Journal of Neurochemistry
© International Society for Neurochemistry
Edited By: Jörg Schulz
Impact Factor: 3.842
ISI Journal Citation Reports © Ranking: 2015: 71/256 (Neurosciences); 83/289 (Biochemistry & Molecular Biology)
Online ISSN: 1471-4159
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Recently Published Articles
- Serotonin 5-HT7 receptor increases the density of dendritic spines and facilitates synaptogenesis in forebrain neurons
Luisa Speranza, Josephine Labus, Floriana Volpicelli, Daria Guseva, Enza Lacivita, Marcello Leopoldo, Gian Carlo Bellenchi, Umberto di Porzio, Monika Bijata, Carla Perrone-Capano and Evgeni Ponimaskin
Version of Record online: 24 MAR 2017 | DOI: 10.1111/jnc.13962
Serotonin 5-HT7 receptor (5-HT7R) promotes formation of dendritic spines and facilitates synaptogenesis in postnatal cortical and striatal neurons. These morphogenic effects are mediated by cyclin-dependent kinase 5 (Cdk5) and small GTPase Cdc42. Thus, 5-HT7R-mediated structural reorganization during the postnatal development might have a crucial role for the development and plasticity of forebrain areas, and thereby can be implicated in regulation of the higher cognitive functions.
Read the Editorial Highlight for this article on doi: 10.1111/jnc.13981.
- You have free access to this content5-HT7 receptor shapes spinogenesis in cortical and striatal neurons : An Editorial Highlight for ‘Serotonin 5-HT7 receptor increases the density of dendritic spines and facilitates synaptogenesis in forebrain neurons’
Philippe Marin and Alexander Dityatev
Version of Record online: 24 MAR 2017 | DOI: 10.1111/jnc.13981
In this issue of the Journal of Neurochemistry, Speranza et al. demonstrated that 5-HT7 serotonin receptors stimulate neurite outgrowth and spinogenesis of cortical and striatal neurons in agonist-dependent and independent manners. The underlying signalling was found to involve Cdk5 and Cdc42. These data are of potential relevance for the understanding and treatment of neurodevelopmental psychiatric disorders.
- New mechanisms for pain: from neurons to glia; from spinal cord to cortex
Version of Record online: 22 MAR 2017 | DOI: 10.1111/jnc.13985
Cortical neurons in the anterior cingulate cortex (ACC) and insular cortex (IC), as well as somatosensory cortices (S1 and S2), receive nociceptive sensory inputs from the periphery through the spinal cord dorsal horn and several subcortical structures. Sensory inputs also innervate neurons in emotion-related brain areas such as the amygdala. The chemical interactions between neurons and non-neurons, such as glial cells, influence the process and storage of nociceptive information at different levels of the central nervous system, from the spinal cord to the brain.
- Type-I interferons mediate the neuroinflammatory response and neurotoxicity induced by rotenone (pages 75–85)
Bevan S. Main, Moses Zhang, Kate M. Brody, Francis J. Kirby, Peter J. Crack and Juliet M. Taylor
Version of Record online: 22 MAR 2017 | DOI: 10.1111/jnc.13940
We confirm the mitochondrial complex I inhibitor, rotenone induces both a type-1 IFN and pro-inflammatory response (increased TNF-α, IL-1β, IL-6 expression) in primary cultured neurons and mixed glia. This response was attenuated in cells lacking the type-1 IFN receptor, IFNAR1, with IFNAR1−/− neurons also neuroprotected against cell death induced by rotenone. Targeting this detrimental response through the use of IFNAR1−/− glia or a blocking monoclonal antibody to IFNAR1, conferred protection against rotenone-induced neuronal cell death.
Read the Editorial Comment for this article on page 9.
- You have free access to this contentType-I interferons in Parkinson's disease: innate inflammatory response drives fate of neurons in model of degenerative brain disorder: An editorial comment on ‘Type-I interferons mediate the neuroinflammatory response and neurotoxicity induced by rotenone’ (pages 9–11)
Katja M. Kanninen and Anthony R. White
Version of Record online: 22 MAR 2017 | DOI: 10.1111/jnc.13983
Rotenone induces up-regulation of type-I interferons (IFN-I) from microglia and astrocytes. These cytokines interact with neurons and also drive release of further pro-inflammatory cytokines from glial cells and neurons. The combined pro-inflammatory assault results in neuronal cell death. This is a new understanding of how rotenone drives neurotoxicity through IFN-I inflammation.
Read the commented article ‘Type-I interferons mediate the neuroinflammatory response and neurotoxicity induced by rotenone’ on page 75.