Neuroscience (NEUROSCIENCE)

Publisher: International Brain Research Organization, Elsevier

Journal description

Neuroscience publishes papers describing the results of original research on any aspect of the scientific study of the nervous system. Any paper, however short, will be considered for publication provided that it reports significant, new and carefully confirmed findings with full experimental details. For Instructions to Authors click on "Guide to Authors" in the left-hand column.

Current impact factor: 3.36

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 3.357
2013 Impact Factor 3.327
2012 Impact Factor 3.122
2011 Impact Factor 3.38
2010 Impact Factor 3.215
2009 Impact Factor 3.292
2008 Impact Factor 3.556
2007 Impact Factor 3.352
2006 Impact Factor 3.427
2005 Impact Factor 3.41
2004 Impact Factor 3.456
2003 Impact Factor 3.601
2002 Impact Factor 3.457
2001 Impact Factor 3.219
2000 Impact Factor 3.563
1999 Impact Factor 3.924
1998 Impact Factor 3.591
1997 Impact Factor 3.594

Impact factor over time

Impact factor

Additional details

5-year impact 3.42
Cited half-life 8.60
Immediacy index 0.77
Eigenfactor 0.07
Article influence 1.05
Website Neuroscience website
Other titles Neuroscience (Online)
ISSN 0306-4522
OCLC 39098294
Material type Document, Periodical, Internet resource
Document type Journal / Magazine / Newspaper, Computer File, Internet Resource

Publisher details


  • 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: The effects of sensory loss on central processing in various sensory systems have already been described. The olfactory system holds the special ability to be activated by a sensorimotor act, without the presentation of an odor. In this study, we investigated brain changes related to chronic peripheral smell loss. We included 11 anosmic patients (8f, 3m; mean age, 43.5 years) with smell loss after an infection of the upper respiratory tract (mean disease duration, 4.64 years) and 14 healthy controls (7f, 7m; mean age, 30.1 years) in a functional magnetic resonance imaging experiment with a sniffing paradigm. Data were analyzed using group-independent component analysis (ICA) and functional connectivity analysis. Our results revealed a spatially intact olfactory network in patients, whereas major aberrations due to peripheral loss were observed in functional connectivity through a variety of distributed brain areas. This is the first study to show the re-organization caused by the lack of peripheral input. The results of this study indicate that anosmic patients hold the ability to activate an olfaction-related functional network through the sensorimotor component of odor-perception (sniffing). The areas involved were not different from those that emerged in healthy controls. However, functional connectivity appears to be different between the two groups, with a decrease of functional connectivity in the brain in patients with chronic peripheral sensory loss. We further can conclude that the loss of the sense of smell may induce far-reaching effects in the whole brain, which lead to compensatory mechanisms from other sensory systems due to the close interconnectivity of the olfactory system with other functional networks.
    Neuroscience 09/2015; DOI:10.1016/j.neuroscience.2015.09.045
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    ABSTRACT: Volatile organic solvent abuse continues to be a worldwide health problem, including the neurobehavioral teratogenic sequelae of toluene abuse during pregnancy. Although abuse levels of prenatal toluene exposure can lead to a Fetal Solvent Syndrome, there is little research examining these effects on memory. Consumption of toluene can have detrimental effects on the developing hippocampus which could lead to specific spatial learning and memory deficits. This study used a rat model to determine how prenatal exposure to abuse levels of toluene would affect performance in a spatial learning and memory task, the Morris Water Maze (MWM). Pregnant Sprague-Dawley rats were exposed to 0, 8000 or 12,000 parts per million (ppm) of toluene for 15 min twice daily from gestation day 8 (GD8) through GD20. Male and female offspring (N= 104) were observed in the MWM for 5 days beginning on postnatal day (PN) 28 and again on PN44. While prenatal toluene exposed animals did not differ in initial acquisition in the MWM, rats prenatally exposed to 12,000 ppm toluene displayed performance deficits during a probe trial and in reversal learning on PN44. Overall, this study indicates that prenatal exposure to repeated inhaled abuse patterns of high concentrations of toluene can impair spatial memory function that persists into adolescence. Copyright © 2015. Published by Elsevier Ltd.
    Neuroscience 08/2015; DOI:10.1016/j.neuroscience.2015.08.050
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    ABSTRACT: It has been proposed that spontaneous panic attacks are the outcome of the misfiring of an evolved suffocation alarm system. Evidence gathered in the last year is suggestive that the dorsal periaqueductal gray (dPAG) in the midbrain harbors a hypoxia-sensitive suffocation alarm system. We here investigated whether facilitation of 5-HT-mediated neurotransmission within the dPAG changes panic-like defensive reactions expressed by male Wistar rats submitted to a hypoxia challenge (7% O2), as observed in other animal models of panic. Intra-dPAG injection of 5-HT (20 nmol), 8-OH-DPAT (8 nmol), a 5-HT1A receptor agonist, or DOI (16 nmol), a preferential 5-HT2A agonist, reduced the number of upward jumps directed to the border of the experimental chamber during hypoxia, interpreted as escape attempts, without affecting the rats' locomotion. These effects were similar to those caused by chronic, but not acute, intraperitoneal administration of the antidepressant fluoxetine (5 -15 mg/kg), or acute systemic administration of the benzodiazepine receptor agonist alprazolam (1 - 4 mg/kg), both drugs clinically used in the treatment of panic disorder. Our findings strengthen the view that the dPAG is a key encephalic area involved in the defensive behaviors triggered by activation of the suffocation alarm system. They also support the use of hypoxia-evoked escape as a model of respiratory-type panic attacks. Copyright © 2015. Published by Elsevier Ltd.
    Neuroscience 08/2015; DOI:10.1016/j.neuroscience.2015.08.045
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    ABSTRACT: Transient receptor potential canonical channel-6 (TRPC6) forms Ca(2+)-permeable non-selective cation channels in neurons. Although TRPC6 plays an important role in neurite outgrowth and neuronal survival during development, TRPC6 expression profiles available to identify distinctive hippocampal neuronal damage and hippocampal excitability in epilepsy are less defined. As compared to normal animals, TRPC6 expression was down-regulated in chronic epileptic rats showing spontaneous recurrent seizures. TRPC6 knockdown increased seizure susceptibility, excitability ratio and paired-pulse inhibition in the dentate gyrus of normal animals. Furthermore, TRPC6 knockdown promoted programmed neuronal necrosis in dentate granule cells, but prevented it in CA1 and CA3 neurons following status epilepticus. The present data suggest for the first time that TRPC6 may inhibit seizure susceptibility and neuronal vulnerability in the rat dentate gyrus. Copyright © 2015. Published by Elsevier Ltd.
    Neuroscience 08/2015; DOI:10.1016/j.neuroscience.2015.08.054
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    ABSTRACT: The experience of pain is a highly complex and personal experience, characterized by tremendous inter-individual variability. The purpose of this study was to use functional magnetic resonance imaging (fMRI) to characterize responses in the brainstem and spinal cord to the same heat stimulus in healthy participants, to further our understanding of individual differences in pain perception. Responses to noxious heat stimuli at 49 °C were investigated in 20 healthy individuals by means of fMRI of the brainstem and spinal cord, at 3 tesla, and were compared with brain fMRI and quantitative sensory testing. Blood oxygenation-level dependent (BOLD) responses were detected with a General Linear Model (GLM) and effective connectivity was examined with Structural Equation Modeling (SEM). Reported pain ratings ranged from 18 to 84 /100 across the participants. Consistent with previous research, brain fMRI results show that BOLD responses in a number of cortical regions are correlated with individual pain ratings. Correlations between pain scores and BOLD responses are also demonstrated in the spinal cord dorsal horn, locus coeruleus, and thalamus. SEM results demonstrate the network of brainstem and spinal cord regions that contribute to the pain response, and reveal differences related to individual pain sensitivity. The results of this study are consistent with the conclusion that individual differences in pain perception in healthy participants are a consequence of differences in descending modulation of spinal nociceptive processes from brainstem regions. Copyright © 2015. Published by Elsevier Ltd.
    Neuroscience 08/2015; DOI:10.1016/j.neuroscience.2015.08.059
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    ABSTRACT: Interleukin-6 (IL-6) has been shown to promote post-stroke angiogenesis and long-term functional recovery; however, whether IL-6 could promote post-stroke neurogenesis remains unclear. This study aims to investigate the effects of IL-6 on neurogenesis after ischemic stroke. We also investigated whether pair housing (PH) could improve the experimental stroke outcome through IL-6. Transient middle cerebral artery occlusion (tMCAO) was induced in mice treated with recombinant IL-6 (rIL-6) or anti-IL-6 neutralizing antibodies (anti-IL-6 mAbs). Another set of mice were pair-housed (PH; male and ovariectomized female) for 2 weeks, subjected to tMCAO and then assigned to a housing condition (isolated or PH). Pair-housed mice were treated with anti-IL-6 mAbs. Behavioral assessments were made 3 days before tMCAO and after 28 days of reperfusion. Neural progenitor cells (NPCs) isolated from ipsilateral subventricular zone (SVZ) at 14 days post-ischemia were treated with rIL-6 plus soluble IL-6 receptor (sIL-6R). The effects of IL-6 on the proliferation and differentiation of NPCs were examined in vivo and in vitro. The role and mechanism of IL-6 in PH-mediated enhancement of NPCs proliferation and functional recovery were investigated in vivo. We found that anti-IL-6 mAbs significantly reduced the proliferation and neuronal differentiation of NPCs in the ipsilateral SVZ, as well as functional recovery; whereas rIL-6 conferred the opposite effects. PH significantly promoted NPCs proliferation and functional recovery compared with socially isolated cohorts; blockade of IL-6 with anti-IL-6 mAbs prevented this promoting effect. In conclusion, our results suggest that IL-6 is an important mediator of social interaction on neurogenesis and long-term functional recovery after ischemic stroke. Copyright © 2015. Published by Elsevier Ltd.
    Neuroscience 08/2015; DOI:10.1016/j.neuroscience.2015.08.055
  • [Show abstract] [Hide abstract]
    ABSTRACT: Dorsoventral patterning and EGFR signaling genes are essential for determining neural identity and differentiation of the Drosophila nervous system. Their role in glial cell development in the Drosophila nervous system is not clearly established. Our study demonstrated that the dorsoventral patterning genes, vnd, ind, and msh, are intrinsically essential for the proper expression of a master glial cell regulator, gcm, and a differentiation gene, repo, in the lateral glia. In addition, we showed that esg is particularly required for their expression in the peripheral glia. These results indicate that the dorsoventral patterning and EGFR signaling genes are essential for identity determination and differentiation of the lateral glia by regulating proper expression of gcm and repo in the lateral glia from the early glial development. In contrast, overexpression of vnd, msh, spi, and Egfr genes repressed the expression of Repo in the ventral neuroectoderm, indicating that maintenance of correct columnar identity along the dorsoventral axis by proper expression of these genes is essential for restrictive formation of glial precursor cells in the lateral neuroectoderm. Therefore, the dorsoventral patterning and EGFR signaling genes play essential roles in correct identity determination and differentiation of lateral glia in the Drosophila nervous system. Copyright © 2015. Published by Elsevier Ltd.
    Neuroscience 08/2015; DOI:10.1016/j.neuroscience.2015.08.049