Abstract
The formation of imprinted memories during a critical period is crucial for vital behaviors, including filial attachment. Yet, little is known about the underlying molecular mechanisms. Using a combination of behavior, pharmacology, in vivo surface sensing of translation (SUnSET) and DiOlistic labeling we found that, translational control by the eukaryotic translation initiation factor 2 alpha (eIF2α) bidirectionally regulates auditory but not visual imprinting and related changes in structural plasticity in chickens. Increasing phosphorylation of eIF2α (p-eIF2α) reduces translation rates and spine plasticity, and selectively impairs auditory imprinting. By contrast, inhibition of an eIF2α kinase or blocking the translational program controlled by p-eIF2α enhances auditory imprinting. Importantly, these manipulations are able to reopen the critical period. Thus, we have identified a translational control mechanism that selectively underlies auditory imprinting. Restoring translational control of eIF2α holds the promise to rejuvenate adult brain plasticity and restore learning and memory in a variety of cognitive disorders.
Highlights
Imprinting is a form of early learning where exposure to a stimulus becomes the triggering signal of a vital behavior (Jin et al, 2016; Horn, 2004)
Our results show that both auditory and visual imprinting trigger new protein synthesis, which is required for both auditory and visual imprinting
Given that (a) long-term remodeling of spines requires protein synthesis (Nishiyama and Yasuda, 2015) and (b) translational control by p-eukaryotic translation initiation factor 2 alpha (eIF2a) selectively regulates auditory imprinting, we examined the role of this translational control mechanism in structural plasticity in imprinting-relevant brain regions
Summary
Imprinting is a form of early learning where exposure to a stimulus becomes the triggering signal of a vital behavior (Jin et al, 2016; Horn, 2004). Imprinting drives a vigorous following behavior in chickens, key for filial attachment (Horn, 2004; Insel and Young, 2001). This rather unique and precocious behavior is advantageous for investigating experience-driven activation of molecular pathways around birth (Bredenkotter and Braun, 1997; Bock and Braun, 1999; McCabe et al, 1982, 1981).
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