TY - JOUR
T1 - Translational control of auditory imprinting and structural plasticity by eIF2α
AU - Batista, Gervasio
AU - Johnson, Jennifer Leigh
AU - Dominguez, Elena
AU - Costa-Mattioli, Mauro
AU - Pena, Jose L.
N1 - Publisher Copyright:
© Batista et al.
PY - 2016/12/23
Y1 - 2016/12/23
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=85010694740&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85010694740&partnerID=8YFLogxK
U2 - 10.7554/eLife.17197
DO - 10.7554/eLife.17197
M3 - Article
C2 - 28009255
AN - SCOPUS:85010694740
SN - 2050-084X
VL - 5
JO - eLife
JF - eLife
IS - DECEMBER2016
M1 - e17197
ER -