PKMζ inhibition disrupts reconsolidation and erases object recognition memory

Rossato, Janine I.; Gonzalez, Maria Carolina; Radiske, Andressa; Apolinário, Gênedy; Conde-Ocazionez, Sergio; Bevilaqua, Lia Rejane Müller; Cammarota, Martín Pablo

PKMζ inhibition disrupts reconsolidation and erases object recognition memory

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dc.contributor.author	Rossato, Janine I.
dc.contributor.author	Gonzalez, Maria Carolina
dc.contributor.author	Radiske, Andressa
dc.contributor.author	Apolinário, Gênedy
dc.contributor.author	Conde-Ocazionez, Sergio
dc.contributor.author	Bevilaqua, Lia Rejane Müller
dc.contributor.author	Cammarota, Martín Pablo
dc.date.accessioned	2019-03-13T19:31:55Z
dc.date.available	2019-03-13T19:31:55Z
dc.date.issued	2019-03-06
dc.description.resumo	Object recognition memory (ORM) confers the ability to discriminate the familiarity of previously encountered items. Reconsolidation is the process by which reactivated memories become labile and susceptible to modifications. The hippocampus is specifically engaged in reconsolidation to integrate new information into the original ORM through a mechanism involving activation of brain-derived neurotrophic factor (BDNF) signaling and induction of LTP. It is known that BDNF can control LTP maintenance through protein kinase Mζ (PKMζ), an atypical protein kinase C isoform that is thought to sustain memory storage by modulating glutamatergic neurotransmission. However, the potential involvement of PKMζ in ORM reconsolidation has never been studied. Using a novel ORM task combined with pharmacological, biochemical, and electrophysiological tools, we found that hippocampal PKMζ is essential to update ORM through reconsolidation, but not to maintain the inactive recognition memory trace stored over time, in adult male Wistar rats. Our results also indicate that hippocampal PKMζ acts downstream of BDNF and controls AMPAR synaptic insertion to elicit reconsolidation and suggest that blocking PKMζ activity during this process deletes active ORM.SIGNIFICANCE STATEMENT Object recognition memory (ORM) is essential to remember facts and events. Reconsolidation integrates new information into ORM through changes in hippocampal plasticity and brain-derived neurotrophic factor (BDNF) signaling. In turn, BDNF enhances synaptic efficacy through protein kinase Mζ (PKMζ), which might preserve memory. Here, we present evidence that hippocampal PKMζ acts downstream of BDNF to regulate AMPAR recycling during ORM reconsolidation and show that this kinase is essential to update the reactivated recognition memory trace, but not to consolidate or maintain an inactive ORM. We also demonstrate that the amnesia provoked by disrupting ORM reconsolidation through PKMζ inhibition is due to memory erasure and not to retrieval failure.	pt_BR
dc.identifier.citation	ROSSATO, J. I. et al. PKMζ inhibition disrupts reconsolidation and erases object recognition memory. J Neurosci., v. 39, n. 10, p. 1828-1841, mar. 2019.	pt_BR
dc.identifier.doi	10.1523/JNEUROSCI.2270-18.2018
dc.identifier.uri	https://repositorio.ufrn.br/jspui/handle/123456789/26760
dc.language	en	pt_BR
dc.subject	PKMζ	pt_BR
dc.subject	memory	pt_BR
dc.subject	reconsolidation	pt_BR
dc.title	PKMζ inhibition disrupts reconsolidation and erases object recognition memory	pt_BR
dc.type	article	pt_BR