Abstract
Neuroplasticity is an “umbrella term” referring to the complex, multifaceted physiological processes that mediate the ongoing structural and functional modifications occurring, at various time- and size-scales, in the ever-changing immature and adult brain, and that represent the basis for fundamental neurocognitive behavioral functions; in addition, maladaptive neuroplasticity plays a role in the pathophysiology of neuropsychiatric dysfunctions. Experiential cues and several endogenous and exogenous factors can regulate neuroplasticity; among these, vitamin E, and in particular α-tocopherol (α-T), the isoform with highest bioactivity, exerts potent effects on many plasticity-related events in both the physiological and pathological brain. In this review, the role of vitamin E/α-T in regulating diverse aspects of neuroplasticity is analyzed and discussed, focusing on the hippocampus, a brain structure that remains highly plastic throughout the lifespan and is involved in cognitive functions. Vitamin E-mediated influences on hippocampal synaptic plasticity and related cognitive behavior, on post-natal development and adult hippocampal neurogenesis, as well as on cellular and molecular disruptions in kainate-induced temporal seizures are described. Besides underscoring the relevance of its antioxidant properties, non-antioxidant functions of vitamin E/α-T, mainly involving regulation of cell signaling molecules and their target proteins, have been highlighted to help interpret the possible mechanisms underlying the effects on neuroplasticity.
Highlights
Neural plasticity is an “umbrella term” used to describe lasting changes to the brain occurring throughout an individual’s lifespan due to an external or internal events
Among the most remarkable forms of neural plasticity is the ability of the hippocampus to continuously generate functional neurons during adulthood, a highly regulated process known as adult hippocampal neurogenesis, which is integral for the hippocampus functions [3,4]
We have found that adult (60–90 days) rats maternally exposed to α-T loads exhibit a marked reduction of the ability to induce long-term potentiation (LTP) in CA1 hippocampal slices, indicating that the impairment in long-term synaptic plasticity observed in juvenile offspring persists in adulthood long after suspension of tocopherol exposure, when hippocampal α-T concentration, as well as protein kinase C (PKC) and PKC-substrate phosphorylation had returned to control levels [78]
Summary
Neural plasticity is an “umbrella term” used to describe lasting changes to the brain occurring throughout an individual’s lifespan due to an external or internal events. The hippocampal formation, an important brain structure involved in learning and memory and in emotions, appears to be affected by plastic processes throughout the lifespan of mammalians, including human. Plastic changes triggered by intense and prolonged negative stimuli could be responsible for disease progression; this particular aspect of neural plasticity could be referred to as maladaptive [9] In this context, the discovery of molecules capable of enhancing hippocampal plasticity and restoring dysfunctional hippocampal plasticity in pathological conditions is one of the relevant targets of neuroscience. We aimed at describing and discussing the role of vitamin E, with particular attention paid to α-tocopherol (α-T, the isoform showing the highest in vivo bioactivity and bioavailability) on neural plasticity processes occurring in the hippocampus during brain development, structural and functional synaptic remodeling, cognition, and pathology
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