2014
DOI: 10.1371/journal.pone.0084086
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Local Plasticity of Dendritic Excitability Can Be Autonomous of Synaptic Plasticity and Regulated by Activity-Based Phosphorylation of Kv4.2

Abstract: While plasticity is typically associated with persistent modifications of synaptic strengths, recent studies indicated that modulations of dendritic excitability may form the other part of the engram and dynamically affect computational processing and output of neuronal circuits. However it remains unknown whether modulation of dendritic excitability is controlled by synaptic changes or whether it can be distinct from them. Here we report the first observation of the induction of a persistent plastic decrease … Show more

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Cited by 11 publications
(11 citation statements)
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References 53 publications
(54 reference statements)
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“…In contrast, we found neuronal excitability, but not excitatory synaptic physiology, to be altered by devaluation. In line with our findings, previous studies have reported excitability changes independently of synaptic plasticity (Egorov et al, 2002; Labno et al, 2014). It is proposed that alterations in excitability may serve as a transient priming mechanism for initial associative memory formation before synaptic changes take place (Moyer et al, 1996; Janowitz and Van Rossum, 2006; Mozzachiodi and Byrne, 2010).…”
Section: Discussionsupporting
confidence: 93%
“…In contrast, we found neuronal excitability, but not excitatory synaptic physiology, to be altered by devaluation. In line with our findings, previous studies have reported excitability changes independently of synaptic plasticity (Egorov et al, 2002; Labno et al, 2014). It is proposed that alterations in excitability may serve as a transient priming mechanism for initial associative memory formation before synaptic changes take place (Moyer et al, 1996; Janowitz and Van Rossum, 2006; Mozzachiodi and Byrne, 2010).…”
Section: Discussionsupporting
confidence: 93%
“…This confirms a similar finding on the effect of global CaMKII overexpression (thus increasing CaMKII*) on fear conditioning, see (Cao et al, 2008; Wang et al, 2003). On any simple model, such memory deficits would not be expected if processes unrelated to CaMKII stored memory, as proposed by (Murakoshi et al, 2017); in this case, such processes could serve as a basis of memory recall even when CaMKII-dependent effects on synapses or other cellular properties (Fan et al, 2005; Labno et al, 2014; Sametsky et al, 2009) were saturated.…”
Section: Discussionmentioning
confidence: 98%
“…Expressed in the dendritic spines of the post-synaptic density (PSD) [39,40], this protein is an actin-crosslinking protein [41] that is involved with synaptic plasticity [39]. This is interesting because changes in dendrite activity might be related to synaptic plasticity [42,43].…”
Section: Discussionmentioning
confidence: 99%