Abstract
Calcium-calmodulin/dependent protein kinase II (CaMKII) plays an essential role in LTP induction, but since it has the capacity to remain persistently activated even after the decay of external stimuli it has been proposed that it can also be necessary for LTP maintenance and therefore for memory persistence. It has been shown that basolateral amygdaloid nucleus (Bla) stimulation induces long-term potentiation (LTP) in the insular cortex (IC), a neocortical region implicated in the acquisition and retention of conditioned taste aversion (CTA). Our previous studies have demonstrated that induction of LTP in the Bla-IC pathway before CTA training increased the retention of this task. Although it is known that IC-LTP induction and CTA consolidation share similar molecular mechanisms, little is known about the molecular actors that underlie their maintenance. The purpose of the present study was to evaluate the role of CaMKII in the maintenance of in vivo Bla-IC LTP as well as in the persistence of CTA long-term memory (LTM). Our results show that acute microinfusion of myr-CaMKIINtide, a selective inhibitor of CaMKII, in the IC of adult rats during the late-phase of in vivo Bla-IC LTP blocked its maintenance. Moreover, the intracortical inhibition of CaMKII 24 h after CTA acquisition impairs CTA-LTM persistence. Together these results indicate that CaMKII is a central key component for the maintenance of neocortical synaptic plasticity as well as for persistence of CTA-LTM.
Highlights
Learning and memory rely on long-lasting changes in synaptic efficiency within neural networks
Since little is known about the molecular actors implicated in the maintenance of synaptic plasticity and long-term memory (LTM), in the present work we evaluated the role of calmodulin/dependent protein kinase II (CaMKII) in the maintenance of in vivo basolateral amygdaloid nucleus (Bla)-insular cortex (IC) Long-term potentiation (LTP) as well as in the persistence of conditioned taste aversion (CTA)-LTM
The application of the inhibitor in the absence of high frequency stimulation (HFS) did not have any effect over baseline transmission (CaMKIINtide group)
Summary
Learning and memory rely on long-lasting changes in synaptic efficiency within neural networks. Long-term potentiation (LTP) is a long-lasting and activity-dependent enhancement of synaptic strength that is widely expressed across the brain (Malenka and Bear, 2004; Rodríguez-Durán et al, 2011). Studies in the neocortex and hippocampus have demonstrated that training in several learning tasks drive modifications of synaptic strength (Rioult-Pedotti et al, 2000; Whitlock et al, 2006; Cooke and Bear, 2010; Liu et al, 2017; Rodríguez-Durán et al, 2017). We have shown that induction of LTP in the Bla-IC pathway before CTA training enhances the retention of this task (Escobar and Bermúdez-Rattoni, 2000; Castillo et al, 2006)
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