Criteria for identifying the molecular basis of the engram (CaMKII, PKMzeta)

Lisman, John

doi:10.1186/s13041-017-0337-4

Cited by 51 publications

(55 citation statements)

References 62 publications

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“…There is an ongoing debate over whether the effect of ZIP on memory is due to PKM inhibition or if it results from nonspecific mechanisms of action (Lisman, 2012(Lisman, , 2017. Actually, PKM knock-out mice can form ZIP-sensitive memories (Lee et al, 2013;Volk et al, 2013) and ZIP induces seizures and reduces spontaneous hippocampal LFPs in anesthetized rats when used at concentrations 10 or more times higher than in our experiments (LeBlancq et al, 2016).…”

Section: Zip Does Not Affect Spontaneous Oscillatory Activity or Basamentioning

confidence: 59%

PKMζ Inhibition Disrupts Reconsolidation and Erases Object Recognition Memory

et al. 2019

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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 M (PKM), an atypical protein kinase C isoform that is thought to sustain memory storage by modulating glutamatergic neurotransmission. However, the potential involvement of PKM in ORM reconsolidation has never been studied. Using a novel ORM task combined with pharmacological, biochemical, and electrophysiological tools, we found that hippocampal PKM 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 PKM acts downstream of BDNF and controls AMPAR synaptic insertion to elicit reconsolidation and suggest that blocking PKM activity during this process deletes active ORM.

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Section: Zip Does Not Affect Spontaneous Oscillatory Activity or Basamentioning

confidence: 59%

PKMζ Inhibition Disrupts Reconsolidation and Erases Object Recognition Memory

et al. 2019

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“…The critical role of AMPARs in memory stabilization and maintenance is well established at both the systems level and within the LTP/LTD model 31 ; during learning there is a rapid increase in the number of AMPAR subunits, as noted above. The upstream control of trafficking these receptors is more controversial, although it is becoming clearer that both PKMζ-PKCι/λ and protein kinase Ca2+/calmodulin-dependent protein kinase II (CaMKII) are important in memory maintenance in adults 37 , 38 , 56 . We focused on PKMζ-PKCι/λ because infant levels are high and remain relatively unchanged during development, while CaMKII levels are low 40 , 41 , 73 .…”

Section: Discussionmentioning

confidence: 99%

Developmental transitions in amygdala PKC isoforms and AMPA receptor expression associated with threat memory in infant rats

Opendak

Zanca

Anane

et al. 2018

Sci Rep

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Although infants learn and remember, they rapidly forget, a phenomenon known as infantile amnesia. While myriad mechanisms impact this rapid forgetting, the molecular events supporting memory maintenance have yet to be explored. To explore memory mechanisms across development, we used amygdala-dependent odor-shock conditioning and focused on mechanisms important in adult memory, the AMPA receptor subunits GluA1/2 and upstream protein kinases important for trafficking AMPAR, protein kinase M zeta (PKMζ) and iota/lambda (PKCι/λ). We use odor-shock conditioning in infant rats because it is late-developing (postnatal day, PN10) and can be modulated by corticosterone during a sensitive period in early life. Our results show that memory-related molecules did not change in pups too young to learn threat (PN8) but were activated in pups old enough to learn (PN12), with increased PKMζ-PKCι/λ and GluA2 similar to that observed in adult memory, but with an uncharacteristic decrease in GluA1. This molecular signature and behavioral avoidance of the conditioned odor was recapitulated in PN8 pups injected with CORT before conditioning to precociously induce learning. Blocking learning via CORT inhibition in older pups (PN12) blocked the expression of these molecules. PN16 pups showed a more adult-like molecular cascade of increased PKMζ-PKCι/λ and GluA1–2. Finally, at all ages, zeta inhibitory peptide (ZIP) infusions into the amygdala 24 hr after conditioning blocked memory. Together, these results identify unique features of memory processes across early development: AMPAR subunits GluA1/2 and PKC isoform expression are differentially used, which may contribute to mechanisms of early life forgetting.

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“…This facilitation might be due to a "real" stronger synaptic transmission after learning or to a decrease of baseline synaptic activity (Lisman, 2017), which might be occluded in D 1 -CB 1 -KO mice. The fact that partial blockade of GABA A receptors in trained WT mice does not alter the LTP facilitation, suggests that this phenomenon is due to a genuine increase of LTP.…”

Section: Discussionmentioning

confidence: 99%

Specific hippocampal interneurons shape consolidation of recognition memory

Cruz

Busquets-García

Zhao

et al. 2019

Preprint

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A complex array of different inhibitory interneurons tightly controls hippocampal activity, but how such diversity specifically impacts on memory processes is scantly known. We found that a small subclass of type-1 cannabinoid receptor (CB 1 )-expressing hippocampal interneurons determines episodic-like memory consolidation by linking dopamine D 1 receptor signaling to GABAergic transmission.Mice lacking CB 1 in D 1 -positive cells (D 1 -CB 1 -KO) displayed impaired long-term, but not short-term, object recognition memory. Re-expression of CB 1 in hippocampal, but not striatal, D 1 -positive cells rescued this memory impairment.Learning induced a facilitation of in vivo hippocampal long-term potentiation (LTP), which was abolished in mutant mice. Chemogenetic and pharmacological experiments revealed that both CB 1 -mediated memory and associated LTP facilitation involves the local control of GABAergic inhibition in a D 1 -dependent manner.This study reveals that CB 1 -/D 1 -expressing interneurons shape hippocampal circuits to sustain recognition memory, thereby identifying a mechanism linking the diversity of hippocampal interneurons to specific behavioral and cognitive outcomes.

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Criteria for identifying the molecular basis of the engram (CaMKII, PKMzeta)

Cited by 51 publications

References 62 publications

PKMζ Inhibition Disrupts Reconsolidation and Erases Object Recognition Memory

PKMζ Inhibition Disrupts Reconsolidation and Erases Object Recognition Memory

Developmental transitions in amygdala PKC isoforms and AMPA receptor expression associated with threat memory in infant rats

Specific hippocampal interneurons shape consolidation of recognition memory

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