The Role of Synaptic Zinc in Experience-Dependent Plasticity
Date
2015-07-29
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Abstract
Experience-dependent plasticity is a fundamental component of the brain’s ability to adapt to its environment. An increasing amount of research suggests that synaptic zinc could be an important mediator of plasticity within the brain. Although a role for synaptic zinc in modulating experience-dependent plasticity has been hypothesized, to date no research has determined if synaptic zinc is necessary for experience-dependent plasticity. The goal of this thesis was to determine if synaptic zinc is an important mediator of experience-dependent plasticity within the hippocampus and neocortex.
The mechanisms through which the brain can respond to experience differ depending on the area of the brain being examined. For example, the extent of hippocampal neurogenesis can be increased by experiences such as environmental enrichment. Our experiments demonstrate that synaptic zinc is necessary for the enhancement of adult hippocampal neurogenesis by environmental enrichment. GPR39 is a zinc-sensing receptor that might transduce the zinc signal that is ultimately responsible for modulating adult hippocampal neurogenesis. We found that ablation of GPR39 signalling also prevented environmental enrichment-dependent increases in neurogenesis. Together these experiments demonstrate a novel role for synaptic zinc and GPR39 in contributing to experience-dependent plasticity in the hippocampus.
Experience can also shape the functioning of the neocortex. Depriving neurons of the primary somatosensory cortex (or barrel cortex) of sensory input by whisker trimming can depress sensory-evoked responses in these neurons. In addition, sensory deprivation can increase the amount of synaptic zinc within sensory deprived regions of the barrel cortex. The regulation of synaptic zinc by sensory experience suggests its mechanistic involvement in experience-dependent plasticity. Utilizing voltage-sensitive dye imaging, which allows for in vivo imaging of sensory-evoked activity in the barrel cortex, we examined sensory deprivation-induced decreases in cortical activity in the barrel cortex. Our results show that ablation of synaptic zinc prevented sensory deprivation-induced reductions in cortical activity. These results demonstrate a role for synaptic zinc for experience-dependent plasticity within the neocortex.
Together, this research provides substantive support for a role for synaptic zinc as an essential regulator of experience-dependent plasticity in both the hippocampus and neocortex.
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Neuroscience
Citation
Chrusch, M. (2015). The Role of Synaptic Zinc in Experience-Dependent Plasticity (Doctoral thesis, University of Calgary, Calgary, Canada). Retrieved from https://prism.ucalgary.ca. doi:10.11575/PRISM/28358