telomere length. The authors indicated that their analysis was conducted with a cohort of approximately 11,000 twins and claimed that their sample size was several-fold larger than the sample in our study. However, their maximum number of subjects appears to be 550, and the number reporting a history of abuse was, at most, 34 (with 20 in the analysis of physical abuse and 34 in the analysis of sexual abuse.)In Response to “No Correlation Between Childhood Maltreatment and Telomere Length”Audrey R. Tyrka, Lawrence H. Price, Hung-Teh Kao, Barbara Porton, Linda L. Carpenter10.1016/j.biopsych.2010.04.040Biological Psychiatry 68, 6 (2010)2010-08-04Biological Psychiatry2010-08-04686S0006-3223(10)X0016-6Correspondencee23e24http://www.biologicalpsychiatryjournal.com/article/PIIS0006322310004786/abstract?rss=yesWe read with interest Garriock and colleagues' article “A Genomewide Association Study of Citalopram Response in Major Depressive Disorder” (). This work is an important step in analyzing the Sequenced Treatment Alternatives to Relieve Depression (STAR*D) genomewide single-nucleotide polymorphism (SNP) data. Given STAR*D's complexity, many additional analyses will undoubtedly be required to realize the full potential of this valuable resource. In this spirit, we quantitatively model response as measured by the Quick Inventory of Depressive Symptoms (QIDS). The gains to quantitatively modeling response are evident in our results; unlike the initial analysis, we identify multiple genomewide significant SNPs.A Genomewide Association Study of Citalopram Response in Major Depressive Disorder—A Psychometric ApproachDaniel E. Adkins, Karolina Åberg, Joseph L. McClay, John M. Hettema, Susan G. Kornstein, József Bukszár, Edwin J.C.G. van den Oord10.1016/j.biopsych.2010.05.018Biological Psychiatry 68, 6 (2010)2010-07-12Biological Psychiatry2010-07-12686S0006-3223(10)X0016-6Correspondencee25e27http://www.biologicalpsychiatryjournal.com/article/PIIS0006322310007882/abstract?rss=yesEditorial Board10.1016/S0006-3223(10)00788-2Biological Psychiatry 68, 6 (2010)2010-09-15Biological Psychiatry2010-09-15686S0006-3223(10)X0016-6FrontmatterA1A1http://www.biologicalpsychiatryjournal.com/article/PIIS0006322310007894/abstract?rss=yesBiological Psychiatry (ISSN 0006-3223) is published semimonthly by Elsevier Inc., 360 Park Avenue South, New York, NY 10010-1710. Periodicals postage paid at New York, NY and additional mailing offices.Subscribers Page10.1016/S0006-3223(10)00789-4Biological Psychiatry 68, 6 (2010)2010-09-15Biological Psychiatry2010-09-15686S0006-3223(10)X0016-6FrontmatterA2A2http://www.biologicalpsychiatryjournal.com/article/PIIS0006322310007900/abstract?rss=yesTable of Contents10.1016/S0006-3223(10)00790-0Biological Psychiatry 68, 6 (2010)2010-09-15Biological Psychiatry2010-09-15686S0006-3223(10)X0016-6FrontmatterA3A4http://www.biologicalpsychiatryjournal.com/article/PIIS0006322310007924/abstract?rss=yesBiological Psychiatry is the official journal of the Society of Biological Psychiatry. The Journal rapidly publishes reports of novel results on a broad range of topics related to the pathophysiology and treatment of major neuropsychiatric disorders. Both basic and clinical neuroscience contributions are encouraged, particularly those addressing genetic and environmental risk factors, neural circuitry and neurochemistry, and important new therapeutic approaches.Guide for Authors10.1016/S0006-3223(10)00792-4Biological Psychiatry 68, 6 (2010)2010-09-15Biological Psychiatry2010-09-15686S0006-3223(10)X0016-6FrontmatterA5A6http://www.biologicalpsychiatryjournal.com/article/PIIS0006322310007936/abstract?rss=yesThis form should be completed by every author and accompany every new manuscript submission. It must be fully complete and accurate, with signatures from ALL authors, before a manuscript will be officially accepted. Please scan the completed form(s) and attach them electronically during the submission process. If you are unable to do so, fax the completed form(s) to the Editorial Office at (214) 648-0881.Manuscript Submission Form10.1016/S0006-3223(10)00793-6Biological Psychiatry 68, 6 (2010)2010-09-15Biological Psychiatry2010-09-15686S0006-3223(10)X0016-6FrontmatterA7A7