Trends in Neurosciences (TRENDS NEUROSCI)

Publisher: Elsevier

Journal description

The breadth of subject areas that fall into the classification of Neuroscience is possibly the widest in the biomedical sciences. As a results, researchers, students and teachers need access to a source of articles that summarise topics of interest outside their own specialities. Trends in Neurosciences (TINS) fulfils that need.In over twenty years TINS has emerged as the leading current awareness journal in the neurosciences (#1 monthly review journal in the ISI SCI Journals Citation Reports® 1996; Impact Factor, 17.755), publishing succinct and readable articles in a monthly magazine format. Short, focused topical reviews make up the core of each issue. News items, meeting reports, commentaries, letters and the most extensive range of neuroscience book reviews are also published, with occasional centrefolds and special thematic issues adding to the variety.The importance of the interface between basic research and clinical applications is emphasised by a regular column reporting on recent advances in our understanding of the general biology of neurological disorders.

Current impact factor: 13.56

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 13.555
2013 Impact Factor 12.902
2012 Impact Factor 13.582
2011 Impact Factor 14.235
2010 Impact Factor 13.32
2009 Impact Factor 12.794
2008 Impact Factor 12.817
2007 Impact Factor 12.479
2006 Impact Factor 13.494
2005 Impact Factor 14.325
2004 Impact Factor 14.794
2003 Impact Factor 12.631
2002 Impact Factor 14.474
2001 Impact Factor 16.475
2000 Impact Factor 17.417
1999 Impact Factor 19.925
1998 Impact Factor 18.463
1997 Impact Factor 17.084

Impact factor over time

Impact factor

Additional details

5-year impact 14.70
Cited half-life >10.0
Immediacy index 2.44
Eigenfactor 0.03
Article influence 6.26
Website Trends in Neurosciences website
Other titles Trends in neurosciences (Monthly), Trends in neurosciences, TINS
ISSN 0166-2236
OCLC 4124768
Material type Periodical, Internet resource
Document type Journal / Magazine / Newspaper, Internet Resource

Publisher details


  • Pre-print
    • Author cannot archive a pre-print version
  • Post-print
    • Author cannot archive a post-print version
  • Restrictions
    • 12 months embargo
  • Conditions
    • On non-commercial hosting platforms including institutional repository
    • Published source must be acknowledged
    • Must link to journal homepage with DOI
    • Publisher's version/PDF cannot be used
    • Publisher last reviewed on 05/08/2015
    • 'Elsevier (Cell Press)' is an imprint of 'Elsevier'
  • Classification
    ​ white

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: In the neocortex, different types of excitatory and inhibitory neurons connect to one another following a detailed blueprint, defining functionally-distinct subnetworks, whose activity and modulation underlie complex cognitive functions. We review the cell-autonomous plasticity of perisomatic inhibition onto principal excitatory neurons. We propose that the tendency of different cortical layers to exhibit depression or potentiation of perisomatic inhibition is dictated by the specific identities of principal neurons (PNs). These are mainly defined by their projection targets and by their preference to be innervated by specific perisomatic-targeting basket cell types. Therefore, principal neurons responsible for relaying information to subcortical nuclei are differentially inhibited and show specific forms of plasticity compared to other PNs that are specialized in more associative functions. Copyright © 2015 Elsevier Ltd. All rights reserved.
    Trends in Neurosciences 08/2015; DOI:10.1016/j.tins.2015.07.008
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    ABSTRACT: Astrocytes have emerged as important partners of neurons in information processing. Important progress has been made in the past two decades in understanding the role of astrocytes in the generation of neuron-astrocyte network outputs resulting in behavior. We review evidence for astrocyte involvement across four different behavioral domains: cognition, emotion, motor, and sensory processing. Accumulating evidence from animal models has provided a wealth of data that largely supports a direct involvement of astrocytes on diverse aspects of behavior. The development of tools for selectively controlling the temporal and spatial properties of astrocyte activity will help to consolidate our knowledge of the mechanisms underlying this involvement. Copyright © 2015 Elsevier Ltd. All rights reserved.
    Trends in Neurosciences 08/2015; DOI:10.1016/j.tins.2015.07.006
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    ABSTRACT: The past two decades have witnessed a rise in the 'NMDA receptor hypofunction' hypothesis for schizophrenia, a devastating disorder that affects around 1% of the population worldwide. A variety of presynaptic, postsynaptic, and regulatory proteins involved in glutamatergic signaling have thus been proposed as potential therapeutic targets. This review focuses on positive allosteric modulation of metabotropic glutamate 2 receptors (mGlu2Rs) and discusses how recent preclinical epigenetic data may provide a molecular explanation for the discrepant results of clinical studies, further stimulating the field to exploit the promise of mGlu2R as a target for schizophrenia treatment. Copyright © 2015. Published by Elsevier Ltd.
    Trends in Neurosciences 07/2015; 38(8). DOI:10.1016/j.tins.2015.06.002
  • Trends in Neurosciences 06/2015; 38(7). DOI:10.1016/j.tins.2015.05.002
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    ABSTRACT: Tau is a microtubule-associated-protein that is sorted into neuronal axons in physiological conditions. In Alzheimer disease (AD) and other tauopathies, Tau sorting mechanisms fail and Tau becomes missorted into the somatodendritic compartment. In AD, aberrant amyloid-β (Aβ) production might trigger Tau missorting. The physiological axonal sorting of Tau depends on the developmental stage of the neuron, the phosphorylation state of Tau and the microtubule cytoskeleton. Disease-associated missorting of Tau is connected to increased phosphorylation and aggregation of Tau, and impaired microtubule interactions. Disease-causing mechanisms involve impaired transport, aberrant kinase activation, non-physiological interactions of Tau, and prion-like spreading. In this review we focus on the physiological and pathological (mis)sorting of Tau, the underlying mechanisms, and effects in disease.
    Trends in Neurosciences 12/2014; 37(12). DOI:10.1016/j.tins.2014.08.004
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    ABSTRACT: Unlike the nonexcitable cell membranes that are ubiquitous in all domains of life, excitable membranes are found almost exclusively in animal organisms (Protozoa and Metazoa). Their transient permeability to ion flow makes possible the rapid detection of, and response to, external stimuli, and results in the phenomena that most clearly distinguish fauna from flora: perception, cognition, and motor activity. Interestingly, all known forms of membrane excitability are a consequence of one unique mechanism: the influx of positively charged ions into the normally alkaline cytoplasm. Here, we suggest that the sudden reversal of the membrane potential during the sensory potential and the action potential is an electrostatic disturbance of homeostasis that is the necessary first step in the processes of ‘sentience’ and ‘irritability’.
    Trends in Neurosciences 12/2014; 37(12). DOI:10.1016/j.tins.2014.07.011
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    ABSTRACT: The use of autism as a diagnostic category guiding translational research is fraught with so many problems that the validity of research conclusions is suspect. Neuroscientists would benefit from attending to nosological difficulties to formulate meaningful research bridging basic biological systems and human disease. I propose a diagnostic schema that could translate more efficiently between the clinical and the neuroscience perspective as a step to improve the effectiveness of this type of research. Copyright © 2014 Elsevier Ltd. All rights reserved.
    Trends in Neurosciences 11/2014; 37(12). DOI:10.1016/j.tins.2014.10.003
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    ABSTRACT: Chronic microinflammation is a hallmark of many aging-related neurodegenerative diseases as well as metabolic syndrome-driven diseases. Recent research indicates that chronic caloric excess can lead to hypothalamic microinflammation, which in turn participates in the development and progression of metabolic syndrome disorders such as obesity, glucose intolerance, and hypertension. Additionally, it was recently shown that increasing age after young adulthood can cause hypothalamic microinflammation independently of nutritional status, mediating a central mechanism of systemic aging. Taken together, these findings suggest that the hypothalamus has a fundamental role, via hypothalamic microinflammation, in translating overnutrition and aging into complex outcomes. Here we summarize recent work and suggest a conceptual model in which hypothalamic microinflammation is a common mediator of metabolic syndrome and aging. Copyright © 2014 Elsevier Ltd. All rights reserved.
    Trends in Neurosciences 11/2014; 38(1). DOI:10.1016/j.tins.2014.10.002
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    ABSTRACT: Long-term depression (LTD) of the efficacy of synaptic transmission is now recognized as an important mechanism for the regulation of information storage and the control of actions, as well as for synapse, neuron, and circuit development. Studies of LTD mechanisms have focused mainly on postsynaptic AMPA-type glutamate receptor trafficking. However, the focus has now expanded to include presynaptically expressed plasticity, the predominant form being initiated by presynaptically expressed Gi/o-coupled metabotropic receptor (Gi/o-GPCR) activation. Several forms of LTD involving activation of different presynaptic Gi/o-GPCRs as a ‘common pathway’ are described. We review here the literature on presynaptic Gi/o-GPCR-mediated LTD, discuss known mechanisms, gaps in our knowledge, and evaluate whether all Gi/o-GPCRs are capable of inducing presynaptic LTD.
    Trends in Neurosciences 11/2014; 37(11). DOI:10.1016/j.tins.2014.07.010
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    ABSTRACT: Stem cell technologies have created new opportunities to generate unlimited numbers of human neurons in the lab and study neurodegenerative disorders such as amyotrophic lateral sclerosis (ALS) and spinal muscular atrophy (SMA). Although some disease hallmarks have been reported in patient-derived stem cell models, it is proving more difficult to recapitulate the full phenotypic extent of these disorders. The problem with these stem cell models lies in the disparity between the advanced age of onset of neurodegenerative disorders and the embryonic nature of the in vitro derived cell types. In this review we discuss experimental methods of in vitro aging of neural cell types as a means to elicit late-onset symptoms in induced pluripotent stem cell (iPSC) models of neurodegenerative disease.
    Trends in Neurosciences 11/2014; 37(11). DOI:10.1016/j.tins.2014.07.008