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Example of Frontiers in Molecular Neuroscience format Example of Frontiers in Molecular Neuroscience format Example of Frontiers in Molecular Neuroscience format Example of Frontiers in Molecular Neuroscience format Example of Frontiers in Molecular Neuroscience format Example of Frontiers in Molecular Neuroscience format Example of Frontiers in Molecular Neuroscience format Example of Frontiers in Molecular Neuroscience format Example of Frontiers in Molecular Neuroscience format Example of Frontiers in Molecular Neuroscience format Example of Frontiers in Molecular Neuroscience format Example of Frontiers in Molecular Neuroscience format Example of Frontiers in Molecular Neuroscience format Example of Frontiers in Molecular Neuroscience format
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Example of Frontiers in Molecular Neuroscience format Example of Frontiers in Molecular Neuroscience format Example of Frontiers in Molecular Neuroscience format Example of Frontiers in Molecular Neuroscience format Example of Frontiers in Molecular Neuroscience format Example of Frontiers in Molecular Neuroscience format Example of Frontiers in Molecular Neuroscience format Example of Frontiers in Molecular Neuroscience format Example of Frontiers in Molecular Neuroscience format Example of Frontiers in Molecular Neuroscience format Example of Frontiers in Molecular Neuroscience format Example of Frontiers in Molecular Neuroscience format Example of Frontiers in Molecular Neuroscience format Example of Frontiers in Molecular Neuroscience format
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open access Open Access

Frontiers in Molecular Neuroscience — Template for authors

Publisher: Frontiers Media
Categories Rank Trend in last 3 yrs
Molecular Biology #75 of 382 up up by 112 ranks
Cellular and Molecular Neuroscience #19 of 88 up up by 38 ranks
journal-quality-icon Journal quality:
High
calendar-icon Last 4 years overview: 1414 Published Papers | 11906 Citations
indexed-in-icon Indexed in: Scopus
last-updated-icon Last updated: 18/07/2020
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Springer

Quality:  
Good
CiteRatio: 5.3
SJR: 1.748
SNIP: 1.079

Journal Performance & Insights

CiteRatio

SCImago Journal Rank (SJR)

Source Normalized Impact per Paper (SNIP)

A measure of average citations received per peer-reviewed paper published in the journal.

Measures weighted citations received by the journal. Citation weighting depends on the categories and prestige of the citing journal.

Measures actual citations received relative to citations expected for the journal's category.

8.4

45% from 2019

CiteRatio for Frontiers in Molecular Neuroscience from 2016 - 2020
Year Value
2020 8.4
2019 5.8
2018 4.1
2017 4.5
2016 6.1
graph view Graph view
table view Table view

1.989

7% from 2019

SJR for Frontiers in Molecular Neuroscience from 2016 - 2020
Year Value
2020 1.989
2019 1.851
2018 1.844
2017 2.128
2016 2.59
graph view Graph view
table view Table view

1.224

25% from 2019

SNIP for Frontiers in Molecular Neuroscience from 2016 - 2020
Year Value
2020 1.224
2019 0.976
2018 0.92
2017 1.003
2016 1.052
graph view Graph view
table view Table view

insights Insights

  • CiteRatio of this journal has increased by 45% in last years.
  • This journal’s CiteRatio is in the top 10 percentile category.

insights Insights

  • SJR of this journal has increased by 7% in last years.
  • This journal’s SJR is in the top 10 percentile category.

insights Insights

  • SNIP of this journal has increased by 25% in last years.
  • This journal’s SNIP is in the top 10 percentile category.

Frontiers in Molecular Neuroscience

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Frontiers Media

Frontiers in Molecular Neuroscience

Approved by publishing and review experts on SciSpace, this template is built as per for Frontiers in Molecular Neuroscience formatting guidelines as mentioned in Frontiers Media author instructions. The current version was created on 18 Jul 2020 and has been used by 698 authors to write and format their manuscripts to this journal.

Neuroscience

i
Last updated on
18 Jul 2020
i
ISSN
1662-5099
i
Impact Factor
Medium - 0.667
i
Open Access
No
i
Sherpa RoMEO Archiving Policy
Green faq
i
Plagiarism Check
Available via Turnitin
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Endnote Style
Download Available
i
Bibliography Name
frontiersinSCNS_ENG_HUMS
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Citation Type
Numbered
[25]
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Bibliography Example
Blonder GE, Tinkham M, Klapwijk TM. Transition from metallic to tunneling regimes in superconducting microconstrictions: Excess current, charge imbalance, and supercurrent conversion. Phys. Rev. B 25 (1982) 4515–4532.

Top papers written in this journal

open accessOpen access Journal Article DOI: 10.3389/FNMOL.2011.00051
PI3K/AKT/mTOR Pathway in Angiogenesis
Jayashree Karar1, Amit Maity1

Abstract:

The phosphatidylinositol 3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) pathway is activated in the majority of human cancers. This pathway is known to play a key role in numerous cellular functions including proliferation, adhesion, migration, invasion, metabolism, and survival, but in the current review we focus o... The phosphatidylinositol 3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) pathway is activated in the majority of human cancers. This pathway is known to play a key role in numerous cellular functions including proliferation, adhesion, migration, invasion, metabolism, and survival, but in the current review we focus on its role in angiogenesis. PI3K activation may occur via RAS mutation, loss of phosphatase and tensin homolog (PTEN), or by increased expression of growth factor receptors such as epidermal growth factor receptor. There is a connection between the PI3K pathway and angiogenesis. Hypoxia leads to HIF-1α stabilization and is a major stimulus for increased vascular endothelial growth factor (VEGF) production by tumor cells. However, activation of the PI3K/AKT pathway in tumor cells can also increase VEGF secretion, both by hypoxia-inducible factor 1 (HIF-1) dependent and independent mechanisms. The PI3K/AKT pathway also modulates the expression of other angiogenic factors such as nitric oxide and angiopoietins. Numerous inhibitors targeting the PI3K/AKT/mTOR pathway have been developed, and these agents have been shown to decrease VEGF secretion and angiogenesis. The effect of these inhibitors on tumor vasculature can be difficult to predict. The vasculature of tumors is aberrant, leading to sluggish bloodflow and elevated interstitial blood pressure, which can be perpetuated by the high levels of VEGF. Hence, decreasing VEGF expression can paradoxically lead to vascular normalization and improved bloodflow in some tumors. In addition to its importance in cancer, the PI3K pathway also plays an essential role in the formation of normal blood vessels during development. Embryos with kinase-dead p110α catalytic subunit of PI3K develop vascular defects. Stimulation of endothelial cells by VEGF leads to activation of the PI3K pathway within these cells, which is important for cell migration. Sustained endothelial activation of AKT1 has been shown to induce the formation of structurally abnormal blood vessels that recapitulate the aberrations of tumor vessels. Hence, the PI3K pathway plays an important role in regulating angiogenesis both in normal tissues and in cancers. read more read less

Topics:

PI3K/AKT/mTOR pathway (69%)69% related to the paper, Angiogenesis (63%)63% related to the paper, Vascular endothelial growth factor (62%)62% related to the paper, Protein kinase B (61%)61% related to the paper, PTEN (57%)57% related to the paper
965 Citations
open accessOpen access Journal Article DOI: 10.3389/NEURO.02.001.2010
A simple role for BDNF in learning and memory
Carlos Cunha1, Ricardo Brambilla2, Kerrie L. Thomas3

Abstract:

Since its discovery almost three decades ago, the secreted neurotrophin brain-derived neurotrophic factor (BDNF) has been firmly implicated in the differentiation and survival of neurons of the CNS. More recently, BDNF has also emerged as an important regulator of synaptogenesis and synaptic plasticity mechanisms underlying l... Since its discovery almost three decades ago, the secreted neurotrophin brain-derived neurotrophic factor (BDNF) has been firmly implicated in the differentiation and survival of neurons of the CNS. More recently, BDNF has also emerged as an important regulator of synaptogenesis and synaptic plasticity mechanisms underlying learning and memory in the adult CNS. In this review we will discuss our knowledge about the multiple intracellular signalling pathways activated by BDNF, and the role of this neurotrophin in long-term synaptic plasticity and memory formation as well as in synaptogenesis. We will show that maturation of BDNF, its cellular localisation and its ability to regulate both excitatory and inhibitory synapses in the CNS may result in conflicting alterations in synaptic plasticity and memory formation. Lack of a precise knowledge about the mechanisms by which BDNF influences higher cognitive functions and complex behaviours may constitute a severe limitation in the possibility to devise BDNF-based therapeutics for human disorders of the CNS. read more read less

Topics:

Synaptic plasticity (55%)55% related to the paper, Synaptogenesis (55%)55% related to the paper, Neurotrophic factors (51%)51% related to the paper
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673 Citations
open accessOpen access Journal Article DOI: 10.3389/FNMOL.2013.00002
Genetically encoded calcium indicators for multi-color neural activity imaging and combination with optogenetics.

Abstract:

Genetically encoded calcium indicators (GECIs) are powerful tools for systems neuroscience. Here we describe red, single-wavelength GECIs, "RCaMPs," engineered from circular permutation of the thermostable red fluorescent protein mRuby. High-resolution crystal structures of mRuby, the red sensor RCaMP, and the recently publis... Genetically encoded calcium indicators (GECIs) are powerful tools for systems neuroscience. Here we describe red, single-wavelength GECIs, "RCaMPs," engineered from circular permutation of the thermostable red fluorescent protein mRuby. High-resolution crystal structures of mRuby, the red sensor RCaMP, and the recently published red GECI R-GECO1 give insight into the chromophore environments of the Ca(2+)-bound state of the sensors and the engineered protein domain interfaces of the different indicators. We characterized the biophysical properties and performance of RCaMP sensors in vitro and in vivo in Caenorhabditis elegans, Drosophila larvae, and larval zebrafish. Further, we demonstrate 2-color calcium imaging both within the same cell (registering mitochondrial and somatic [Ca(2+)]) and between two populations of cells: neurons and astrocytes. Finally, we perform integrated optogenetics experiments, wherein neural activation via channelrhodopsin-2 (ChR2) or a red-shifted variant, and activity imaging via RCaMP or GCaMP, are conducted simultaneously, with the ChR2/RCaMP pair providing independently addressable spectral channels. Using this paradigm, we measure calcium responses of naturalistic and ChR2-evoked muscle contractions in vivo in crawling C. elegans. We systematically compare the RCaMP sensors to R-GECO1, in terms of action potential-evoked fluorescence increases in neurons, photobleaching, and photoswitching. R-GECO1 displays higher Ca(2+) affinity and larger dynamic range than RCaMP, but exhibits significant photoactivation with blue and green light, suggesting that integrated channelrhodopsin-based optogenetics using R-GECO1 may be subject to artifact. Finally, we create and test blue, cyan, and yellow variants engineered from GCaMP by rational design. This engineered set of chromatic variants facilitates new experiments in functional imaging and optogenetics. read more read less

Topics:

GCaMP (62%)62% related to the paper, Calcium imaging (58%)58% related to the paper, Optogenetics (56%)56% related to the paper, Channelrhodopsin (55%)55% related to the paper
View PDF
657 Citations
open accessOpen access Journal Article DOI: 10.3389/FNMOL.2015.00077
NF-kappaB Signaling Pathways in Neurological Inflammation: A Mini Review.
Ruey-Horng Shih1, Chen-Yu Wang2, Chuen-Mao Yang2

Abstract:

The NF-κB (nuclear factor κ-light-chain-enhancer of activated B cells) transcription factor family is a pleiotropic regulator of many cellular signaling pathways, providing a mechanism for the cells in response to a wide variety of stimuli linking to inflammation. The stimulated cells will be regulated by not only the canonic... The NF-κB (nuclear factor κ-light-chain-enhancer of activated B cells) transcription factor family is a pleiotropic regulator of many cellular signaling pathways, providing a mechanism for the cells in response to a wide variety of stimuli linking to inflammation. The stimulated cells will be regulated by not only the canonical but also non-canonical NF-κB pathways. To initiate both of these pathways, IκB-degradation triggers NF-κB release and the nuclear translocated-heterodimer (or homodimer) can associate with the κB sites of promoter to regulate the gene transcriptions. NF-κB ubiquitously expresses in neurons and the constitutive NF-κB activation is associated with processing of neuronal information. NF-κB can regulate the transcription of genes such as chemokines, cytokines, proinflammatory enzymes, adhesion molecules, proinflammatory transcription factors, and other factors to modulate the neuronal survival. In neuronal insult, NF-κB constitutively active in neuron cell bodies can protect neurons against different injuries and regulate the neuronal inflammatory reactions. Besides neurons, NF-κB transcription factors are abundant in glial cells and cerebral blood vessels and the diverse functions of NF-κB also regulate the inflammatory reaction around the neuronal environment. NF-κB transcription factors are abundant in the brain and exhibit diverse functions. Several central nerve system (CNS) diseases are linked to NF-κB activated by inflammatory mediators. The RelA and c-Rel expression produce opposite effects on neuronal survival. Importantly, c-Rel expression in CNS plays a critical role in anti-apoptosis and reduces the age-related behaviors. Moreover, the different subunits of NF-κB dimer formation can modulate the neuroninflammation, neuronal protection, or neurotoxicity. The diverse functions of NF-κB depend on the subunits of the NF-κB dimer-formation which enable us to develop a therapeutic approach to neuroinflammation based on a new concept of inflammation as a strategic tool in neuronal cells. However, the detail role of NF-κB in neuroinflammation, remains to be clarified. In the present article, we provide an updated review of the current state of our knowledge about relationship between NF-κB and neuroinflammation. read more read less

Topics:

Neuroinflammation (56%)56% related to the paper, Neuroprotection (55%)55% related to the paper, Proinflammatory cytokine (55%)55% related to the paper, Transcription factor (54%)54% related to the paper, Cell signaling (52%)52% related to the paper
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596 Citations
open accessOpen access Journal Article DOI: 10.3389/FNMOL.2017.00284
Methods Used to Evaluate Pain Behaviors in Rodents
Jennifer R. Deuis1, Lucie Sam Dvorakova1, Irina Vetter1

Abstract:

Rodents are commonly used to study the pathophysiological mechanisms of pain as studies in humans may be difficult to perform and ethically limited. As pain cannot be directly measured in rodents, many methods that quantify "pain-like" behaviors or nociception have been developed. These behavioral methods can be divided into ... Rodents are commonly used to study the pathophysiological mechanisms of pain as studies in humans may be difficult to perform and ethically limited. As pain cannot be directly measured in rodents, many methods that quantify "pain-like" behaviors or nociception have been developed. These behavioral methods can be divided into stimulus-evoked or non-stimulus evoked (spontaneous) nociception, based on whether or not application of an external stimulus is used to elicit a withdrawal response. Stimulus-evoked methods, which include manual and electronic von Frey, Randall-Selitto and the Hargreaves test, were the first to be developed and continue to be in widespread use. However, concerns over the clinical translatability of stimulus-evoked nociception in recent years has led to the development and increasing implementation of non-stimulus evoked methods, such as grimace scales, burrowing, weight bearing and gait analysis. This review article provides an overview, as well as discussion of the advantages and disadvantages of the most commonly used behavioral methods of stimulus-evoked and non-stimulus-evoked nociception used in rodents. read more read less

Topics:

Nociception assay (60%)60% related to the paper, Nociception (50%)50% related to the paper
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578 Citations
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Frontiers in Molecular Neuroscience format uses frontiersinSCNS_ENG_HUMS citation style.

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Yes, the template is compliant with the Frontiers in Molecular Neuroscience guidelines. Our experts at SciSpace ensure that. If there are any changes to the journal's guidelines, we'll change our algorithm accordingly.

3. Can I cite my article in multiple styles in Frontiers in Molecular Neuroscience?

Of course! We support all the top citation styles, such as APA style, MLA style, Vancouver style, Harvard style, and Chicago style. For example, when you write your paper and hit autoformat, our system will automatically update your article as per the Frontiers in Molecular Neuroscience citation style.

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13. What is Sherpa RoMEO Archiving Policy for Frontiers in Molecular Neuroscience?

SHERPA/RoMEO Database

We extracted this data from Sherpa Romeo to help researchers understand the access level of this journal in accordance with the Sherpa Romeo Archiving Policy for Frontiers in Molecular Neuroscience. The table below indicates the level of access a journal has as per Sherpa Romeo's archiving policy.

RoMEO Colour Archiving policy
Green Can archive pre-print and post-print or publisher's version/PDF
Blue Can archive post-print (ie final draft post-refereeing) or publisher's version/PDF
Yellow Can archive pre-print (ie pre-refereeing)
White Archiving not formally supported
FYI:
  1. Pre-prints as being the version of the paper before peer review and
  2. Post-prints as being the version of the paper after peer-review, with revisions having been made.

14. What are the most common citation types In Frontiers in Molecular Neuroscience?

The 5 most common citation types in order of usage for Frontiers in Molecular Neuroscience are:.

S. No. Citation Style Type
1. Author Year
2. Numbered
3. Numbered (Superscripted)
4. Author Year (Cited Pages)
5. Footnote

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16. Can I download Frontiers in Molecular Neuroscience in Endnote format?

Yes, SciSpace provides this functionality. After signing up, you would need to import your existing references from Word or Bib file to SciSpace. Then SciSpace would allow you to download your references in Frontiers in Molecular Neuroscience Endnote style according to Elsevier guidelines.

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