Ca2+-dependent synaptic signalling malfunctions in experimental optic neuritis.

点击翻译按钮获取中文摘要

Synaptic degeneration is a common feature of many neurodegenerative and neuroinflammatory conditions, but the relevance of synaptic Ca2+ signalling and function in the retina is at present unclear. In order to analyse Ca2+ signalling malfunctions in retinal photoreceptor synapses in mouse models of neurodegeneration and neuroinflammation (using CSP¿ and Unc119 knockouts and a model of optic neuritis), we will employ both genetically engineered synaptic Ca2+ reporter mice and a novel mouse strain carries a genetically encoded reporter for exo- and endo-cytotic process, the SypHy mouse. These reporter mice will allow us to monitor synaptic alterations in Ca2+ signalling and vesicle recycling and correlate them with the neurodegenerative process. Furthermore, we plan to characterise the influence of inflammatory cytokines on synaptic transmission in the retina using both these reporter mice and other tools such as cytokine antagonism.