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

2016 Impact Factor Available summer 2017
2014 / 2015 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
Year

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

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: cAMP response-element binding protein (CREB) dependent genes are differentially expressed in brains of temporal lobe epilepsy (TLE) patients and also in animal models of TLE. Previous studies have demonstrated the importance of CREB regulated transcription in TLE. However, the role of the key regulator of CREB activity, CREB-regulated transcription coactivator 1 (CRTC1), has not been explored in epilepsy. In the present study the pilocarpine-induced status epilepticus (SE) model of TLE was used to study the regulation of CRTC1 during and following SE. Nuclear translocation of CRTC1 is critical for its transcriptional activity, and dephosphorylation at serine 151 residue via calcineurin phosphatase regulates cytoplasmic to nuclear transit of CRTC1. Here, we examined the localization and phosphorylation (Ser151) of CRTC1 in SE-induced rat hippocampus at two different time points after SE onset.
    No preview · Article · Feb 2016 · Neuroscience
  • Ying Jin · Julien Bouyer · Jed S Shumsky · Christopher Haas · Itzhak Fischer

    No preview · Article · Feb 2016 · Neuroscience
  • M. Alejandra Lopez-Verrilli · Ariel Caviedes · Alex Cabrera · Soledad Sandoval · Ursula Wyneken · Maroun Khoury

    No preview · Article · Feb 2016 · Neuroscience
  • Doron Bushi · Orna Gera · Genady Kostenich · Efrat Shavit-Stein · Ronen Weiss · Joab Chapman · David Tanne

    No preview · Article · Feb 2016 · Neuroscience
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    ABSTRACT: Prenatal stress and overexposure to glucocorticoids (GC) during development may be associated with an increased susceptibility to a number of diseases in adulthood including neuropsychiatric disorders, such as depression and anxiety. In animal models, prenatal overexposure to GC results in hyper-responsiveness to stress in adulthood, and females appear to be more susceptible than males. Here, we tested the hypothesis that overexposure to GC during fetal development has sex-specific programming effects on the brain, resulting in altered behaviors in adulthood. We examined the effects of dexamethasone (DEX; a synthetic GC) during prenatal life on stress-related behaviors in adulthood and on the tryptophan hydroxylase-2 (TpH2) gene expression in the adult dorsal raphe nucleus (DRN). TpH2 is the rate-limiting enzyme for serotonin (5-HT) synthesis and has been implicated in the etiology of human affective disorders. Timed-pregnant rats were treated with DEX from gestational days 18-22. Male and female offspring were sacrificed on the day of birth (postnatal day 0; P0), P7, and in adulthood (P80-84) and brains were examined for changes in TpH2 mRNA expression. Adult animals were also tested for anxiety- and depressive- like behaviors. In adulthood, prenatal DEX increased anxiety- and depressive- like behaviors selectively in females, as measured by decreased time spent in the center of the open field and increased time spent immobile in the forced swim test, respectively. Prenatal DEX increased TpH2 mRNA selectively in the female caudal DRN at P7, whereas it decreased TpH2 mRNA selectively in the female caudal DRN in adulthood. In animals challenged with restraint stress in adulthood, TpH2 mRNA was significantly lower in rostral DRN of prenatal DEX treated females compared to vehicle treated females. These data demonstrated that prenatal overexposure to GC alter the development of TpH2 gene expression and these alterations correlated with lasting behavioral changes found in adult female offspring.
    No preview · Article · Feb 2016 · Neuroscience

  • No preview · Article · Feb 2016 · Neuroscience
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    ABSTRACT: It is well established that multisensory integration is a functional characteristic of the superior colliculus that disambiguates external stimuli and therefore reduces the reaction times towards simple audiovisual targets in space. However, in a condition where complex audiovisual stimuli, such as the optical flow in the presence of modulated audio signals, little is known about the processing of the multisensory integration in the superior colliculus. Furthermore, since visual and auditory deficits constitute hallmark signs during aging, we sought to gain some insight on whether audiovisual processes in the superior colliculus are altered with age. Extracellular single-unit recordings were conducted in the superior colliculus of anaesthetized Sprague-Dawley adult (10-12 months) and aged (21-22 months) rats. Looming circular concentric sinusoidal gratings were presented alone and in the presence of sinusoidally amplitude modulated white noise. In both groups of rats, two different audiovisual response interactions were encountered in the spatial domain: superadditive, and suppressive. In contrast, additive audiovisual interactions were found only in adults rats. Hence, superior colliculus audiovisual interactions were more numerous in adult rats (38%) than in aged rats (8%). These results suggest that intersensory interactions in the superior colliculus play an essential role in space processing towards audiovisual moving objects during self-motion. Moreover, aging has a deleterious effect on complex audiovisual interactions.
    No preview · Article · Feb 2016 · Neuroscience

  • No preview · Article · Feb 2016 · Neuroscience
  • Joshua A. Gordon · Kafui Dzirasa

    No preview · Article · Feb 2016 · Neuroscience
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    ABSTRACT: Studies on classification learning suggested that altered dopamine function in Parkinson’s Disease (PD) specifically affects learning from feedback. In patients OFF medication, enhanced learning from negative feedback has been described. This learning bias was not seen in observational learning from feedback, indicating different neural mechanisms for this type of learning. The present study aimed to compare the acquisition of stimulus-response-outcome associations in PD patients OFF medication and healthy control subjects in active and observational learning. 16 PD patients OFF medication and 16 controls were examined with three parallel learning tasks each, two feedback-based (active and observational) and one non-feedback based paired associates task. No acquisition deficit was seen in the patients for any of the tasks. More detailed analyses on the learning strategies did, however, reveal that the patients showed more lose-shift responses during active feedback learning than controls, and that lose-shift and win-stay responses more strongly determined performance accuracy in patients than controls. For observational feedback learning, the performance of both groups correlated similarly with the performance in non-feedback-based paired associates learning and with the accuracy of observed performance. Also, patients and controls showed comparable evidence of feedback processing in observational learning. In active feedback learning, PD patients use alternative learning strategies than healthy controls. Analyses on observational learning did not yield differences between patients and controls, adding to recent evidence of a differential role of the human striatum in active and observational learning from feedback.
    No preview · Article · Feb 2016 · Neuroscience
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    ABSTRACT: The choroid plexus (CP) located in the brain ventricles, by forming the interface between the blood and the cerebrospinal fluid (CSF) are in a privileged position to monitor the composition of these body fluids. Yet, the mechanisms involved in this surveillance system remain to be identified. The taste transduction pathway senses some types of molecules, thereby evaluating the chemical content of fluids, not only in the oral cavity but also in other tissues throughout the body, such as some cell types of the airways, the gastrointestinal tract, testis and skin. Therefore, we hypothesized that the taste transduction pathway could be also operating in the CP to assess the composition of the CSF. We found transcripts for some taste receptors (Tas1R1, Tas1R2, Tas1R3, Tas2R109 and Tas2R144) and for downstream signaling molecules (α-Gustducin, Plcβ2, ItpR3 and TrpM5) that encode this pathway, and confirmed the expression of the corresponding proteins in Wistar rat CP explants and in the CP epithelial cells (CPEC). The functionality of the T2R receptor expressed in CP cells was assessed by calcium imaging, of CPEC stimulated with the bitter compound D-Salicin, which elicited a rise in the intracellular Ca2+. This effect was diminished in the presence of the bitter receptor blocker Probenecid. In summary, we described the expression of the taste-related components involved in the transduction signaling cascade in CP. Taken together, our results suggest that the taste transduction pathway in CPEC makes use of T2R receptors in the chemical surveillance of the CSF composition, in particular to sense bitter noxious compounds.
    No preview · Article · Feb 2016 · Neuroscience
  • Gregory B. Bissonette · Matthew R. Roesch

    No preview · Article · Feb 2016 · Neuroscience

  • No preview · Article · Feb 2016 · Neuroscience
  • [Show abstract] [Hide abstract]
    ABSTRACT: We explored the changes in multi-finger synergies in patients after a single cortical stroke with mild motor impairments. We hypothesized that both synergy indices and anticipatory synergy adjustments prior to the initiation of a self-paced quick action would be diminished in the patients compared to age-matched controls. The patients with history of cortical stroke, and age-matched controls (n = 12 in each group) performed one-finger and multi-finger accurate force production tasks involving both steady-state and quick force pulse production. Finger interdependence (enslaving) and multi-finger synergies stabilizing total force were quantified. The stroke patients showed lower maximal finger forces, in particular in the contralesional hand, which also showed increased enslaving indices. Multi-finger synergies during steady-state force production were, however, unchanged after stroke. In contrast, a drop in the synergy index prior to the force pulse generation was significantly delayed in the stroke patients. Our results show that mild cortical stroke leads to no significant changes in multifinger synergies, but there is impairment in feed-forward adjustments of the synergies prior to a quick action, a drop in the maximal force production, and an increase in enslaving. We conclude that studies of synergies reveal two aspects of synergic control differentially affected by cortical stroke.
    No preview · Article · Jan 2016 · Neuroscience
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    ABSTRACT: Pain is an ambiguous perception: the same pain stimulation can be perceived differently in different contexts, producing different experiences, ranging from mild to unbearable pain. It can be even experienced as a rewarding sensation within the appropriate context. Overall, placebo and nocebo effects appear to be very good models to understand how the psychosocial context modulates the experience of pain. In this review, we examine the effects of different contexts on pain, with a specific focus on the neurobiological mechanisms. Positive and rewarding contexts inform the patients that an effective treatment is being delivered and are capable of producing pain relief through the activation of specific systems such as opioids, cannabinoids and dopamine. Conversely, a negative context can produce pain exacerbation and clinical worsening through the modulation of different systems, such as the activation of cholecystokinin and the deactivation of opioids and dopamine. In addition, when a therapy is delivered unbeknownst to the patient, its effects are reduced. A better understanding of the neurobiological underpinnings of the context-pain interaction is a challenge both for future pain research and for good clinical practice.
    No preview · Article · Jan 2016 · Neuroscience
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    ABSTRACT: The objective of the study was to examine whether axotomy and 17β-estradiol affects P2X7 receptor expression and distribution in the hypoglossal nucleus. The left hypoglossal nerve of ovariectomized mice was cut and animals received a single injection of 17β-estradiol (25μg/100 g b. w. in 20% (2- hydroxypropyl) - β- cyclodextrin) or vehicle one hour after axotomy. Mice were sacrificed on day 4 following surgery. The area fraction of P2X7 receptor immunoreactive structures and of CD11b immunolabeled microglia, P2X7 protein concentration, and the immunoreactivity pattern of estrogen receptor alpha / beta were analyzed on both sides of the hypoglossal nucleus. Following axotomy the area fraction of P2X7 immunoreactive neurons showed a decreasing tendency, while the area fraction of P2X7 immunolabeled microglia increased significantly on the axotomized side compared with the control side in mice injected with vehicle. In animals treated with 17β-estradiol the decrease in area fraction of neural and the increase in area fraction of microglial P2X7 immunostaining on the axotomized side were significantly enhanced compared with animals injected with vehicle. The P2X7 immunoreactivity pattern on the control side of the nucleus remained unchanged after 17β-estradiol injection. Semi-quantitative Western blots revealed no significant difference in P2X7 protein concentration comparing the axotomized side with the control side in either experimental group. The CD11b immunoreactive microglia area fraction increased significantly following axotomy, but was not affected by 17β-estradiol. Neither estrogen receptor alpha, nor beta colocalized with CD11b. Our results suggest that axotomy induces cell-type specific changes in P2X7 receptor expression, which may be directly regulated by 17β-estradiol through estrogen receptor alpha or beta in neurons, but not in activated microglia.
    No preview · Article · Jan 2016 · Neuroscience
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    ABSTRACT: It has previously been shown in rats that acute administration of THC exerts a dose-dependent effect on simple locomotor activity, with low doses of THC causing hyper-locomotion and high doses causing hypo-locomotion. However the effect of acute THC administration on cortical movement representations (motor maps) and skilled learned movements is completely unknown. It is important to determine the effects of THC on motor maps and skilled learned behaviors because behaviors like driving place people at heightened risk. Three doses of THC were used in the current study: 0.2 mg/kg, 1.0 mg/kg and 2.5 mg/kg representing the approximate range of the low to high levels of available THC one would consume from recreational use of cannabis. Acute peripheral administration of THC to drug naïve rats resulted in dose-dependent alterations in motor map expression using high resolution short duration intracortical microstimulation (SD-ICMS). THC at 0.2 mg/kg decreased movement thresholds and increased motor map size, while 1.0 mg/kg had the opposite effect, and 2.5 mg/kg had an even more dramatic effect. Deriving complex movement maps using long duration (LD)-ICMS at 1.0 mg/kg resulted in fewer complex movements. Dosages of 1.0 mg/kg and 2.5 mg/kg THC reduced the number of reach attempts but did not affect percentage of success or the kinetics of reaching on the single pellet skilled reaching task. Rats that received 2.5 mg/kg THC did show an increase in latency of forelimb removal on the bar task, while dose-dependent effects of THC on unskilled locomotor activity using the rotorod and horizontal ladder tasks were not observed. Rats may be employing compensatory strategies after receiving THC, which may account for the robust changes in motor map expression but moderate effects on behavior.
    No preview · Article · Jan 2016 · Neuroscience
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    ABSTRACT: Microglia have multiple functions in regulating homeostasis in the central nervous system (CNS), and microglial inflammation is thought to play a role in the etiology of the neurodegenerative diseases. When endogenous or exogenous stimuli trigger disorders in microenvironmental homeostasis in CNS, microglia critically determine the fate of other neural cells. Recently, it was reported that autophagy might influence inflammation and activation of microglia. Though the interaction between autophagy and macrophages has been reported and reviewed in length, the role of autophagy in microglia has yet to be reviewed. Herein, we will highlight recent advances on the emerging role of autophagy in microglia, focusing on the regulation of autophagy during microglial inflammation, and the possible mechanism involved.
    No preview · Article · Jan 2016 · Neuroscience
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    ABSTRACT: Minocycline, a second-generation tetracycline, is well known for its antibiotic, anti-inflammatory, and antinociceptive effects. Modulation of synaptic transmission is one of the analgesic mechanisms of minocycline. Although it has been reported that minocycline may suppress excitatory glutamatergic synaptic transmission, it remains unclear whether it could affect inhibitory synaptic transmission, which also plays a key role in modulating pain signaling. To examine the effect of minocycline on synaptic transmission in rat spinal substantia gelatinosa neurons, we recorded spontaneous inhibitory postsynaptic currents (sIPSCs) using whole-cell patch clamp recording at a holding potential of 0 mV. Bath application of minocycline significantly increased the frequency but not the amplitude of sIPSCs in a reversible and concentration-department manner with an EC50 of 85. The enhancement of inhibitory synaptic transmission produced by minocycline was not affected by the glutamate receptor antagonists CNQX and D-APV or by the voltage-gated sodium channel blocker tetrodotoxin. Moreover, the potency of minocycline for facilitating sIPSC frequency was the same in both glycinergic and GABAergic sIPSCs without changing their decay phases. However, the facilitatory effect of minocycline on sIPSCs was eliminated in a Ca2+-free Krebs solution or by co-administration with calcium channel blockers. In summary, our data demonstrate that baseline inhibitory synaptic transmission in substantia gelatinosa neurons is markedly enhanced by minocycline. This may function to decrease the excitability of substantia gelatinosa neurons, thus leading to a modulation of nociceptive transmission.
    Full-text · Article · Jan 2016 · Neuroscience
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    ABSTRACT: κ Opioid receptor agonists produce aversive effects in rodents, however the underlying mechanisms remain unclear. Activation of p38 mitogen-activated protein kinase (MAPK) has been discovered to play a critical role in the modulation of affective behaviors. The present study was undertaken to detect the possible involvement of p38 MAPK in the aversive effects induced by κ opioid receptor activation. We found that the κ opioid receptor agonist trans-(±)-3,4-Dichloro-N-methyl-N-[2-(1-pyrrolidinyl)-cyclohexyl] benzenacetamide methanesulfonate salt (U50,488H) produced significant place aversion in mice as measured by the conditioned place preference procedure, accompanied with significant p38 MAPK activation in the amygdala, but not in the nucleus accumbens and hippocampus. Stereotaxic microinjection of the p38 MAPK inhibitor 4-(4-fluorophenyl)-2-(4-methylsulfonylphenyl)-5-(4-pyridy-l)-1H-imidazole (SB203580) into amygdala significantly inhibited p38 MAPK activation and completely blocked the conditioned place aversion in mice. Thus, these results suggested that activation of p38 MAPK in the amygdala was required to mediate κ opioid receptor-induced aversive behavior.
    No preview · Article · Jan 2016 · Neuroscience