The role of zincergic neurons, and zinc signalling, in cortical plasticity

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A fundamental property of the brain is that it is highly plastic, meaning that it is capable of changing and adapting as a result of experiences provided by sensory inputs, learning, social and physical interactions, exposure to drugs and hormones, or injury. This plasticity is mediated by changes to the structure and function of neural cells at molecular, cellular, synaptic and network levels. Plasticity can involve the experience-dependent strengthening of synaptic connections, or the formation of new cells or synapses. As importantly, plasticity can involve the experience-dependent weakening of synaptic connections, or the loss of cells or synapses. The mammalian cerebral cortex is of key interest with regard to plasticity because it carries out many of the highest levels of mental functioning. Our goal is to advance our understanding of the cellular, molecular and behavioural mechanisms responsible for mediating experience-dependent plasticity in the mammalian cerebral cortex using an animal model. Specifically, we use the whisker somatosensory system pathway, where we can easily manipulate sensory experience at the level of the somatosensory cortex. We can drive specific patterns of activity by passively stimulating a whisker, or we can deprive the cortex of sensory input by trimming or plucking the whisker.