Articles by Stephanie Rainey-Smith in JoVE
Regular Care and Maintenance of a Zebrafish (Danio rerio) Laboratory: An Introduction Avdesh Avdesh*1,2, Mengqi Chen*1,3, Mathew T. Martin-Iverson1,2,4, Alinda Mondal1,3, Daniel Ong1, Stephanie Rainey-Smith1,3, Kevin Taddei1,3, Michael Lardelli5, David M. Groth6, Giuseppe Verdile1,3, Ralph N. Martins1,2,3,7 1Centre of Excellence for Alzheimer's Disease Research and Care, School of Medical sciences, Edith Cowan University, 2Centre for Clinical Research in Neuropsychiatry, Graylands Hospital, University of Western Australia, 3McCusker Alzheimer's Research foundation, 4School of Medicine and Pharmacology, University of Western Australia, 5Department of Molecular and Biomedical Sciences, University of Adelaide, 6School of Biomedical Sciences, Curtin University of Technology, 7School of Psychiatry and Clinical Neurosciences, University of Western Australia This protocol outlines regular maintenance and care to maintain optimal conditions for zebrafish husbandry. The video illustrates the protocol for system maintenance, regular housing, feeding, breeding, and raising of zebrafish larvae.
Other articles by Stephanie Rainey-Smith on PubMed
Neuroprotective Effects of Hesperetin in Mouse Primary Neurones Are Independent of CREB Activation Neuroscience Letters. Jun, 2008 | Pubmed ID: 18467030 Dietary flavonoids, including the citrus flavanone hesperetin, may have stimulatory effects on cytoprotective intracellular signalling pathways. In primary mouse cortical neurone cultures, but not SH-SY5Y human neuroblastoma cells or human primary dermal fibroblasts (Promocells), hesperetin (100-300nM, 15min) caused significant increases in the level of ERK1/2 phosphorylation, but did not increase CREB phosphorylation. Administration of hesperetin for 18h did not alter gene expression driven by the cyclic AMP response element (CRE), assessed using a luciferase reporter system, but 300nM hesperetin partially reversed staurosporine-induced cell death in primary neurones. Our data show that hesperetin is a neuroprotective compound at concentrations where antioxidant effects are unlikely to predominate. The effects of hesperetin are cell-type dependent and, unlike the flavanol (-)epicatechin, neuroprotection in vitro is not associated with enhanced CREB phosphorylation or CRE-mediated gene expression.
Tumour Necrosis Factor Alpha Induces Rapid Reduction in AMPA Receptor-mediated Calcium Entry in Motor Neurones by Increasing Cell Surface Expression of the GluR2 Subunit: Relevance to Neurodegeneration Journal of Neurochemistry. May, 2010 | Pubmed ID: 20132465 The alpha-amino-3-hydroxyl-5-methyl-4-isoxazole-propionate receptor (AMPAR) subunit GluR2, which regulates excitotoxicity and the inflammatory cytokine tumour necrosis factor alpha (TNFalpha) have both been implicated in motor neurone vulnerability in amyotrophic lateral sclerosis/motor neurone disease. TNFalpha has been reported to increase cell surface expression of AMPAR subunits to increase synaptic strength and enhance excitotoxicity, but whether this mechanism occurs in motor neurones is unknown. We used primary cultures of mouse motor neurones and cortical neurones to examine the interaction between TNFalpha receptor activation, GluR2 availability, AMPAR-mediated calcium entry and susceptibility to excitotoxicity. Short exposure to a physiologically relevant concentration of TNFalpha (10 ng/mL, 15 min) caused a marked redistribution of both GluR1 and GluR2 to the cell surface as determined by cell surface biotinylation and immunofluorescence. Using fura-2-acetoxymethyl ester microfluorimetry, we showed that exposure to TNFalpha caused a rapid reduction in the peak amplitude of AMPA-mediated calcium entry in a PI3-kinase and p38 kinase-dependent manner, consistent with increased insertion of GluR2-containing AMPAR into the plasma membrane. This resulted in a protection of motor neurones against kainate-induced cell death. Our data therefore, suggest that TNFalpha acts primarily as a physiological regulator of synaptic activity in motor neurones rather than a pathological drive in amyotrophic lateral sclerosis.