European Neuropsychopharmacology (EUR NEUROPSYCHOPHARM)
European Neuropsychopharmacology provides a medium for the prompt publication of articles in the field of neuropsychopharmacology. Its scope encompasses clinical and basic research relevant to the effects of centrally acting agents in its broadest sense. Types of Papers:Full length Research Papers: detailing findings of original experimental or clinical research in any area of neuropsychopharmacology; Short Communications: brief research reports or results that have reached a stage where they are ready for preliminary communication; Reviews on specialised topics. Letters to the Editor relating to material published in the journal are also welcomed.
- Impact factor4.05Show impact factor historyHide impact factor history
- WebsiteEuropean Neuropsychopharmacology website
Other titlesEuropean neuropsychopharmacology (Online)
Material typeDocument, Periodical, Internet resource
Document typeInternet Resource, Computer File, Journal / Magazine / Newspaper
- Author can archive a pre-print version
- Author can archive a post-print version
- 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
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- 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
Publications in this journal
Article: Chronic effects of corticosterone on GIRK1-3 subunits and 5-HT(1A) receptor expression in rat brain and their reversal by concurrent fluoxetine treatment[show abstract] [hide abstract]
ABSTRACT: Dysregulation of the serotonergic system and abnormalities of the hypothalamic-pituitary-adrenal axis have been demonstrated in major depression. Animal studies indicate that 5-HT receptor expression may be reduced by long-term administration of corticosterone. However, similar studies on the regulation of GIRK channels, one of the most important effectors of the neuronal 5-HT receptor, are limited. In order to address these issues, slow-release corticosterone pellets were implanted subcutaneously to adrenal intact male rats (200mg pellets, 35 days release). Starting on day 15, animals were treated for 21 days with fluoxetine (5mg/kg/day, i.p.), or vehicle. Using in situ hybridization histochemistry and receptor autoradiography, we found that chronic corticosterone treatment was accompanied by a significant decrease on the mRNAs coding for mineralocorticoid receptors in hippocampal areas. Under these conditions, 5-HT receptor mRNA expression decreased in dorsal raphe nucleus and dentate gyrus. However, 5-HT receptor levels, as measured by [H]-8-OH-DPAT binding, diminished significantly only in dentate gyrus. It is noteworthy that chronic treatment with fluoxetine reversed the alterations on 5-HT receptor mRNA levels only in dorsal raphe. Finally, chronic corticosterone treatment produced an increase on the mRNA coding for the GIRK2 subunit in several hypothalamic and thalamic areas, which was reversed by fluoxetine. Measurements of cell density and volume of the granular layer of the dentate gyrus did not reveal significant changes after corticosterone or corticosterone plus fluoxetine treatments. These data are relevant for a better understanding of the differential regulation of pre- and postsynaptic 5-HT receptors by corticosterone flattened rhythm.European Neuropsychopharmacology 01/2013; 23(3):229-239.
European Neuropsychopharmacology 06/2012; 8(3-12).
Article: Evaluation of a pharmacist intervention on patients initiating pharmacological treatment for depression: a randomized controlled superiority trial.European Neuropsychopharmacology 01/2012;
European Neuropsychopharmacology 01/2012; 22(2):139-140.
Article: Psychiatric co-morbidity and suicidality among methamphetamine dependent patients who seek treatment in MalaysiaEuropean Neuropsychopharmacology 01/2011; 21.
Article: Influence of catecholamine depletion on the striatal activation associated with appetitive conditioning.European Neuropsychopharmacology 01/2011; 21(3):S318.
Article: The use of psychopharmacological agents in a sample of patients with obsessive-compulsive disorder and their relationship to symptomsEuropean Neuropsychopharmacology 01/2011;
[show abstract] [hide abstract]
ABSTRACT: In humans, most physiological and behavioural functions demonstrate a circadian rhythmicity, which is essential to adequately cope with dramatic fluctuations occurring in the external environment. Therefore, it is intuitive that alterations in the endogenous machinery regulating circadian oscillations may lead to physical and mental symptoms and morbidities. Mood disorders, especially unipolar depression and seasonal affective disorder, have been linked to circadian rhythm abnormalities. This paper provides a brief description of the molecular and genetic mechanisms regulating the endogenous clock system and reviews selected studies describing circadian abnormalities in patients with depression. Evidence is emerging that a disruption of the normal circadian rhythmicity occurs at least in a subgroup of depressed patients and that interventions able to resynchronize the human circadian system, including sleep deprivation, light therapy and drugs specifically acting on the endogenous clock system, have proven antidepressant effects. It seems likely that, in the future, the knowledge coming from the exploration of molecular and genetic mechanisms involved in the physiology of the circadian clock system will be fruitful for a deeper understanding of the etiopathogenesis of mood disorders and the development of more effective therapeutic strategies.European Neuropsychopharmacology 11/2008; 18(10):701-11.
Article: Glutamatergic dysfunction in schizophrenia: from basic neuroscience to clinical psychopharmacology.[show abstract] [hide abstract]
ABSTRACT: The underlying cellular mechanisms leading to frontal cortical hypofunction (i.e., hypofrontality) in schizophrenia remain unclear. Both hypoactive and hyperreactive prefrontal cortical (PFC) states have been reported in schizophrenia patients. Recent proton magnetic resonance spectroscopy studies revealed that antipsychotic-naïve patients with first psychotic episode exhibit a hyperactive PFC. Conversely, PFC activity seems to be diminished in patients chronically exposed to conventional antipsychotic treatments, an effect that could reflect the therapeutic action as well as some of the impairing side effects induced by long-term blockade of dopamine transmission. In this review, we will provide an evolving picture of the pathophysiology of schizophrenia moving from dopamine to a more glutamatergic-centered hypothesis. We will discuss how alternative antipsychotic strategies may emerge by using drugs that reduce excessive glutamatergic response without altering the balance of synaptic and extrasynaptic normal glutamatergic neurotransmission. Preclinical studies indicate that acamprosate, a FDA approved drug for relapse prevention in detoxified alcoholic patients, reduces the glutamatergic hyperactivity triggered by ethanol withdrawal without depressing normal glutamatergic transmission. Whether this effect is mediated by a direct modulation of NMDA receptors or by antagonism of metabotropic glutamate receptor remains to be determined. We hypothesize that drugs with similar pharmacological actions to acamprosate may provide a better and safer approach to reverse psychotic symptoms and cognitive deficits without altering the balance of excitation and inhibition of the corticolimbic dopamine-PFC system. It is predicted that schizophrenia patients treated with acamprosate-like compounds will not exhibit progressive cortical atrophy associated with the anti-dopaminergic effect of classical antipsychotic exposure.European Neuropsychopharmacology 11/2008; 18(11):773-86.
Article: Experimentally induced various inflammatory models and seizure: understanding the role of cytokine in rat.[show abstract] [hide abstract]
ABSTRACT: The mechanism of epileptogenesis is not well established. There is higher incidence of seizures among patients with chronic inflammatory disease. Cytokines are rapidly induced in the brain after a variety of stimuli including inflammation. Aim of this study was to produce various inflammatory models and seizure to understand the role of TNFalpha in above mentioned models. A total of 54 male rats were included in the study. Animals were divided into 3 groups of colitis, arthritis, and cotton wool granuloma. Each group had 3 subgroups of control, model and treatment. At the end of 3 days in colitis, 17 days in arthritis and 7 days in cotton wool granuloma groups a subconvulsive dose of PTZ (40 mg/kg i.p) was injected to note seizure onset and seizure score. Brain samples were subjected to DNA fragmentation testing. Presence of inflammation was confirmed by morphology and histology. Plasma and brain TNFalpha levels were measured. The models of colitis, arthritis and CWG were effectively produced as evidenced by morphology and histology scores (p<0.001). Seizure onset was reduced and grade was increased (p<0.001). Thalidomide reduced the morphological, histological (p<0.002), DNA fragmentation and seizure grade (p<0.001) while increased seizure onset (p<0.001) in the arthritis group. TNFalpha levels in both plasma and brain were reduced following thalidomide treatment (p<0.002) in arthritis group. There were no significant findings in colitis or cotton wool granuloma groups. Inflammation was associated with decreased threshold to PTZ induced seizure. Thalidomide is effective in reducing the extent of arthritis as well as reducing the seizure scoring and increasing seizure onset in the adjuvant arthritis group. Thalidomide was also effective in reducing TNFalpha levels thus contributing to its antiepileptic activity.European Neuropsychopharmacology 11/2008; 18(10):760-7.
Article: Dopamine and serotonin levels following prenatal viral infection in mouse--implications for psychiatric disorders such as schizophrenia and autism.[show abstract] [hide abstract]
ABSTRACT: Prenatal viral infection has been associated with neurodevelopmental disorders such as schizophrenia and autism. It has previously been demonstrated that viral infection causes deleterious effects on brain structure and function in mouse offspring following late first trimester (E9) and middle-late second trimester (E18) administration of influenza virus. Neurochemical analysis following infection on E18 using this model has revealed significantly altered levels of serotonin, 5-hydroxyindoleacetic acid, and taurine, but not dopamine. In order to monitor these different patterns of monoamine expression in exposed offspring in more detail and to see if there are changes in the dopamine system at another time point, pregnant C57BL6J mice were infected with a sublethal dose of human influenza virus or sham-infected using vehicle solution on E16. Male offspring of the infected mice were collected at P0, P14, and P56, their brains removed and cerebellum dissected and flash frozen. Dopamine and serotonin levels were then measured using HPLC-ED technique. When compared to controls, there was a significant decrease in serotonin levels in the cerebella of offspring of virally exposed mice at P14. No differences in levels of dopamine were observed in exposed and control mice, although there was a significant decrease in dopamine at P14 and P56 when compared to P0. The present study shows that the serotonergic system is disrupted following prenatal viral infection, potentially modelling disruptions that occur in patients with schizophrenia and autism.European Neuropsychopharmacology 11/2008; 18(10):712-6.
Article: Reduced serum concentrations of nerve growth factor, but not brain-derived neurotrophic factor, in chronic cannabis abusers.[show abstract] [hide abstract]
ABSTRACT: Chronic cannabis use produces effects within the central nervous system (CNS) which include deficits in learning and attention tasks and decreased brain volume. Neurotrophins, in particular nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF), are proteins that serve as survival factors for CNS neurons. Deficits in the production and utilization of these proteins can lead to CNS dysfunctions including those associated with cannabis abuse. In this study we measured by enzyme-linked immunosorbent assay (ELISA) the NGF and BDNF serum levels in two groups of subjects: cannabis-dependent patients and healthy subjects. We found that NGF serum levels were significantly reduced in cannabis abusers as compared to healthy subjects. These findings indicate that NGF may have a role in the central action of cannabis and potentially in the neurotoxicity induced by this drug. These data also suggest that chronic cannabis consumption may be a risk factor for developing psychosis among drug users.European Neuropsychopharmacology 10/2008; 18(12):882-7.
Article: Cellular and behavioural profile of the novel, selective neurokinin1 receptor antagonist, vestipitant: a comparison to other agents.[show abstract] [hide abstract]
ABSTRACT: This study characterized the novel neurokinin (NK)(1) antagonist, vestipitant, under clinical evaluation for treatment of anxiety and depression. Vestipitant possessed high affinity for human NK(1) receptors (pK(i), 9.4), and potently blocked Substance P-mediated phosphorylation of Extracellular-Regulated-Kinase. In vivo, it occupied central NK(1) receptors in gerbils (Inhibitory Dose(50), 0.11 mg/kg). At similar doses, it abrogated nociception elicited by formalin in gerbils, and blocked foot-tapping and locomotion elicited by the NK(1) agonist, GR73632, in gerbils and guinea pigs, respectively. Further, vestipitant attenuated fear-induced foot-tapping in gerbils, separation-induced distress-vocalizations in guinea pigs, marble-burying behaviour in mice, and displayed anxiolytic actions in Vogel conflict and fear-induced ultrasonic vocalization procedures in rats. These actions were mimicked by CP99,994, L733,060 and GR205,171 which acted stereoselectively vs its less active isomer, GR226,206. In conclusion, vestipitant is a potent NK(1) receptor antagonist: its actions support the utility of NK(1) receptor blockade in the alleviation of anxiety and, possibly, depression.European Neuropsychopharmacology 10/2008; 18(10):729-50.
Article: Catechol-O-methyltransferase Val158Met polymorphism in relation to aggressive schizophrenia in a Korean population.[show abstract] [hide abstract]
ABSTRACT: We examined the association between the Catechol-O-methyltransferase (COMT) Val158Met polymorphism and aggressive schizophrenia. The sample included 61 aggressive schizophrenic patients as well as 104 non-aggressive patients from psychiatric hospitals and 415 healthy volunteers in South Korea. In the case-control comparisons, there was no significant association between the aggressive schizophrenic patients and the COMT Val158Met polymorphism. Looking only at the subgroup of aggressive schizophrenic patients, however, we found a dose-dependent relationship between the Met allele and verbal aggression. In this subgroup, the Met carriers showed a higher verbal aggression score than those with the Val/Val homozygote. These findings support the hypothesized moderating role of the COMT gene in the aggressive behaviour in some schizophrenic patients, though they do not support the existence of a direct association between the COMT Val158Met polymorphism and aggressive schizophrenia case status in the Korean population.European Neuropsychopharmacology 10/2008; 18(11):820-5.
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.
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