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

Publisher: Elsevier

Journal 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.

Current impact factor: 3.69

Impact Factor Rankings

2016 Impact Factor Available summer 2017
2014 / 2015 Impact Factor 3.689
2013 Impact Factor 4.025
2012 Impact Factor 3.552
2011 Impact Factor 3.247
2010 Impact Factor 2.877
2009 Impact Factor 2.823
2008 Impact Factor 2.638
2007 Impact Factor 2.802
2006 Impact Factor 2.584
2005 Impact Factor 2.769
2004 Impact Factor 2.149
2003 Impact Factor 1.827
2002 Impact Factor 1.433
2001 Impact Factor 1.058
2000 Impact Factor 1.078
1999 Impact Factor 1.389
1998 Impact Factor 1.114
1997 Impact Factor 0.819

Impact factor over time

Impact factor
Year

Additional details

5-year impact 3.80
Cited half-life 5.90
Immediacy index 1.34
Eigenfactor 0.02
Article influence 1.00
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
    • Authors pre-print on any website, including arXiv and RePEC
    • Author's post-print on author's personal website immediately
    • Author's post-print on open access repository after an embargo period of between 12 months and 48 months
    • Permitted deposit due to Funding Body, Institutional and Governmental policy or mandate, may be required to comply with embargo periods of 12 months to 48 months
    • Author's post-print may be used to update arXiv and RepEC
    • Publisher's version/PDF cannot be used
    • Must link to publisher version with DOI
    • Author's post-print must be released with a Creative Commons Attribution Non-Commercial No Derivatives License
    • Publisher last reviewed on 03/06/2015
  • Classification
    green

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: A combination of cannabis and ecstasy may change the cognitive functions more than either drug alone. The present study was designed to investigate the possible involvement of dorsal hippocampal NMDA receptors in the interactive effects of arachidonylcyclopropylamide (ACPA) and ecstasy/MDMA on memory retrieval. Adult male Wistar rats were cannulated into the CA1 regions of the dorsal hippocampus (intra-CA1) and memory retrieval were examined using the step-through type of passive avoidance task. Intra-CA1 microinjection of a selective CB1 receptor agonist, ACPA (0.5-4ng/rat) immediately before the testing phase (pre-test), but not after the training phase (post-training), impaired memory retrieval. In addition, pre-test intra-CA1 microinjection of MDMA (0.5-1μg/rat) dose-dependently decreased step-trough latency, indicating an amnesic effect of the drug by itself. Interestingly, pre-test microinjection of a higher dose of MDMA into the CA1 regions significantly improved ACPA-induced memory impairment. Moreover, pre-test intra-CA1 microinjection of a selective NMDA receptor antagonist, D-AP5 (1 and 2μg/rat) inhibited the reversal effect of MDMA on the impairment of memory retrieval induced by ACPA. Pre-test intra-CA1 microinjection of the same doses of D-AP5 had no effect on memory retrieval alone. These findings suggest that ACPA or MDMA consumption can induce memory retrieval impairment, while their co-administration improves this amnesic effect through interacting with hippocampal glutamatergic-NMDA receptor mechanism. Thus, it seems that the tendency to abuse cannabis with ecstasy may be for avoiding cognitive dysfunction.
    No preview · Article · Apr 2016 · Progress in Neuro-Psychopharmacology and Biological Psychiatry
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    ABSTRACT: αO-conotoxin GeXIVA (GeXIVA) is a potent antagonist of α9α10 nicotinic acetylcholine receptors (nAChRs), which has four Cys residues and three disulfide isomers. Among the 3 isomers, both GeXIVA[1,2] (bead isomer) and GeXIVA[1,4] (ribbon isomer) showed potent block on α9α10 nAChRs with close low nanomolar IC50s. Here we report that anti-hypersensitive effects of the bead and ribbon isomers in the chronic constriction injury (CCI) model of neuropathic pain and acute pain model of tail flick test. Treatment was started and continued for 7 or 14days after the development of hyperalgesia which was induced by CCI surgery. GeXIVA[1,2] and GeXIVA[1,4] significantly reduced mechanical allodynia in CCI rats without tolerance, in which GeXIVA[1,2] remained upto two weeks after intramuscular administration of the toxins were ceased. The pain reliever effect of GeXIVA[1,2] on neuropathic rats was slightly better than GeXIVA[1,4]. The two isomers did not suppress the acute thermal pain behaviors significantly when they were tested in the tail flick model by intramuscular bolus injection. Both GeXIVA[1,2] and GeXIVA[1,4] had no significant effect on performance of rats in the accelerating rotarod test after intramuscular injections. This suggests that αO-conotoxin GeXIVA[1,2] and GeXIVA[1,4] may offer new strategies to the treatment of neuropathic pain.
    No preview · Article · Apr 2016 · Progress in Neuro-Psychopharmacology and Biological Psychiatry
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    ABSTRACT: Attention-deficit/hyperactivity disorder (ADHD) is a common childhood psychiatric disorder that often persists into adulthood. While several studies have identified altered functional connectivity in brain networks during rest in children with ADHD, few studies have been performed on adults with ADHD. Existing studies have generally investigated small samples. We therefore investigated aberrant functional connectivity in a large sample of adult patients with childhood-onset ADHD, using a data-driven, whole-brain approach. Adults with a clinical ADHD diagnosis (N = 99) and healthy, adult comparison subjects (N = 113) underwent a 9-minute resting-state fMRI session in a 1.5 T MRI scanner. After elaborate preprocessing including a thorough head-motion correction procedure, group independent component analysis (ICA) was applied from which we identified six networks of interest: cerebellum, executive control, left and right frontoparietal and two default-mode networks. Participant-level network maps were obtained using dual-regression and tested for differences between patients with ADHD and controls using permutation testing. Patients showed significantly stronger connectivity in the anterior cingulate gyrus of the executive control network. Trends were also observed for stronger connectivity in the cerebellum network in ADHD patients compared to controls. However, there was considerable overlap in connectivity values between patients and controls, leading to relatively low effect sizes despite the large sample size. These effect sizes were slightly larger when testing for correlations between hyperactivity/impulsivity symptoms and connectivity strength in the executive control and cerebellum networks. This study provides important insights for studies on the neurobiology of adult ADHD; it shows that resting-state functional connectivity differences between adult patients and controls exist, but have smaller effect sizes than existing literature suggested.
    No preview · Article · Jan 2016 · Progress in Neuro-Psychopharmacology and Biological Psychiatry
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    ABSTRACT: Kindling is a form of behavioral sensitization that is related to the progression of several neuropsychiatric disorders such as bipolar disorder. We recently demonstrated that female periadolescent rats are more vulnerable to nicotine (NIC)-induced kindling than their male counterparts. Furthermore, we evidenced that decreases in brain antioxidative defenses may contribute to this gender difference. Here we aimed to determine the preventive effects of the antioxidant N-acetyl cysteine (NAC) against NIC-kindling in female periadolescent rats. To do this female Wistar rats at postnatal day 30 received repeated injections of NIC 2 mg/kg, i.p. every weekday for up to 19 days. NAC90, 180 or 270 mg/kg, i.p. was administered 30 min before NIC. The levels of glutathione (GSH), superoxide dismutase (SOD) activity, lipid peroxidation (LP) and nitrite were determined in the prefrontal cortex (PFC), hippocampus (HC) and striatum (ST). The development of kindling occurred at a median time of 16.5 days with 87.5% of NIC animals presenting stage 5 seizures in the last day of drug administration. NAC270 prevented the occurrence of kindling. NIC-kindled animals presented decreased levels of GSH and increased LP in the PFC, HC and ST, while SOD activity was decreased in the ST. NAC180 or 270 prevented the alterations in GSH induced by NIC, but only NAC270 prevented the alterations in LP. Nitrite levels increased in the ST of NAC270 pretreated NIC-kindled animals. Taken together we demonstrated that NAC presents anti-kindling effects in female animals partially through the restoration of oxidative alterations.
    No preview · Article · Jan 2016 · Progress in Neuro-Psychopharmacology and Biological Psychiatry
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    ABSTRACT: JWH-250 and JWH-073 are two synthetic cannabinoid agonists with nanomolar affinity at CB1 and CB2 receptors. They are illegally marketed within “herbal blend” for theirs psychoactive effects greater than those produced by Cannabis. Recently, we analyzed an “herbal” preparation containing a mixture of both JWH-250 and JWH-073. The present study was aimed at investigating the in vitro and in vivo pharmacological activity of JWH-250 and JWH-073 in male CD-1 mice. In vitro competition binding experiments performed on mouse and human CB1 and CB2 receptors revealed a nanomolar affinity and potency of the JWH-250 and JWH-073. In vivo studies showed that JWH-250 and JWH-073, administered separately, induced a marked hypothermia, increased pain threshold to both noxious mechanical and thermal stimuli, caused catalepsy, reduced motor activity, impaired sensorimotor responses (visual, acoustic and tactile), caused seizures, myoclonia, hyperreflexia and promote aggressiveness in mice. Moreover, microdialysis study in freely moving mice showed that systemic administration of JWH-250 and JWH-073 stimulated dopamine release in the nucleus accumbens in a dose-dependent manner. Behavioral, neurological and neurochemical effects were fully prevented by the selective CB1 receptor antagonist/inverse agonist AM 251. Co-administration of ineffective doses of JWH-250 and JWH-073 impaired visual sensorimotor responses, improved mechanical pain threshold and stimulated mesolimbic DA transmission in mice, living unchanged all other behavioral and physiological parameters. For the first time the present study demonstrates the overall pharmacological effects induced by the administration of JWH-250 and JWH-073 in mice and it reveals their potentially synergistic action suggesting that co-administration of different synthetic cannabinoids may potentiate the detrimental effects of individual compounds increasing their dangerousness and abuse potential.
    No preview · Article · Jan 2016 · Progress in Neuro-Psychopharmacology and Biological Psychiatry
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    ABSTRACT: Major depression (MDD) is a chronic psychiatric condition in which patients often show increasing cognitive impairment with recurring episodes. Neurodegeneration may play an important component in the pathogenesis of MDD associated with cognitive complaints. In agreement with this, patients with MDD show decreased brain volumes in areas implicated in emotional regulation and cognition, neuronal and glial cell death as well as activation of various pathways that can contribute to cell death. Therefore, the aim of this review is to provide an integrative overview of potential contributing factors to neurodegeneration in MDD. Studies have reported increased neuronal and glial cell death in the frontal cortex, amygdala, and hippocampus of patients with MDD. This may be due to decreased neurogenesis from lower levels of brain-derived neurotrophic factor (BDNF), excitotoxicity from increased glutamate signaling, and lower levels of gamma-aminobutyric acid (GABA) signaling. In addition, mitochondrial dysfunction and oxidative stress are found in similar brain areas where evidence of excitotoxicity has been reported. Also, levels of antioxidant enzymes were reported to be increased in patients with MDD. Inflammation may also be a contributing factor, as levels of inflammatory cytokines were reported to be increased in the prefrontal cortex of patients with MDD. While preliminary, studies have also reported neuropathological alterations in patients with MDD. Together, these studies suggest that lower BDNF levels, mitochondrial dysfunction, oxidative stress, inflammation and excitotoxicity may be contributing to neuronal and glial cell death in MDD, leading to decreased brain volume and cognitive dysfunction with multiple recurrent episodes. This highlights the need to identify specific pathways involved in neurodegeneration in MDD, which may elucidate targets that can be treated to ameliorate the effects of disease progression in this disorder.
    No preview · Article · Jan 2016 · Progress in Neuro-Psychopharmacology and Biological Psychiatry
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    ABSTRACT: Attention deficit hyperactivity disorder (ADHD) is a common neurodevelopmental condition charactetised by impulsivity, inattention and hyperactivity. Aside from these core psychopathologies, sleep disturbances are found to be highly comorbid with ADHD, and indeed dysregulated sleep may contribute to some of the symptoms of the disorder. It is not clear how sleep disturbances come to be so common in ADHD, but one putative mechanism is through the circadian timekeeping system. This system underpins the genertaion of near twenty four hour rhythms in a host of physiological, behavioural and psychological parameters, and is a key determinant of the sleep/wake cycle. In this paper we review the evidence for sleep and circadian rhythm disturbance in ADHD, examine the possible mechanistic links between these factors and the disorder and discuss future directions through which the circadian clock can be targetted for ADHD symptom relief.
    No preview · Article · Jan 2016 · Progress in Neuro-Psychopharmacology and Biological Psychiatry
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    ABSTRACT: Adverse environmental factors including prenatal maternal infection are capable of inducing long-lasting behavioral and neural alterations which can enhance the risk to develop schizophrenia. It is so far not clear whether supportive postnatal environments are able to modify such prenatally-induced alterations. In rodent models, environmental enrichment influences behavior and cognition, for instance by affecting endocrinologic, immunologic, and neuroplastic parameters. The current study was designed to elucidate the influence of postnatal environmental enrichment on schizophrenia-like behavioral alterations induced by prenatal polyI:C immune stimulation at gestational day 9 in mice. Adult offspring were tested for amphetamine-induced locomotion, social interaction, and problem-solving behavior as well as expression of dopamine D1 and D2 receptors and associated molecules, microglia density and adult neurogenesis. Prenatal polyI:C treatment resulted in increased dopamine sensitivity and dopamine D2 receptor expression in adult offspring which was not reversed by environmental enrichment. Prenatal immune activation prevented the effects of environmental enrichment which increased exploratory behavior and microglia density in NaCl treated mice. Problem-solving behavior as well as the number of immature neurons was affected by neither prenatal immune stimulation nor postnatal environmental enrichment. The behavioral and neural alterations that persist into adulthood could not generally be modified by environmental enrichment. This might be due to early neurodevelopmental disturbances which could not be rescued or compensated for at a later developmental stage.
    No preview · Article · Jan 2016 · Progress in Neuro-Psychopharmacology and Biological Psychiatry
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    ABSTRACT: Objective: Abnormal brain networks have been observed in patients with obsessive-compulsive disorder (OCD). However, detailed network hub and connectivity changes remained unclear in treatment-naive patients with OCD. Here, we sought to determine whether patients show hub-related connectivity changes in their whole-brain functional networks. Methods: We used resting-state functional magnetic resonance imaging data and voxel-based graph-theoretic analysis to investigate functional connectivity strength and hubs of whole-brain networks in 29 treatment-naive patients with OCD and 29 age- and gender-matched healthy controls. Correlation analysis was applied for potential associations with OCD symptom severity. Results: OCD selectively targeted brain regions of higher functional connectivity strength than the average including brain network hubs, mainly distributed in the cortico-striato-thalamo-cortical (CSTC) circuits and additionally parietal, occipital, temporal and cerebellar regions. Moreover, affected functional connectivity strength in the cerebellum, the medial orbitofrontal cortex and superior occipital cortex was significantly associated with global OCD symptom severity. Conclusion: Our results provide the evidence about OCD-related brain network hub changes, not only in the CSTC circuits but more distributed in whole brain networks. Data suggest that whole brain network hub analysis is useful for understanding the pathophysiology of OCD.
    No preview · Article · Dec 2015 · Progress in Neuro-Psychopharmacology and Biological Psychiatry

  • No preview · Article · Dec 2015 · Progress in Neuro-Psychopharmacology and Biological Psychiatry
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    ABSTRACT: Obsessive compulsive disorder (OCD) is a chronic and debilitating disorder. As can be seen in other psychiatric disorders, refractoriness to treatment is an important problem for patients with OCD. OCD is a chronic disorder like collagen tissue disorders, with symptoms tending to wax and wane but rarely remitting spontaneously through the course of the disorder. An important part of OCD patients respond to serotonin reuptake inhibitors alone or in combination with other medications, and cognitive behavior therapy. However, up to 30%–40% of patients do not respond to the available treatment modalities. The present paper tried to review the current state of knowledge on definition, clinical aspects, etiopathogenesis, and treatment strategies of patients with refractory OCD.
    No preview · Article · Dec 2015 · Progress in Neuro-Psychopharmacology and Biological Psychiatry