Example of Neurotoxicity Research format
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Example of Neurotoxicity Research format Example of Neurotoxicity Research format Example of Neurotoxicity Research format Example of Neurotoxicity Research format Example of Neurotoxicity Research format Example of Neurotoxicity Research format Example of Neurotoxicity Research format Example of Neurotoxicity Research format Example of Neurotoxicity Research format Example of Neurotoxicity Research format Example of Neurotoxicity Research format Example of Neurotoxicity Research format Example of Neurotoxicity Research format Example of Neurotoxicity Research format Example of Neurotoxicity Research format Example of Neurotoxicity Research format Example of Neurotoxicity Research format Example of Neurotoxicity Research format
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Example of Neurotoxicity Research format Example of Neurotoxicity Research format Example of Neurotoxicity Research format Example of Neurotoxicity Research format Example of Neurotoxicity Research format Example of Neurotoxicity Research format Example of Neurotoxicity Research format Example of Neurotoxicity Research format Example of Neurotoxicity Research format Example of Neurotoxicity Research format Example of Neurotoxicity Research format Example of Neurotoxicity Research format Example of Neurotoxicity Research format Example of Neurotoxicity Research format Example of Neurotoxicity Research format Example of Neurotoxicity Research format Example of Neurotoxicity Research format Example of Neurotoxicity Research format
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Neurotoxicity Research — Template for authors

Publisher: Springer
Categories Rank Trend in last 3 yrs
Toxicology #33 of 122 up up by 6 ranks
Neuroscience (all) #41 of 110 up up by 10 ranks
journal-quality-icon Journal quality:
Good
calendar-icon Last 4 years overview: 582 Published Papers | 3239 Citations
indexed-in-icon Indexed in: Scopus
last-updated-icon Last updated: 05/06/2020
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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.

2.992

10% from 2018

Impact factor for Neurotoxicity Research from 2016 - 2019
Year Value
2019 2.992
2018 3.311
2017 3.186
2016 2.942
graph view Graph view
table view Table view

5.6

10% from 2019

CiteRatio for Neurotoxicity Research from 2016 - 2020
Year Value
2020 5.6
2019 5.1
2018 4.4
2017 4.7
2016 5.7
graph view Graph view
table view Table view

insights Insights

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

insights Insights

  • CiteRatio of this journal has increased by 10% 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.

0.923

4% from 2019

SJR for Neurotoxicity Research from 2016 - 2020
Year Value
2020 0.923
2019 0.889
2018 0.941
2017 1.063
2016 1.142
graph view Graph view
table view Table view

0.877

12% from 2019

SNIP for Neurotoxicity Research from 2016 - 2020
Year Value
2020 0.877
2019 0.785
2018 0.812
2017 0.8
2016 0.828
graph view Graph view
table view Table view

insights Insights

  • SJR of this journal has increased by 4% in last years.
  • This journal’s SJR is in the top 10 percentile category.

insights Insights

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

Neurotoxicity Research

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Springer

Neurotoxicity Research

Neurotoxicity Research is an international, interdisciplinary broad-based journal for reporting both basic and clinical research on classical neurotoxicity effects and mechanisms associated with neurodegeneration, necrosis, neuronal apoptosis, nerve regeneration, neurotrophin ...... Read More

Toxicology

General Neuroscience

Pharmacology, Toxicology and Pharmaceutics

i
Last updated on
05 Jun 2020
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ISSN
1029-8428
i
Impact Factor
Medium - 0.99
i
Open Access
No
i
Sherpa RoMEO Archiving Policy
Green faq
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Plagiarism Check
Available via Turnitin
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Endnote Style
Download Available
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Bibliography Name
SPBASIC
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Citation Type
Author Year
(Blonder et al, 1982)
i
Bibliography Example
Beenakker CWJ (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: 10.1007/BF03033808
Dopamine and Reward: The Anhedonia Hypothesis 30 years on
Roy A. Wise1
01 Oct 2008 - Neurotoxicity Research

Abstract:

The anhedonia hypothesis — that brain dopamine plays a critical role in the subjective pleasure associated with positive rewards — was intended to draw the attention of psychiatrists to the growing evidence that dopamine plays a critical role in the objective reinforcement and incentive motivation associated with food and wat... The anhedonia hypothesis — that brain dopamine plays a critical role in the subjective pleasure associated with positive rewards — was intended to draw the attention of psychiatrists to the growing evidence that dopamine plays a critical role in the objective reinforcement and incentive motivation associated with food and water, brain stimulation reward, and psychomotor stimulant and opiate reward. The hypothesis called to attention the apparent paradox that neuroleptics, drugs used to treat a condition involving anhedonia (schizophrenia), attenuated in laboratory animals the positive reinforcement that we normally associate with pleasure. The hypothesis held only brief interest for psychiatrists, who pointed out that the animal studies reflected acute actions of neuroleptics whereas the treatment of schizophrenia appears to result from neuroadaptations to chronic neuroleptic administration, and that it is the positive symptoms of schizophrenia that neuroleptics alleviate, rather than the negative symptoms that include anhedonia. Perhaps for these reasons, the hypothesis has had minimal impact in the psychiatric literature. Despite its limited heuristic value for the understanding of schizophrenia, however, the anhedonia hypothesis has had major impact on biological theories of reinforcement, motivation, and addiction. Brain dopamine plays a very important role in reinforcement of response habits, conditioned preferences, and synaptic plasticity in cellular models of learning and memory. The notion that dopamine plays a dominant role in reinforcement is fundamental to the psychomotor stimulant theory of addiction, to most neuroadaptation theories of addiction, and to current theories of conditioned reinforcement and reward prediction. Properly understood, it is also fundamental to recent theories of incentive motivation. read more read less

Topics:

Anhedonia (60%)60% related to the paper, Addiction (58%)58% related to the paper, Brain stimulation reward (52%)52% related to the paper, Pleasure (50%)50% related to the paper
540 Citations
Journal Article DOI: 10.1007/BF03033137
Dopamine- or L-DOPA-induced neurotoxicity: the role of dopamine quinone formation and tyrosinase in a model of Parkinson's disease.
Masato Asanuma1, Ikuko Miyazaki1, Norio Ogawa1
01 Jan 2003 - Neurotoxicity Research

Abstract:

Dopamine (DA)- or L-dihydroxyphenylalanine-(L-DOPA-) induced neurotoxicity is thought to be involved not only in adverse reactions induced by long-term L-DOPA therapy but also in the pathogenesis of Parkinson's disease. Numerous in vitro and in vivo studies concerning DA- or L-DOPA-induced neurotoxicity have been reported in ... Dopamine (DA)- or L-dihydroxyphenylalanine-(L-DOPA-) induced neurotoxicity is thought to be involved not only in adverse reactions induced by long-term L-DOPA therapy but also in the pathogenesis of Parkinson's disease. Numerous in vitro and in vivo studies concerning DA- or L-DOPA-induced neurotoxicity have been reported in recent decades. The reactive oxygen or nitrogen species generated in the enzymatical oxidation or auto-oxidation of an excess amount of DA induce neuronal damage and/or apoptotic or non-apoptotic cell death; the DA-induced damage is prevented by various intrinsic and extrinsic antioxidants. DA and its metabolites containing two hydroxyl residues exert cytotoxicity in dopaminergic neuronal cells mainly due to the generation of highly reactive DA and DOPA quinones which are dopaminergic neuron-specific cytotoxic molecules. DA and DOPA quinones may irreversibly alter protein function through the formation of 5-cysteinyl-catechols on the proteins. For example, the formation of DA quinone-alpha-synuclein consequently increases cytotoxic protofibrils and the covalent modification of tyrosine hydroxylase by DA quinones. The melanin-synthetic enzyme tyrosinase in the brain may rapidly oxidize excess amounts of cytosolic DA and L-DOPA, thereby preventing slowly progressive cell damage by auto-oxidation of DA, thus maintainng DA levels. Since tyrosinase also possesses catecholamine-synthesizing activity in the absence of tyrosine hydroxylase (TH), the double-edged synthesizing and oxidizing functions of tyrosinase in the dopaminergic system suggest its potential for application in the synthesis of DA, instead of TH in the degeneration of dopaminergic neurons, and in the normalization of abnormal DA turnover in the long-term L-DOPA-treated Parkinson's disease patients. read more read less

Topics:

Dopaminergic (58%)58% related to the paper, Tyrosine hydroxylase (57%)57% related to the paper, Dopamine (54%)54% related to the paper, Tyrosinase (53%)53% related to the paper, Neurotoxicity (53%)53% related to the paper
473 Citations
Journal Article DOI: 10.1007/BF03033565
The 6-hydroxydopamine model of Parkinson's disease.
Nicola Simola1, Micaela Morelli, Anna R. Carta1
01 Apr 2007 - Neurotoxicity Research

Abstract:

The neurotoxin 6-hydroxydopamine (6-OHDA) continues to constitute a valuable topical tool used chiefly in modeling Parkinson’s disease in the rat. The classical method of intracerebral infusion of 6-OHDA, involving a massive destruction of nigrostriatal dopaminergic neurons, is largely used to investigate motor and biochemica... The neurotoxin 6-hydroxydopamine (6-OHDA) continues to constitute a valuable topical tool used chiefly in modeling Parkinson’s disease in the rat. The classical method of intracerebral infusion of 6-OHDA, involving a massive destruction of nigrostriatal dopaminergic neurons, is largely used to investigate motor and biochemical dysfunctions in Parkinson’s disease. Subsequently, more subtle models of partial dopaminergic degeneration have been developed with the aim of revealing finer motor deficits. The present review will examine the main features of 6-OHDA models, namely the mechanisms of neurotoxin-induced neurodegeneration as well as several behavioural deficits and motor dysfunctions, including the priming model, modeled by this means. An overview of the most recent morphological and biochemical findings obtained with the 6-OHDA model will also be provided, particular attention being focused on the newly investigated intracellular mechanisms at the striatal level (e.g., A2A and NMDA receptors, PKA, CaMKII, ERK kinases, as well as immediate early genes, GAD67 and peptides). Thanks to studies performed in the 6-OHDA model, all these mechanisms have now been hypothesised to represent the site of pathological dysfunction at cellular level in Parkinson’s disease. read more read less

Topics:

Neurodegeneration (55%)55% related to the paper, Parkinson's disease (54%)54% related to the paper, Hydroxydopamine (53%)53% related to the paper
370 Citations
Journal Article DOI: 10.1007/BF03033567
Neurotoxicity of substituted amphetamines: molecular and cellular mechanisms.
Jean Lud Cadet1, Irina N. Krasnova1, Subramaniam Jayanthi1, Johnalyn Lyles1
01 Apr 2007 - Neurotoxicity Research

Abstract:

The amphetamines, including amphetamine (AMPH), methamphetamine (METH) and 3,4-methylenedioxymethamphetamine (MDMA), are among abused drugs in the US and throughout the world. Their abuse is associated with severe neurologic and psychiatric adverse events including the development of psychotic states. These neuropsychiatric c... The amphetamines, including amphetamine (AMPH), methamphetamine (METH) and 3,4-methylenedioxymethamphetamine (MDMA), are among abused drugs in the US and throughout the world. Their abuse is associated with severe neurologic and psychiatric adverse events including the development of psychotic states. These neuropsychiatric complications might, in part, be related to drug-induced neurotoxic effects, which include damage to dopaminergic and serotonergic terminals, neuronal apoptosis, as well as activated astroglial and microglial cells in the brain. The purpose of the present review is to summarize the toxic effects of AMPH, METH and MDMA. The paper also presents some of the factors that are thought to underlie this toxicity. These include oxidative stress, hyperthermia, excitotoxicity and various apoptotic pathways. Better understanding of the cellular and molecular mechanisms involved in their toxicity should help to generate modern therapeutic approaches to prevent or attenuate the long-term consequences of amphetamine use disorders in humans. read more read less

Topics:

MDMA (54%)54% related to the paper, Meth- (54%)54% related to the paper, Methamphetamine (53%)53% related to the paper, Neurotoxicity Syndrome (52%)52% related to the paper, Neurotoxicity (51%)51% related to the paper
278 Citations
Journal Article DOI: 10.1007/BF03033289
Intraneuronal dopamine-quinone synthesis: a review.
David Sulzer1, Luigi Zecca1
01 Sep 1999 - Neurotoxicity Research

Abstract:

Dopamine-quinone is synthesized by oxidation of the catechol ring of dopamine. If this occurs within the neuronal cytosol, the quinone may react with cytosolic components, particularly with cysteine residues. In contrast, if quinone is produced within neuronal lysosomes it may provide the fundamental building block for neurom... Dopamine-quinone is synthesized by oxidation of the catechol ring of dopamine. If this occurs within the neuronal cytosol, the quinone may react with cytosolic components, particularly with cysteine residues. In contrast, if quinone is produced within neuronal lysosomes it may provide the fundamental building block for neuromelanin. Since the population of neurons that die in Parkinson's disease are those that display obvious intralysosomal neuromelanin and since cytosolic dopamine-dependent oxyradical formation may underlie methamphetamine toxicity and other specific forms of neurodegeneration in dopaminergic neurons, it is important to elucidate the pathways leading to production of dopamine-quinone. Here we review pathways by which intracellular catechols may be oxidized to quinones, either enzymatically or via reduction of ferric iron or other metals. These metabolites can be adduced by cysteine, could underlie aberrant metabolism and ubiquitination pathways, may induce Lewy body formation, and mediate the synthesis of hydroxyl radical and oxyradical species. Finally, we suggest that by accumulating excess cytosolic catecholamine, neuromelanin synthesis may safely sequester quinones that would otherwise be produced in the neuronal cytosol. read more read less

Topics:

Neuromelanin (61%)61% related to the paper, Population (51%)51% related to the paper, Dopaminergic (51%)51% related to the paper, Substantia nigra (50%)50% related to the paper
270 Citations
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13. What is Sherpa RoMEO Archiving Policy for Neurotoxicity Research?

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 Neurotoxicity Research. 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 Neurotoxicity Research?

The 5 most common citation types in order of usage for Neurotoxicity Research 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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