Progress in Neuro-Psychopharmacology and Biological Psychiatry (PROG NEURO-PSYCHOPH )

Publisher: Elsevier

Description

Progress in Neuro-Psychopharmacology & Biological Psychiatry is an international and multidisciplinary research, review and news journal. One of its main aims is to assure rapid publication of authoritative reviews and research papers dealing with experimental and clinical aspects of neuro-psychopharmacology and biological psychiatry. Another important aim of the journal is to supply pertinent information, provided by national and international bodies, that contributes to progress in the scientific and professional fields. Finally, the journal intends to foster and encourage communications between members of the communities of neuro-psychopharmacology and biological psychiatry.

  • Impact factor
    3.55
  • 5-year impact
    3.51
  • Cited half-life
    5.30
  • Immediacy index
    0.66
  • Eigenfactor
    0.02
  • Article influence
    0.94
  • Website
    Progress in Neuro-Psychopharmacology and Biological Psychiatry website
  • Other titles
    Progress in neuro-psychopharmacology & biological psychiatry (Online), Progress in neuro psychopharmacology and biological psychiatry
  • ISSN
    1878-4216
  • OCLC
    39196483
  • Material type
    Document, Periodical, Internet resource
  • Document type
    Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

Elsevier

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • Voluntary deposit by author of pre-print allowed on Institutions open scholarly website and pre-print servers
    • Voluntary deposit by author of authors post-print allowed on institutions open scholarly website including Institutional Repository
    • Deposit due to Funding Body, Institutional and Governmental mandate only allowed where separate agreement between repository and publisher exists
    • Set statement to accompany deposit
    • Published source must be acknowledged
    • Must link to journal home page or articles' DOI
    • Publisher's version/PDF cannot be used
    • Articles in some journals can be made Open Access on payment of additional charge
    • NIH Authors articles will be submitted to PMC after 12 months
    • Authors who are required to deposit in subject repositories may also use Sponsorship Option
    • Pre-print can not be deposited for The Lancet
  • Classification
    ​ green

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Rats selectively bred for deficient prepulse inhibition (PPI), an operant measure of sensorimotor gating in which a weak prepulse stimulus attenuates the response to a subsequent startling stimulus, may be used to study certain pathophysiological mechanisms and therapeutic strategies for neuropsychiatric disorders with abnormalities in information processing, such as schizophrenia and Tourette`s syndrome (TS). Little is known about neuronal activity in the medial prefrontal cortex (mPFC) and the nucleus accumbens (NAC), which are involved in the modulation of PPI. Here, we examined neuronal activity in these structures, and also in the entopeduncular nucleus (EPN), since lesions of this region alleviate the PPI deficit. Male rats with breeding-induced high and low expression of PPI (n=7, each) were anesthetized with urethane (1.2mg/kg). Single-unit activity and local field potentials were recorded in the mPFC, the NAC and in the EPN. In the mPFC discharge rate, measures of irregularity and burst activity were significantly reduced in PPI low compared to PPI high rats (p<0.05), while analysis in the NAC showed approximately inverse behavior. In the EPN no difference between groups was found. Additionally, the oscillatory theta band activity (4-8Hz) was enhanced and the beta band (13-30Hz) and gamma band (30-100Hz) activity was reduced in the NAC in PPI low rats. Reduced neuronal activity in the mPFC and enhanced activity in the NAC of PPI low rats, together with altered oscillatory behavior are clearly associated with reduced PPI. PPI low rats may thus be used to study the pathophysiology and therapeutic strategies for neuropsychiatric disorders accompanied by deficient sensorimotor gating.
    Progress in Neuro-Psychopharmacology and Biological Psychiatry 09/2014;
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    ABSTRACT: This study examined how Internet gaming disorder (IGD) subjects modulating reward and risk at a neural level under a probability-discounting task with functional magnetic resonance imaging (fMRI). Behavioral and imaging data were collected from 19 IGD subjects (22.2 ± 3.08 years) and 21 healthy controls (HC, 22.8 ± 3.5 years). Behavior results showed that IGD subjects prefer the probabilistic options to fixed ones and were associated with shorter reaction time, when comparing to HC. The fMRI results revealed that IGD subjects show decreased activation in inferior frontal gyrus and the precentral gyrus when choosing the probabilistic options than HC. Correlations were also calculated between behavioral performances and brain activities in relevant brain regions. Both of the behavioral performance and fMRI results indicate that people with IGD show impaired risk evaluation, which might be the reason why IGD subjects continue playing online games despite the risks of widely known negative consequence.
    Progress in Neuro-Psychopharmacology and Biological Psychiatry 09/2014;
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    ABSTRACT: Patients with schizophrenia using antipsychotics often develop metabolic side effects, especially with clozapine. Previous studies indicated that antipsychotics could activate the pathway of the sterol regulatory element-binding protein (SREBP). The SREBF2 gene (encoding SREBP2) mainly regulates the cholesterol biosynthetic gene. Therefore, we hypothesized that the SREBF2 gene would be a candidate gene for interindividual variation in drug-induced metabolic syndrome (MetS). In this genetic case-control study, we examined the SREBF2 gene polymorphisms in the risk of MetS patients treated with clozapine.
    Progress in Neuro-Psychopharmacology and Biological Psychiatry 09/2014;
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    ABSTRACT: Epidemiological studies suggest that perinatal complications, particularly hypoxia-related ones, increase the risk of schizophrenia. Recent genetic studies of the disorder have identified several putative susceptibility genes, some of which are known to be regulated by hypoxia. It can be postulated therefore that birth complications that cause hypoxia in the fetal brain may be associated with a dysregulation in the expression of some of the schizophrenia candidate genes. To test this, we used an animal model of perinatal asphyxia, in which rat pups were exposed to 15min of intrauterine anoxia during Caesarean section birth, and examined the expression of mRNA of five of the putative susceptibility genes (NRG1, ErbB4, AKT1, COMT and BDNF) by real-time quantitative PCR in the medial prefrontal cortex (mPFC) and the hippocampus at 6 and 12weeks after birth. The expression of NRG1 mRNA was significantly decreased in the mPFC, but not in the hippocampus, at 6 and 12weeks after birth. In addition, a significant increase in COMT mRNA expression was observed in the mPFC at 12weeks. The alteration in mRNA levels of NRG1 and COMT was not associated with a change in their protein levels. These results suggest that perinatal asphyxia may lead to disturbances in the PFC, which in turn may exert a long-lasting influence on the expression of specific genes, such as NRG1 and COMT. Our results also suggest that translational interruption may occur in this model of perinatal asphyxia.
    Progress in Neuro-Psychopharmacology and Biological Psychiatry 09/2014;
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    ABSTRACT: The benzodiazepine lorazepam is widely utilized in the treatment of elderly individuals with anxiety disorders and related conditions. Negative effects of acute lorazepam administration on cognitive performance, especially memory, have been reported in both previously untreated elderly and in individuals who have received short term (up to three weeks) treatment with therapeutic doses. However, it remains unclear if these adverse cognitive effects also persist after long-term use, which is frequently found in clinical practice.
    Progress in Neuro-Psychopharmacology and Biological Psychiatry 09/2014;
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    ABSTRACT: Epigenetic regulation may be involved in the pathophysiology of mental disorders, such as schizophrenia and bipolar disorder, and in the pharmacological action of drugs. Characterizing the epigenetic effects of drugs is an important step to optimal treatment. We performed comprehensive and gene-specific DNA methylation analyses of quetiapine using human neuroblastoma cells. Human neuroblastoma cells were cultured with quetiapine for 8days, and DNA methylation analysis was performed using Infinium HumanMethylation27 BeadChip. A total of 1,173 genes showed altered DNA methylation. Altered DNA methylation predominantly occurred as hypomethylation within the CpG island compared to DNA isolated from non-treated cells. Gene ontology analysis revealed that these genes were related to the cellular process of intracellular protein binding. There was no common effect of quetiapine with three mood stabilizers (lithium, valproate, and carbamazepine). However, common DNA methylation changes in eight genes, including ADRA1A, which encodes alpha 1A-adrenoceptor, were found with quetiapine and lithium treatment. Finally, bisulfite-sequencing analysis revealed that quetiapine decreased the DNA methylation level of the promoter region of SLC6A4, where hypermethylation with bipolar disorder and hypomethylation with mood stabilizers have been reported.
    Progress in Neuro-Psychopharmacology and Biological Psychiatry 09/2014;
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    ABSTRACT: Bipolar disorder (BD) is a chronic psychiatric illness of which the pathophysiology remains partially unknown. Abnormalities of neurotrophins and other trophic factors orchestrate important alterations which could be implicated in the etiology of BD. Therefore, the main objective of this review is to examine the recent findings and critically evaluate the potential role of neurotrophins that may allow us to substantially improve the development of novel treatments. The most recently published findings highlight that brain-derived neurotrophic factor (BDNF), insulin-like growth factor (IGF-1) and vascular endothelial growth factor (VEGF) present distinct patterns in the different stages of BD, suggesting their potential in the identification of the BD subgroups and may ultimately advance treatment strategies.
    Progress in Neuro-Psychopharmacology and Biological Psychiatry 09/2014;
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    ABSTRACT: Serum levels of brain-derived neurotrophic factor (BDNF) have been shown to be lower in patients with major depressive disorder (MDD) than in healthy persons. Although several studies have examined the associations between serum BDNF levels and broader categories of depression identified by psychiatrists or depressive symptoms measured with depression scales among nonpatient populations, some of these studies did not consider possible confounders and included mostly young or middle-aged subjects and nonrepresentative control subjects, such as volunteers and patients' relatives. Therefore, whether MDD, broader categories of depression, or depressive symptoms in the elderly are associated with BDNF remains unclear. The present study examined these associations in a community sample and controlled for confounders.
    Progress in Neuro-Psychopharmacology and Biological Psychiatry 08/2014;
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    ABSTRACT: Atomoxetine, a noradrenaline reuptake inhibitor (NRI), which is a non-stimulating medicine that is used for the treatment of patients with attention deficit hyperactivity disorder (ADHD), has been found to be effective in reducing behavioral impulsivity in rodents, but its efficacy in a dorsal noradrenergic ascending bundle (DNAB)-lesioned condition has not been examined. The present study aimed to investigate the effects of DNAB lesions on attention and impulsive control in the five-choice serial reaction time task (5-CSRTT) in rats treated with atomoxetine. The drug-induced changes in noradrenaline efflux in the medial prefrontal cortex were also measured. 5-CSRTT-trained rats were included in one of the following groups: N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP-4)/Atomoxetine, Sham/Atomoxetine, DSP-4/Saline, or Sham/Saline. Acute atomoxetine (0.3mg/kg) was administered 14days after the DSP-4 regime. The behavioral testing included manipulations of the inter-trial interval (ITI), stimulation duration and food satiety. In vivo microdialysis of the noradrenaline efflux in the medial prefrontal cortex and the expression of the noradrenaline transporter (NAT) in the DNAB areas were examined. Atomoxetine reduced impulsivity and perseveration in the long-ITI condition with no effects on any other variables. This phenomenon was not influenced by DSP-4 pre-treatment. The DNAB-lesioned rats had lower noradrenaline efflux in the medial prefrontal cortex. DSP-4 caused no change in NAT expression in the DNAB areas. These findings suggested that noradrenaline reuptake may not be exclusively responsible for the atomoxetine effects in adjusting impulsivity. The role of DNAB should also be considered, particularly in conditions requiring greater behavioral inhibition.
    Progress in Neuro-Psychopharmacology and Biological Psychiatry 08/2014;
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    ABSTRACT: Bipolar disorder (BPD) is a serious and common mental disorder with high heritability. The serotonergic system is known to be implicated in the etiology of the disorder. Tryptophan hydroxylase isoform-2 (TPH2), which controls the synthesis of serotonin in the brain, has been suggested as a candidate gene for BDP. The aim of this study was to examine the association between the polymorphisms in TPH2 and BPD.
    Progress in Neuro-Psychopharmacology and Biological Psychiatry 08/2014;
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    ABSTRACT: Understanding the neurobiological bases for sex differences in alcohol dependence is needed to help guide the development of individualized therapies for alcohol abuse disorders. In the present study, alcohol-induced adaptations in (1) anxiety-like behavior, (2) patterns of c-Fos activation and (3) subcellular distribution of corticotropin releasing factor receptor in locus coeruleus (LC) neurons was investigated in male and female Sprague-Dawley rats that were chronically exposed to ethanol using a liquid diet. Results confirm and extend reports by others showing that chronic ethanol exposure produces an anxiogenic-like response in both male and female subjects. Ethanol-induced sex differences were observed with increased c-Fos expression in LC neurons of female ethanol-treated subjects compared to controls or male subjects. Results also reveal sex differences in the subcellular distribution of the CRFr in LC-noradrenergic neurons with female subjects exposed to ethanol exhibiting a higher frequency of plasmalemmal CRFrs. These adaptations have implications for LC neuronal activity and its neural targets across the sexes. Considering the important role of the LC in ethanol-induced activation of the hypothalamo-pituitary-adrenal (HPA) axis, the present results indicate important sex differences in feed-forward regulation of the HPA axis that may render alcohol dependent females more vulnerable to subsequent stress exposure.
    Progress in Neuro-Psychopharmacology and Biological Psychiatry 08/2014;
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    ABSTRACT: The association between cardiovascular reactivity and major depressive disorder (MDD) remains unclear. This study aimed to examine this association via reactive heart rate variability (HRV) in a well-diagnosed first-episode MDD group and a control group.
    Progress in Neuro-Psychopharmacology and Biological Psychiatry 08/2014;
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    ABSTRACT: Olanzapine is widely prescribed for treating schizophrenia and other mental disorders although it leads to severe body weight gain/obesity. Chronic co-treatment with betahistine has been found to significantly decrease olanzapine-induced weight gain; however it is not clear whether this co-treatment affects the therapeutic effects of olanzapine. This study investigated the effects of chronic treatment of olanzapine and/or betahistine on the binding density of the serotonergic 5-HT2A (5-HT2AR) and 5-HT2C (5-HT2CR) receptors, 5-HT transporter (5-HTT), and dopaminergic D2 receptors (D2R) in the brain regions involved in antipsychotic efficacy, including the prefrontal cortex (PFC), cingulate cortex (Cg), nucleus accumbens (NAc), and caudate putamen (CPu). Rats were treated with olanzapine (1mg/kg, t.i.d.) or vehicle for 3.5weeks, and then olanzapine treatment was withdrawn for 19days. From week 6, the two groups were divided into 4 groups (n=6) for 5weeks' treatment: (1) olanzapine-only (1mg/kg, t.i.d.), (2) betahistine-only (9.6mg/kg, t.i.d.), (3) olanzapine and betahistine co-treatment (O+B), and (4) vehicle. Compared to the control, the olanzapine-only treatment significantly decreased the bindings of 5-HT2AR, 5-HT2CR, and 5-HTT in the PFC, Cg and NAc. Similar changes were observed in the rats receiving the O+B co-treatment. The olanzapine-only treatment significantly increased the D2R binding in the Cg, NAc, and CPu, while the betahistine-only treatment reduced D2R binding. The co-treatment of betahistine reversed the D2R bindings in the NAc and CPu that were increased by olanzapine. Therefore, the chronic O+B co-treatment has similar effects on serotonin transmission as the olanzapine-only treatment, but reverses the D2R that is up-regulated by chronic olanzapine treatment. The co-treatment maintains the therapeutic effects of olanzapine but decreases / prevents the excess weight gain.
    Progress in Neuro-Psychopharmacology and Biological Psychiatry 08/2014;
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    ABSTRACT: Although sub-regional analysis methods of the corpus callosum (CC) have been developed, there has been no in vivo magnetic resonance imaging (MRI) study on a sub-regional volume analysis of the CC of late-onset depression (LOD). The aim of this study was to investigate the CC volume differences between LOD subjects and healthy elderly controls using a sub-regional analysis technique. Forty subjects with LOD and thirty nine group-matched healthy control subjects underwent 3T MRI scanning, and sub-regional volumes of the CC were measured and compared between the groups. The volumes of total (F=5.8, p=0.001), the anterior (F=5.2, p=0.001) and the posterior CC (F=5.1, p=0.001) were significantly reduced in the LOD group as compared to the control group. We measured cognitive functions in several different domains (language functions, verbal learning, visuospatial functions, delayed recall, memory consolidation, recognition memory, and executive functions) through the Korean version of the Consortium to Establish a Registry for Alzheimer's Disease. The anterior CC volume in the LOD group showed significant positive correlation with the verbal fluency scores. The posterior CC volume in the LOD group was positively correlated significantly with the word list memory, the word list recall and the constructional praxis scores. This study is the first to elaborate the sub-regional volume differences of the CC between controls and LOD patients. These structural changes in the CC might be at the core of the underlying neurobiological mechanisms in LOD.
    Progress in Neuro-Psychopharmacology and Biological Psychiatry 08/2014;
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    ABSTRACT: Time perception, which plays a fundamental role in decision making and the evaluation of the environment, is also influenced by emotions. Patients with bipolar disorder have impairments in emotional processing as well as interval timing. We investigated the effects of emotional stimuli on time estimation and reproduction in manic and euthymic bipolar patients compared with healthy controls.
    Progress in Neuro-Psychopharmacology and Biological Psychiatry 08/2014;
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    ABSTRACT: Neuroimaging studies suggest that treatment-naive depression (TD) is characterized by abnormal functional connectivity between specific brain regions. However, the question surrounding the structural basis of functional aberrations in TD patients still remains.
    Progress in Neuro-Psychopharmacology and Biological Psychiatry 08/2014;
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    ABSTRACT: Increasing evidence has implicated the role of Disrupted-in-Schizophrenia-1 (DISC1), a potential susceptibility gene for schizophrenia, in early neurodevelopmental processes. However, the effect of its genotype variation on brain morphologic changes related to neurodevelopmental abnormalities in schizophrenia remains largely unknown. This magnetic resonance imaging study examined the association between DISC1 Ser704Cys polymorphism and a range of brain neurodevelopmental markers [cavum septi pellucidi (CSP), adhesio interthalamica (AI), olfactory sulcus depth, and sulcogyral pattern (Type I, II, III, and IV) in the orbitofrontal cortex (OFC)] in an all Japanese sample of 75 schizophrenia patients and 87 healthy controls. The Cys carriers had significantly larger CSP than the Ser homozygotes for both schizophrenia patients and healthy controls. The Cys carriers also exhibited a reduction in the Type I pattern of the right OFC in the healthy controls, but not in the schizophrenia patients. The DISC1 Ser704Cys polymorphism did not affect the AI and olfactory sulcus depth in either group. These results suggested a possible role of the DISC1 genotype in the early neurodevelopment of human brains, but failed to show its specific role in the neurodevelopmental pathology of schizophrenia.
    Progress in Neuro-Psychopharmacology and Biological Psychiatry 08/2014;
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    ABSTRACT: In Parkinson's disease (PD) and L-3,4-Dihydroxyphenylalanine (L-DOPA)-induced dyskinesias (LID), overactivity of brain glutamate neurotransmission is documented and antiglutamatergic drugs decrease LID. Serotonin (5-HT) receptors and transporter (SERT) are also implicated in LID and we hypothesize that antiglutamatergic drugs can also regulate brain serotoninergic activity. Our aim was to investigate the long-term effect of the prototypal metabotropic glutamate 5 (mGlu5) receptor antagonist 2-methyl-6-(phenylethynyl)pyridine (MPEP) with L-DOPA on basal ganglia SERT, 5-HT1A and 5-HT2A receptor levels in monkeys lesioned with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). MPTP monkeys were treated for one month with L-DOPA and developed LID while those treated with L-DOPA and MPEP (10mg/kg) developed significantly less LID. Normal controls and saline-treated MPTP monkeys were included for biochemical analysis. The MPTP lesion and experimental treatments left unchanged striatal 5-HT concentrations. MPTP lesion induced an increase of striatal 5-HIAA concentrations similar in all MPTP monkeys as compared to controls. [(3)H]-8-OH-DPAT and [(3)H]-citalopram specific binding levels to 5-HT1A receptors and SERT respectively remained unchanged in the striatum and globus pallidus of all MPTP monkeys compared to controls and no difference was observed between groups of MPTP monkeys. [(3)H]-ketanserin specific binding to striatal and pallidal 5-HT2A receptors were increased in L-DOPA-treated MPTP monkeys as compared to controls, saline and L-DOPA+MPEP MPTP monkeys and no difference between the latter groups was observed; dyskinesias scores correlated positively with this binding. In conclusion, reduction of development of LID with MPEP was associated with lower striatal and pallidal 5-HT2A receptors showing that glutamate activity also affects serotoninergic markers.
    Progress in Neuro-Psychopharmacology and Biological Psychiatry 07/2014;

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