Journal of Neurochemistry
© International Society for Neurochemistry
Edited By: Jörg Schulz
Impact Factor: 4.244
ISI Journal Citation Reports © Ranking: 2013: 63/251 (Neurosciences); 74/291 (Biochemistry & Molecular Biology)
Online ISSN: 1471-4159
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Recently Published Articles
- HIV-1 Tat C modulates NOX2 and NOX4 expressions through miR-17 in a human microglial cell line
Vaishnavi Sunil Jadhav, Karl-Heinz Krause and Sunit K. Singh
Accepted manuscript online: 21 AUG 2014 08:50AM EST | DOI: 10.1111/jnc.12933
- Bioenergetic adaptation in response to autophagy regulators during rotenone exposure
Samantha Giordano, Matthew Dodson, Saranya Ravi, Matthew Redmann, Xiaosen Ouyang, Victor M. Darley Usmar and Jianhua Zhang
Article first published online: 21 AUG 2014 | DOI: 10.1111/jnc.12844
Exposure to the neurotoxin rotenone is a risk factor for Parkinson's disease. We tested the hypothesis that autophagy is protective against rotenone toxicity in primary neurons. Exposure to nanomolar concentrations of rotenone caused immediate mitochondrial dysfunction, associated with a suppression of macroautophagy. However, mitophagy occurred that was independent of LC3II accumulation, and the surviving neurons exhibited adaptations to their cellular bioenergetic profiles. Cotreatment with the autophagy enhancer rapamycin was protective, whereas further inhibition of autophagy with 3-methyladenine (3-MA) exacerbated cell death, resulting in additional bioenergetic adaptations in the surviving neurons.
- Striatal serotonin 2C receptors decrease nigrostriatal dopamine release by increasing GABA-A receptor tone in the substantia nigra
Mary V. Burke, Christine Nocjar, Alex J. Sonneborn, Andrew C. McCreary and Elizabeth A. Pehek
Article first published online: 21 AUG 2014 | DOI: 10.1111/jnc.12842
Dopamine (DA) neurons in the substantia nigra pars compacta (SNpc) project to the caudate-putamen (CP; striatum). This circuitry is implicated in numerous pathologies including Parkinson's disease. Using in vivo microdialysis, we demonstrated that blockade of serotonin (5-HT) 2C receptors in the CP increased nigrostriatal DA release. Infusions of a GABA-A agonist into the substantia nigra pars reticulata (SNpr) blocked this increase. This work indicates that striatal serotonin 2C receptors regulate GABAergic tone in the SNpr, which in turn regulates nigrostriatal DA release.
- Ceramide metabolism analysis in a model of binge drinking reveals both neuroprotective and toxic effects of ethanol
Mihyun Bae, Veera Venkata Ratnam Bandaru, Neha Patel and Norman J. Haughey
Article first published online: 21 AUG 2014 | DOI: 10.1111/jnc.12834
We used a mouse model of binge drinking – a common form of alcohol abuse – to directly compare the effects of ethanol (EtOH) during intoxication and acute withdrawal on brain ceramide metabolism. Gene and metabolite analysis suggest that intoxication is associated with a protective phenotype, as evidenced by reductions in several ceramides. By contrast, acute withdrawal was associated with a degenerative phenotype that was manifested by the elevations in several ceramide species. These data suggest that neural damage may occur during the acute EtOH withdrawal phase and may involve increased production of neurotoxic ceramide species. The image depicts primary metabolic pathways regulated during EtOH intoxication (green) and those most active during withdrawal (red). SMase, Sphingomyelin phosphodiesterase; SGMS, sphingomyelin synthase; CerS, ceramid synthase; S1P, sphingosine-1P; sphK, sphingosine kinase.
- Reactive oxygen species and lipid peroxidation inhibitors reduce mechanical sensitivity in a chronic neuropathic pain model of spinal cord injury in rats
Shayne N. Hassler, Kathia M. Johnson and Claire E. Hulsebosch
Article first published online: 21 AUG 2014 | DOI: 10.1111/jnc.12830
We propose that the application of compounds that inhibit reactive oxygen species (ROS) and related downstream molecules will also reduce the behavioral measures of chronic neuropathic pain. Injury or trauma to nervous tissue leads to increased concentrations of ROS in the surviving tissue. Further damage from ROS molecules to dorsal lamina neurons leads to membrane excitability, the physiological correlate of chronic pain. Chronic pain is difficult to treat with current analgesics and this research will provide a novel therapy for this disease.