Munc13-3 mutation prevents critical period neuronal plasticity in visual cortex.

Munc13-3;Visual plasticity;Critical period;Monocular deprivation

James Geoffrey Morris, 1984-

University:University of Louisville

Department:Anatomical Sciences and Neurobiology

关键词: Munc13-3;    Visual plasticity;    Critical period;    Monocular deprivation;   

Others  :  https://ir.library.louisville.edu/cgi/viewcontent.cgi?article=2007&context=etd

美国|英语

来源: The Universite of Louisville's Institutional Repository

【 摘 要 】

Through differential display PCR, Munc13-3 was identified as a gene whose relative expression in the visual cortex corresponds to critical period plasticity. Expression of the gene was low at the peak of the critical period and expression was high in the weeks near the end of the critical period. Expression of the gene also shifted during dark rearing, a process known to delay the time course of the critical period. Using electrophysiology and monocular deprivation (MD) in mice at different points within the critical period, it is possible to compare normal MD mice's visual evoked potentials to Munc13-3 mutant MD mice's visual evoked potentials to see what effect Muncl3-3 has on visual cortical plasticity. Visual evoked potentials from the eyes contralateral and ipsilateral to the recording electrode in the binocular region of the visual cortex were stimulated and recorded in normal wildtype mice, monocular deprived mice and monocular deprived Muncl3-3 mutants at ages 3.5 weeks and 9 weeks. At 3.5 weeks age the normal wildtype mice showed a large contralateral and smaller ipsilateral response, monocular deprived mice showed the same size ipsilateral (non-deprived eye) response, but a smaller contralateral (deprived eye) response. The monocular deprived Munc13-3 mutant mice showed the same as the normal mouse, large contralateral (deprived eye) response and small ipsilateral (non-deprived eye) response. At 9 weeks of age the normal mice showed the same pattern as the 3.5 week old mice, the monocular deprived mice showed an increased ipsilateral response but no change in contralateral response and the monocular deprived Munc13-3 mutants showed no difference in response compared to the normal mice. Monocular deprivation causes a decreased responsiveness from the contralateral eye in young mice, but causes an increased responsiveness from the ipsilateral eye in the adult mice. Munc13-3, a gene seen to be involved with short term synaptic plasticity and vesicle and neurotransmitter release, mutants do not have any change after monocular deprivation, so plasticity is lost. Munc13-3 gene is therefore involved in the regulation of visual cortical plasticity and is required, most likely in conjunction with other genes, to maintain plasticity in the visual cortex during the critical period.