Example of Developmental Neurobiology format
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Example of Developmental Neurobiology format Example of Developmental Neurobiology format Example of Developmental Neurobiology format Example of Developmental Neurobiology format Example of Developmental Neurobiology format Example of Developmental Neurobiology format
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Example of Developmental Neurobiology format Example of Developmental Neurobiology format Example of Developmental Neurobiology format Example of Developmental Neurobiology format Example of Developmental Neurobiology format Example of Developmental Neurobiology format
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Developmental Neurobiology — Template for authors

Publisher: Wiley
Categories Rank Trend in last 3 yrs
Developmental Neuroscience #4 of 35 up up by 4 ranks
Cellular and Molecular Neuroscience #21 of 88 up up by 18 ranks
journal-quality-icon Journal quality:
High
calendar-icon Last 4 years overview: 262 Published Papers | 2038 Citations
indexed-in-icon Indexed in: Scopus
last-updated-icon Last updated: 21/07/2020
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Related Journals

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Springer

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High
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SJR: 1.582
SNIP: 1.194
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SJR: 1.65
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PLOS

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SJR: 1.594
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Journal Performance & Insights

Impact Factor

CiteRatio

Determines the importance of a journal by taking a measure of frequency with which the average article in a journal has been cited in a particular year.

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

3.935

51% from 2018

Impact factor for Developmental Neurobiology from 2016 - 2019
Year Value
2019 3.935
2018 2.6
2017 2.598
2016 2.972
graph view Graph view
table view Table view

7.8

28% from 2019

CiteRatio for Developmental Neurobiology from 2016 - 2020
Year Value
2020 7.8
2019 6.1
2018 5.3
2017 5.8
2016 4.9
graph view Graph view
table view Table view

insights Insights

  • Impact factor of this journal has increased by 51% in last year.
  • This journal’s impact factor is in the top 10 percentile category.

insights Insights

  • CiteRatio of this journal has increased by 28% in last years.
  • This journal’s CiteRatio is in the top 10 percentile category.

SCImago Journal Rank (SJR)

Source Normalized Impact per Paper (SNIP)

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.

1.716

12% from 2019

SJR for Developmental Neurobiology from 2016 - 2020
Year Value
2020 1.716
2019 1.944
2018 1.475
2017 1.661
2016 1.792
graph view Graph view
table view Table view

0.906

11% from 2019

SNIP for Developmental Neurobiology from 2016 - 2020
Year Value
2020 0.906
2019 0.816
2018 0.715
2017 0.77
2016 0.797
graph view Graph view
table view Table view

insights Insights

  • SJR of this journal has decreased by 12% in last years.
  • This journal’s SJR is in the top 10 percentile category.

insights Insights

  • SNIP of this journal has increased by 11% in last years.
  • This journal’s SNIP is in the top 10 percentile category.
Developmental Neurobiology

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Wiley

Developmental Neurobiology

Developmental Neurobiology (previously the Journal of Neurobiology ) publishes original research articles on development, regeneration, repair and plasticity of the nervous system and on the ontogeny of behavior. High quality contributions in these areas are solicited, with an...... Read More

Neuroscience

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Last updated on
21 Jul 2020
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ISSN
1932-8451
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Impact Factor
High - 1.102
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Open Access
Yes
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Sherpa RoMEO Archiving Policy
Yellow faq
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Plagiarism Check
Available via Turnitin
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Endnote Style
Download Available
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Bibliography Name
apa
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Citation Type
Numbered
[25]
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Bibliography Example
Beenakker, C.W.J. (2006) Specular andreev reflection in graphene.Phys. Rev. Lett., 97 (6), 067 007. URL 10.1103/PhysRevLett.97.067007.

Top papers written in this journal

open accessOpen access Journal Article DOI: 10.1002/DNEU.20853
Three groups of interneurons account for nearly 100% of neocortical GABAergic neurons
Bernardo Rudy1, Gordon Fishell1, Soo Hyun Lee1, Jens Hjerling-Leffler1

Abstract:

An understanding of the diversity of cortical GABAergic interneurons is critical to understand the function of the cerebral cortex. Recent data suggest that neurons expressing three markers, the Ca2+-binding protein parvalbumin (PV), the neuropeptide somatostatin (SST), and the ionotropic serotonin receptor 5HT3a (5HT3aR) acc... An understanding of the diversity of cortical GABAergic interneurons is critical to understand the function of the cerebral cortex. Recent data suggest that neurons expressing three markers, the Ca2+-binding protein parvalbumin (PV), the neuropeptide somatostatin (SST), and the ionotropic serotonin receptor 5HT3a (5HT3aR) account for nearly 100% of neocortical interneurons. Interneurons expressing each of these markers have a different embryological origin. Each group includes several types of interneurons that differ in morphological and electrophysiological properties and likely have different functions in the cortical circuit. The PV group accounts for ∼40% of GABAergic neurons and includes fast spiking basket cells and chandelier cells. The SST group, which represents ∼30% of GABAergic neurons, includes the Martinotti cells and a set of neurons that specifically target layerIV. The 5HT3aR group, which also accounts for ∼30% of the total interneuronal population, is heterogeneous and includes all of the neurons that express the neuropeptide VIP, as well as an equally numerous subgroup of neurons that do not express VIP and includes neurogliaform cells. The universal modulation of these neurons by serotonin and acetylcholine via ionotropic receptors suggests that they might be involved in shaping cortical circuits during specific brain states and behavioral contexts. read more read less

Topics:

Parvalbumin (59%)59% related to the paper, GABAergic (52%)52% related to the paper, Neocortex (52%)52% related to the paper, Population (51%)51% related to the paper, Ionotropic effect (50%)50% related to the paper
1,211 Citations
open accessOpen access Journal Article DOI: 10.1002/DNEU.20758
The role of BDNF and its receptors in depression and antidepressant drug action: Reactivation of developmental plasticity.
Eero Castrén1, Tomi Rantamäki1

Abstract:

Recent evidence suggests that neuronal plasticity plays an important role in the recovery from depression. Antidepressant drugs and electroconvulsive shock treatment increase the expression of several molecules, which are associated with neuronal plasticity, in particular the neurotrophin BDNF and its receptor TrkB. Furthermo... Recent evidence suggests that neuronal plasticity plays an important role in the recovery from depression. Antidepressant drugs and electroconvulsive shock treatment increase the expression of several molecules, which are associated with neuronal plasticity, in particular the neurotrophin BDNF and its receptor TrkB. Furthermore, these treatments increase neurogenesis and synaptic numbers in several brain areas. Conversely, depression, at least in its severe form, is associated with reduced volumes of the hippocampus and prefrontal cortex and in at least some cases these neurodegenerative signs can be attenuated by successful treatment. Such observations suggest a central role for neuronal plasticity in depression and the antidepressant effect, and also implicate BDNF signaling as a mediator of this plasticity. The antidepressant fluoxetine can reactivate developmental-like neuronal plasticity in the adult visual cortex, which, under appropriate environmental guidance, leads to the rewiring of a developmentally dysfunctional neural network. These observations suggest that the simple form of the neurotrophic hypothesis of depression, namely, that deficient levels of neurotrophic support underlies mood disorders and increases in these neurotrophic factors to normal levels brings about mood recovery, may not sufficiently explain the complex process of recovery from depression. This review discusses recent data on the role of BDNF and its receptors in depression and the antidepressant response and suggests a model whereby the effects of antidepressant treatments could be explained by a reactivation of activity-dependent and BDNF-mediated cortical plasticity, which in turn leads to the adjustment of neuronal networks to better adapt to environmental challenges. read more read less

Topics:

Metaplasticity (62%)62% related to the paper, Developmental plasticity (57%)57% related to the paper, Tropomyosin receptor kinase B (55%)55% related to the paper, Neurotrophic factors (55%)55% related to the paper, Neuroplasticity (55%)55% related to the paper
View PDF
784 Citations
open accessOpen access Journal Article DOI: 10.1002/DNEU.20765
Postsynaptic BDNF-TrkB signaling in synapse maturation, plasticity, and disease
Akira Yoshii1, Martha Constantine-Paton2, Martha Constantine-Paton1

Abstract:

Brain-derived neurotrophic factor (BDNF) is a prototypic neurotrophin that regulates diverse developmental events from the selection of neural progenitors to the terminal dendritic differentiation and connectivity of neurons. We focus here on activity-dependent synaptic regulation by BDNF and its receptor, full length TrkB. B... Brain-derived neurotrophic factor (BDNF) is a prototypic neurotrophin that regulates diverse developmental events from the selection of neural progenitors to the terminal dendritic differentiation and connectivity of neurons. We focus here on activity-dependent synaptic regulation by BDNF and its receptor, full length TrkB. BDNF-TrkB signaling is involved in transcription, translation, and trafficking of proteins during various phases of synaptic development and has been implicated in several forms of synaptic plasticity. These functions are carried out by a combination of the three signaling cascades triggered when BDNF binds TrkB: the mitogen-activated protein kinase (MAPK), the phospholipase Cγ (PLC PLCγ), and the phosphatidylinositol 3-kinase (PI3K) pathways. MAPK and PI3K play crucial roles in both translation and/or trafficking of proteins induced by synaptic activity while PLCγ regulates intracellular Ca2+ that can drive transcription via cyclic AMP and a Protein Kinase C. Conversely, the abnormal regulation of BDNF is implicated in various developmental and neurodegenerative diseases that perturb neural development and function. We will discuss the current state of understanding BDNF signaling in the context of synaptic development and plasticity with a focus on the post-synaptic cell and close with the evidence that basic mechanisms of BDNF function still need to be understood in order to effectively treat genetic disruptions of these pathways that cause devastating neurodevelopmental diseases. read more read less

Topics:

Tropomyosin receptor kinase B (62%)62% related to the paper, Tropomyosin receptor kinase A (60%)60% related to the paper, Synaptic plasticity (59%)59% related to the paper, Metaplasticity (59%)59% related to the paper, Brain-derived neurotrophic factor (58%)58% related to the paper
View PDF
611 Citations
open accessOpen access Journal Article DOI: 10.1002/DNEU.20774
Brain-Derived Neurotrophic Factor and the Development of Structural Neuronal Connectivity
Susana Cohen-Cory1, Adhanet H. Kidane1, Nicole J. Shirkey1, Sonya Marshak1

Abstract:

Neurotrophins are growth factors with crucial roles in the developing and mature nervous system. They are initially synthesized as precursor proteins (pro-neurotrophins), which are processed intracellularly to be secreted mostly in a mature, biologically active form (Mowla et al., 1999; Mowla et al., 2001; Matsumoto et al., 2... Neurotrophins are growth factors with crucial roles in the developing and mature nervous system. They are initially synthesized as precursor proteins (pro-neurotrophins), which are processed intracellularly to be secreted mostly in a mature, biologically active form (Mowla et al., 1999; Mowla et al., 2001; Matsumoto et al., 2008; for review see Lu et al., 2005). Pro-neurotrophins can also influence developing and mature neural circuits, and may be released in a developmentally regulated manner (Lee et al., 2001; Lu et al., 2005; Teng et al., 2005; Yang et al., 2009). Neurotrophins bind two classes of membrane receptors, the tropomyosin receptor kinase (Trk) family of receptors and the p75 neurotrophin receptor (p75NTR) (for a review see Chao, 2003). The actions of mature neurotrophins are mediated by the high affinity full-length Trk receptors, which signal through their intrinsic tyrosine kinase activity to promote growth. Trk receptors signal by dimerization of receptor molecules, leading to intracellular phosphorylation and activation of intracellular signaling cascades (Ullrich and Schlessinger, 1990; Jing et al., 1992). Truncated Trk receptors (Trk.T) are splice variants of full-length Trks, which lack the intracellular tyrosine kinase domain, and are thought to act as negative effectors of full-length receptors (Luikart et al., 2003), although they may also have their own signaling properties (Rose et al., 2003; Ohira et al., 2006). The neurotrophins show binding specificity for particular Trk receptors: nerve growth factor (NGF) binds to TrkA, brain-derived neurotrophic factor (BDNF) and neurotrophin 4 (NT4) to TrkB, and neurotrophin 3 (NT3) to TrkC (Chao, 2003). The p75NTR has low affinity for the mature neurotrophins, but can form a complex with Trk receptors to form high affinity binding sites for neurotrophins, enabling the receptor to participate in the stimulation of growth processes (Esposito et al., 2001). Moreover, p75NTR displays high affinity binding with pro-neurotrophins, and induces apoptosis by interacting with sortilin (Lee et al., 2001; Nykjaer et al., 2004). Thus, pro-neurotrophins and mature neurotrophins may utilize distinct receptors to mediate divergent neuronal actions. This review focuses on the actions of mature BDNF, highlighting the role that BDNF plays in the development of synaptic connectivity in the central nervous system (CNS). Evidence supporting presynaptic actions by target-released BDNF, and the influence that BDNF exerts during the structural development of neurons are reviewed here. read more read less

Topics:

Trk receptor (64%)64% related to the paper, Tropomyosin receptor kinase B (60%)60% related to the paper, Low-affinity nerve growth factor receptor (60%)60% related to the paper, Neurotrophin (58%)58% related to the paper, Tropomyosin receptor kinase A (58%)58% related to the paper
View PDF
483 Citations
Journal Article DOI: 10.1002/DNEU.20506
PI3K/Akt and CREB regulate adult neural hippocampal progenitor proliferation and differentiation
Joseph Peltier1, Analeah O'Neill1, David V. Schaffer1

Abstract:

The phosphoinositide 3-OH kinase (PI3K)/Akt pathway has been implicated in regulating several important cellular processes, including apoptosis, survival, proliferation, and metabolism. Using both pharmacological and genetic means, we demonstrate here that PI3K/Akt plays a crucial role in the proliferation of adult hippocampa... The phosphoinositide 3-OH kinase (PI3K)/Akt pathway has been implicated in regulating several important cellular processes, including apoptosis, survival, proliferation, and metabolism. Using both pharmacological and genetic means, we demonstrate here that PI3K/Akt plays a crucial role in the proliferation of adult hippocampal neural progenitor cells. PI3K/Akt transduces intracellular signals from multiple mitogens, including basic fibroblast growth factor (FGF-2), Sonic hedgehog (Shh), and insulin-like growth factor 1 (IGF-1). In addition, retroviral vector-mediated over-expression of wild type Akt increased cell proliferation, while a dominant negative Akt inhibited proliferation. Furthermore, wild type Akt over-expression reduced glial (GFAP) and neuronal (β-tubulin III) marker expression during differentiation, indicating that it inhibits cell differentiation. We also show that activation of the cAMP response element binding protein (CREB), which occurs in cells stimulated by FGF-2, is limited when Akt signaling is inhibited, demonstrating a link between Akt and CREB. Over-expression of wild type CREB increases progenitor proliferation, whereas dominant negative CREB only slightly decreases proliferation. These results indicate that PI3K/Akt signaling integrates extracellular signaling information to promote cellular proliferation and inhibit differentiation in adult neural progenitors. © 2007 Wiley Periodicals, Inc. Develop Neurobiol, 2007. read more read less

Topics:

PI3K/AKT/mTOR pathway (74%)74% related to the paper, Protein kinase B (65%)65% related to the paper, CREB (58%)58% related to the paper, Cellular differentiation (57%)57% related to the paper, Growth factor (55%)55% related to the paper
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398 Citations
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Developmental Neurobiology format uses apa citation style.

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Frequently asked questions

1. Can I write Developmental Neurobiology in LaTeX?

Absolutely not! Our tool has been designed to help you focus on writing. You can write your entire paper as per the Developmental Neurobiology guidelines and auto format it.

2. Do you follow the Developmental Neurobiology guidelines?

Yes, the template is compliant with the Developmental Neurobiology 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 Developmental Neurobiology?

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 Developmental Neurobiology citation style.

4. Can I use the Developmental Neurobiology templates for free?

Sign up for our free trial, and you'll be able to use all our features for seven days. You'll see how helpful they are and how inexpensive they are compared to other options, Especially for Developmental Neurobiology.

5. Can I use a manuscript in Developmental Neurobiology that I have written in MS Word?

Yes. You can choose the right template, copy-paste the contents from the word document, and click on auto-format. Once you're done, you'll have a publish-ready paper Developmental Neurobiology that you can download at the end.

6. How long does it usually take you to format my papers in Developmental Neurobiology?

It only takes a matter of seconds to edit your manuscript. Besides that, our intuitive editor saves you from writing and formatting it in Developmental Neurobiology.

7. Where can I find the template for the Developmental Neurobiology?

It is possible to find the Word template for any journal on Google. However, why use a template when you can write your entire manuscript on SciSpace , auto format it as per Developmental Neurobiology's guidelines and download the same in Word, PDF and LaTeX formats? Give us a try!.

8. Can I reformat my paper to fit the Developmental Neurobiology's guidelines?

Of course! You can do this using our intuitive editor. It's very easy. If you need help, our support team is always ready to assist you.

9. Developmental Neurobiology an online tool or is there a desktop version?

SciSpace's Developmental Neurobiology is currently available as an online tool. We're developing a desktop version, too. You can request (or upvote) any features that you think would be helpful for you and other researchers in the "feature request" section of your account once you've signed up with us.

10. I cannot find my template in your gallery. Can you create it for me like Developmental Neurobiology?

Sure. You can request any template and we'll have it setup within a few days. You can find the request box in Journal Gallery on the right side bar under the heading, "Couldn't find the format you were looking for like Developmental Neurobiology?”

11. What is the output that I would get after using Developmental Neurobiology?

After writing your paper autoformatting in Developmental Neurobiology, you can download it in multiple formats, viz., PDF, Docx, and LaTeX.

12. Is Developmental Neurobiology's impact factor high enough that I should try publishing my article there?

To be honest, the answer is no. The impact factor is one of the many elements that determine the quality of a journal. Few of these factors include review board, rejection rates, frequency of inclusion in indexes, and Eigenfactor. You need to assess all these factors before you make your final call.

13. What is Sherpa RoMEO Archiving Policy for Developmental Neurobiology?

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 Developmental Neurobiology. 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 Developmental Neurobiology?

The 5 most common citation types in order of usage for Developmental Neurobiology are:.

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

15. How do I submit my article to the Developmental Neurobiology?

It is possible to find the Word template for any journal on Google. However, why use a template when you can write your entire manuscript on SciSpace , auto format it as per Developmental Neurobiology's guidelines and download the same in Word, PDF and LaTeX formats? Give us a try!.

16. Can I download Developmental Neurobiology 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 Developmental Neurobiology Endnote style according to Elsevier guidelines.

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