Neuroscience & Biobehavioral Reviews (NEUROSCI BIOBEHAV R)

Publisher: Elsevier

Journal description

The journal will publish original and significant review articles dealing with all aspects of neuroscience, where the relationship to the study of psychological processes and behavior is clearly established. Conversely, the journal will also publish articles whose primary focus deals with psychological processes and behavior, and which have relevance to one or more aspects of neuroscience. Submissions to the journal are actively encouraged which deal with topics not only in the more traditional areas, but also in the following areas, whenever the reviews bring new insights into brain-behavior relations: neuropsychology cognitive neuroscience brain imaging in vivo monitoring of the brain's electrical and biochemical activities molecular biology genetics neurocomputation Theoretical articles and mini-reviews, for which the scope and literature coverage are more restricted, will also be published. The table of contents for this journal is now available pre-publication, via e-mail, as part of the free ContentsDirect service from Elsevier Science. Please send an e-mail message to cdhelp@elsevier.co.uk for further information about this service.

Current impact factor: 10.28

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2013 / 2014 Impact Factor 10.284
2012 Impact Factor 9.44
2011 Impact Factor 8.65
2010 Impact Factor 9.015
2009 Impact Factor 7.791
2008 Impact Factor 7.804
2007 Impact Factor 8.147
2006 Impact Factor 8.293
2005 Impact Factor 7.443
2004 Impact Factor 6.346
2003 Impact Factor 5.482
2002 Impact Factor 5.504
2001 Impact Factor 5.212
2000 Impact Factor 3.382
1999 Impact Factor 3.595
1998 Impact Factor 3.316
1997 Impact Factor 2.786

Impact factor over time

Impact factor
Year

Additional details

5-year impact 9.92
Cited half-life 6.80
Immediacy index 2.13
Eigenfactor 0.03
Article influence 3.50
Website Neuroscience & Biobehavioral Reviews website
Other titles Neuroscience and biobehavioral reviews, Neuroscience & biobehavioral reviews
ISSN 1873-7528
OCLC 3552135
Material type Periodical, Internet resource
Document type Journal / Magazine / Newspaper, Internet Resource

Publisher details

Elsevier

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • Pre-print allowed on any website or open access repository
    • Voluntary deposit by author of authors post-print allowed on authors' personal website, arXiv.org or institutions open scholarly website including Institutional Repository, without embargo, where there is not a policy or mandate
    • Deposit due to Funding Body, Institutional and Governmental policy or mandate only allowed where separate agreement between repository and the publisher exists.
    • 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 .
    • 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 PubMed Central after 12 months
    • Publisher last contacted on 18/10/2013
  • Classification
    ​ green

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: GRIMONPREZ A., R. Raedt, C. Baeken, P. Boon and K. Vonck. The antidepressant mechanism of action of vagus nerve stimulation: evidence from preclinical studies. NEUROSCI BIOBEHAV REV, 2015 Vagus nerve stimulation (VNS) is a proposed neuromodulatory treatment for medically refractory major depression. Although VNS is already used in clinical practice, the underlying mechanism of action remains unknown. The present review provides an overview of the preclinical VNS studies in view of two major hypotheses in depression research: the monoaminergic and the neural plasticity hypothesis of depression. Copyright © 2015. Published by Elsevier Ltd.
    Neuroscience & Biobehavioral Reviews 06/2015; DOI:10.1016/j.neubiorev.2015.06.019
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    ABSTRACT: The melanocortin system of the hypothalamus, including the neuropeptides α-melanocyte stimulating hormone (αMSH) and agouti-related protein (AgRP), and their receptors, the melanocortin-3 receptor (MC3R) and melanocortin-4 receptor (MC4R), have been well-studied for their roles in the central control of feeding and body weight. In this review, we discuss the evidence demonstrating that αMSH and AgRP also act on the mesocorticolimbic and mesostriatal dopamine systems to regulate a wide variety of behaviors. In addition to the well described ability of αMSH to increase dopamine transmission and to increase grooming and rearing when injected directly into the ventral tegmental area, a growing body of evidence indicates that αMSH and AgRP can also act on dopamine pathways to regulate feeding and drug abuse, including reward-related behaviors toward food and drugs. Increasing our understanding of how αMSH and AgRP act on dopamine pathways to affect behavior may allow for identification of new strategies to combat disorders involving dysfunction of dopamine pathways, such as obesity and drug abuse. Copyright © 2015. Published by Elsevier Ltd.
    Neuroscience & Biobehavioral Reviews 06/2015; DOI:10.1016/j.neubiorev.2015.06.020
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    ABSTRACT: How much, how often and how fast a drug reaches the brain determine the behavioural and neuroplastic changes associated with the addiction process. Despite the critical nature of these variables, the drug addiction field often ignores pharmacokinetic issues, which we argue can lead to false conclusions. First, we review the clinical data demonstrating the importance of the speed of drug onset and of intermittent patterns of drug intake in psychostimulant drug addiction. This is followed by a review of the preclinical literature demonstrating that pharmacokinetic variables play a decisive role in determining behavioural and neurobiological outcomes in animal models of addiction. This literature includes recent data highlighting the importance of intermittent, 'spiking' brain levels of drug in producing an increase in the motivation to take drug over time. Rapid drug onset and intermittent drug exposure both appear to push the addiction process forward most effectively. This has significant implications for refining animal models of addiction and for better understanding the neuroadaptations that are critical for the disorder. Copyright © 2015. Published by Elsevier Ltd.
    Neuroscience & Biobehavioral Reviews 06/2015; DOI:10.1016/j.neubiorev.2015.06.012
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    ABSTRACT: Inhibition concerns the capacity to suppress on-going response tendencies. Patient data and results from neuro-imaging and magnetic-stimulation studies point to a proactive mechanism involving top-down control signals that potentiate inhibitory sensory-motor connections, depending on whether possibly necessary inhibition is anticipated or not. The proactive mechanism is manifest in stronger sensory-cortex responses to stop signals yielding successful inhibition, observed as a modulation of short-latency human evoked potentials (N1) which may overlap with generic mechanisms for infrequent-event detection. A second, reactive, mechanism would be much more independent of the specific inhibition context, and generalize to situations in which behavioral interrupt is not dictated by task demands but invoked by the salience of task-irrelevant but potentially distracting events. The reactive mechanism is visible in a longer-latency human event-related potential termed frontal P3 (fP3) which is elicited by (successful) stop stimuli and most likely originates from dorsal-medial prefrontal cortex (preSMA), and is dissociated from the reactive mechanism pharmacologically and by individual differences. Implications may arise for more personalized treatments of disorders such as ADHD. Copyright © 2015. Published by Elsevier Ltd.
    Neuroscience & Biobehavioral Reviews 06/2015; DOI:10.1016/j.neubiorev.2015.06.011
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    ABSTRACT: Stress responses entail neuroendocrine, autonomic, and behavioral changes to promote effective coping with real or perceived threats to one's safety. While these responses are critical for the survival of the individual, adverse effects of repeated exposure to stress are widely known to have deleterious effects on health. Thus, a considerable effort in the search for treatments to stress-related CNS disorders necessitates unraveling the brain mechanisms responsible for adaptation under acute conditions and their perturbations following chronic stress exposure. This paper is based upon a symposium from the 2014 International Behavioral Neuroscience Meeting, summarizing some recent advances in understanding the effects of stress on adaptive and maladaptive responses subserved by limbic forebrain networks. An important theme highlighted in this review is that the same networks mediating neuroendocrine, autonomic, and behavioral processes during adaptive coping also comprise targets of the effects of repeated stress exposure in the development of maladaptive states. Where possible, reference is made to the similarity of neurobiological substrates and effects observed following repeated exposure to stress in laboratory animals and the clinical features of stress-related disorders in humans. Copyright © 2015. Published by Elsevier Ltd.
    Neuroscience & Biobehavioral Reviews 06/2015; DOI:10.1016/j.neubiorev.2015.06.018
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    ABSTRACT: The mystery surrounding how plant neurotoxins came to possess reinforcing properties is termed the paradox of drug reward. Here we propose a resolution to this paradox whereby dopamine - which has traditionally been viewed as a signal of reward - initially signaled aversion and encouraged escape. We suggest that after being consumed, plant neurotoxins such as nicotine activated an aversive dopaminergic pathway, thereby deterring predatory herbivores. Later evolutionary events - including the development of a GABAergic system capable of modulating dopaminergic activity - led to the ability to down-regulate and 'control' this dopamine-based aversion. We speculate that this negative reinforcement system evolved so that animals could suppress aversive states such as hunger in order to attend to other internal drives (such as mating, shelter) that would result in improved organismal fitness. Copyright © 2015. Published by Elsevier Ltd.
    Neuroscience & Biobehavioral Reviews 06/2015; DOI:10.1016/j.neubiorev.2015.06.016
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    ABSTRACT: NILSSON, S.R.O., ALSIÖ, J., ELIZABETH M. SOMERVILLE, E.M., CLIFTON, P.G. The Rat's not for Turning: Dissociating the Psychological Components of Cognitive Inflexibility. NEUROSCI BIOBEHAV REV XX(X) XXX-XXX 2015. Executive function is commonly assessed by assays of cognitive flexibility such as reversal learning and attentional set-shifting. Disrupted performance in these assays, apparent in many neuropsychiatric disorders, is frequently interpreted as inability to overcome prior associations with reward. However, non-rewarded or irrelevant associations may be of considerable importance in both discrimination learning and cognitive flexibility. Non-rewarded associations can have greater influence on choice behaviour than rewarded associations in discrimination learning. Pathology-related deficits in cognitive flexibility can produce selective disruptions to both the processing of irrelevant associations and associations with reward. Genetic and pharmacological animal models demonstrate that modulation of reversal learning may result from alterations in either rewarded or non-rewarded associations. Successful performance in assays of cognitive flexibility can therefore depend on a combination of rewarded, non-rewarded, and irrelevant associations derived from previous learning, accounting for some inconsistencies observed in the literature. Taking this combination into account may increase the validity of animal models and may also reveal pathology-specific differences in problem solving and executive function. Copyright © 2015. Published by Elsevier Ltd.
    Neuroscience & Biobehavioral Reviews 06/2015; DOI:10.1016/j.neubiorev.2015.06.015
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    ABSTRACT: Repeated exposure to a wide range of stressors differing in nature and intensity results in a reduced response of prototypical stress markers (i.e. plasma levels of ACTH and adrenaline) after an acute challenge with the same (homotypic) stressor. This reduction has been considered to be a habituation-like phenomenon. However, direct experimental evidence for this assumption is scarce. In the present work we demonstrate in adult male rats that adaptation of the hypothalamus-pituitary-adrenal (HPA) axis to repeated stress does not follow some of the critical rules of habituation. Briefly, adaptation was stronger and faster with more severe stressors, maximally observed even with a single exposure to severe stressors, extremely long-lasting, negatively related to the interval between the exposures and positively related to the length of daily exposure. We offer a new theoretical view to explain adaptation to daily repeated stress. Copyright © 2015. Published by Elsevier Ltd.
    Neuroscience & Biobehavioral Reviews 06/2015; DOI:10.1016/j.neubiorev.2015.06.013
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    ABSTRACT: The functional organization of the parieto-frontal system is crucial for understanding cognitive-motor behavior and provides the basis for interpreting the consequences of parietal lesions in humans from a neurobiological perspective. The parieto-frontal connectivity defines some main information streams that, rather than being devoted to restricted functions, underlie a rich behavioral repertoire. Surprisingly, from macaque to humans, evolution has added only a few, new functional streams, increasing however their complexity and encoding power. In fact, the characterization of the conduction times of parietal and frontal areas to different target structures has recently opened a new window on cortical dynamics, suggesting that evolution has amplified the probability of dynamic interactions between the nodes of the network, thanks to communication patterns based on temporally-dispersed conduction delays. This might allow the representation of sensory-motor signals within multiple neural assemblies and reference frames, as to optimize sensory-motor remapping within an action space characterized by different and more complex demands across evolution. Copyright © 2015. Published by Elsevier Ltd.
    Neuroscience & Biobehavioral Reviews 06/2015; DOI:10.1016/j.neubiorev.2015.06.014
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    ABSTRACT: Imaging and lesion studies have suggested numerous roles for the temporoparietal junction (TPJ), for example in attention and neglect, social cognition, and self/other processing. These studies cannot establish causal relationships, and the importance and relevance of (and interrelationships between) proposed roles remain controversial. This review examined studies that use noninvasive transcranial stimulation (NTS) to explore TPJ function. Of 459 studies identified, 40 met selection criteria. The strengths and weaknesses of NTS-relevant parameters used are discussed, and methodological improvements suggested. These include the need for careful selection of stimulation sites and experimental tasks, and use of neuronavigation and concurrent functional activity measures. Without such improvements, overlapping and discrete functions of the TPJ will be difficult to disentangle. Nevertheless, the contributions of these studies to theoretical models of TPJ function are discussed, and the clinical relevance of TPJ stimulation explored. Some evidence exists for TPJ stimulation in the treatment of auditory hallucinations, tinnitus, and depersonalisation disorder. Further examination of the TPJ in conditions such as autism spectrum disorder is also warranted. Copyright © 2015. Published by Elsevier Ltd.
    Neuroscience & Biobehavioral Reviews 06/2015; 55. DOI:10.1016/j.neubiorev.2015.05.017
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    ABSTRACT: The neural basis of face processing has been extensively studied in the past two decades. The current dominant neural model proposed by Haxby and colleagues (2000, 2007) suggests a division of labor between the fusiform face area (FFA), which processes invariant facial aspects, such as identity, and the posterior superior temporal sulcus (pSTS), which processes changeable facial aspects, such as expression. An extension to this model for the processing of dynamic faces proposed by O'Toole and colleagues (2002) highlights the role of the pSTS in the processing of identity from dynamic familiar faces. To evaluate these models, we reviewed recent neuroimaging studies that examined the processing of identity and expression with static and dynamic faces. Based on accumulated data we propose an updated model, emphasizing the dissociation between form and motion as the primary functional division between a ventral stream that goes through the FFA and a dorsal stream that goes through the STS, respectively, and suggest that future research should expand to further investigate the processing of dynamic faces. Copyright © 2015. Published by Elsevier Ltd.
    Neuroscience & Biobehavioral Reviews 06/2015; 55. DOI:10.1016/j.neubiorev.2015.06.010
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    ABSTRACT: We describe a new type of agnosia consisting of an impairment in the ability to mentally represent or know what one is feeling. Freud the neurologist coined the term "agnosia" in 1891 before creating psychoanalysis in 1895 but the term has not been previously applied to the domain of affective processing. We propose that the concept of "affective agnosia" advances the theory, measurement and treatment of what is now called "alexithymia," meaning "lack of words for emotion." We trace the origin of the alexithymia construct and discuss the strengths and limitations of extant research. We review evidence that the ability to represent and put emotions into words is a developmental achievement that strongly influences one's ability to experience, recognize, understand and use one's own emotional responses. We describe the neural substrates of emotional awareness and affective agnosia and compare and contrast these with related conditions. We then describe how this expansion of the conceptualization and measurement of affective processing deficits has important implications for basic emotion research and clinical practice. Copyright © 2015. Published by Elsevier Ltd.
    Neuroscience & Biobehavioral Reviews 06/2015; 55. DOI:10.1016/j.neubiorev.2015.06.007
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    ABSTRACT: Brain/biological (BR) and cognitive/neural reserve (CR) have increasingly been used to explain some of the variability that occurs as a consequence of normal ageing and neurological injuries or disease. However, research evaluating the impact of reserve on outcomes after adult traumatic brain injury (TBI) has yet to be quantitatively reviewed. This meta-analysis consolidated data from 90 studies (published prior to 2015) that either examined the relationship between measures of BR (genetics, age, sex) or CR (education, premorbid IQ) and outcomes after TBI or compared the outcomes of groups with high and low reserve. The evidence for genetic sources of reserve was limited and often contrary to prediction. APOE ∈4 status has been studied most, but did not have a consistent or sizeable impact on outcomes. The majority of studies found that younger age was associated with better outcomes, however most failed to adjust for normal age-related changes in cognitive performance that are independent of a TBI. This finding was reversed (older adults had better outcomes) in the small number of studies that provided age-adjusted scores; although it remains unclear whether differences in the cause and severity of injuries that are sustained by younger and older adults contributed to this finding. Despite being more likely to sustain a TBI, males have comparable outcomes to females. Overall, as is the case in the general population, higher levels of education and pre-morbid IQ are both associated with better outcomes. Copyright © 2015. Published by Elsevier Ltd.
    Neuroscience & Biobehavioral Reviews 06/2015; 62. DOI:10.1016/j.neubiorev.2015.06.001
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    ABSTRACT: Smokers have substantial individual differences in quit success in response to current treatments for nicotine dependence. This observation may suggest that different underlying motivations for continued tobacco use across individuals and nicotine cessation may require different treatments in different individuals. Although most animal models of nicotine dependence emphasize the positive reinforcing effects of nicotine as the major motivational force behind nicotine use, smokers generally report that other consequences of nicotine use, including the ability of nicotine to alleviate negative affective states or cognitive impairments, as reasons for continued smoking. These states could result from nicotine withdrawal, but also may be associated with premorbid differences in affective and/or cognitive function. Effects of nicotine on cognition and affect may alleviate these impairments regardless of their premorbid or postmorbid origin (e.g., before or after the development of nicotine dependence). The ability of nicotine to alleviate these symptoms would thus negatively reinforce behavior, and thus maintain subsequent nicotine use, contributing to the initiation of smoking, the progression to dependence and relapse during quit attempts. The human and animal studies reviewed here support the idea that self-medication for pre-morbid and withdrawal-induced impairments may be more important factors in nicotine addiction and relapse than has been previously appreciated in preclinical research into nicotine dependence. Given the diverse beneficial effects of nicotine under these conditions, individuals might smoke for quite different reasons. This review suggests that inter-individual differences in the diverse effects of nicotine associated with self-medication and negative reinforcement are an important consideration in studies attempting to understand the causes of nicotine addiction, as well as in the development of effective, individualized nicotine cessation treatments. Copyright © 2015. Published by Elsevier Ltd.
    Neuroscience & Biobehavioral Reviews 06/2015; DOI:10.1016/j.neubiorev.2015.06.004