Different phosphatase‐dependent mechanisms mediate long‐term depression and depotentiation of long‐term potentiation in mouse hippocampal CA1 area

Jouvenceau, Anne; Billard, Jean‐Marie; Haditsch, Ursula; Mansuy, Isabelle M.; Dutar, P.

doi:10.1046/j.1460-9568.2003.02831.x

Cited by 61 publications

(56 citation statements)

References 32 publications

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“…Some studies have mentioned the possible involvement of calcineurin, CB1 receptors, and LVGCCs with LTP reversal or depotentiation (Christie et al 1997;Zhuo et al 1999;Gerdeman et al 2002;Jouvenceau et al 2003;Lin et al 2003b). Interestingly, all three mechanisms seem to interact in endocannabinoid-mediated LTD in the hippocampus, with calcineurin apparently integrating the postsynaptic activation signal provided by LVGCCs and the presynaptic signal mediated by CB1 receptors (Heifets et al 2008).…”

Section: Discussionmentioning

confidence: 99%

Calcineurin inhibition blocks within-, but not between-session fear extinction in mice

et al. 2015

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Memory extinction involves the formation of a new associative memory that inhibits a previously conditioned association. Nonetheless, it could also depend on weakening of the original memory trace if extinction is assumed to have multiple components. The phosphatase calcineurin (CaN) has been described as being involved in extinction but not in the initial consolidation of fear learning. With this in mind, we set to study whether CaN could have different roles in distinct components of extinction. Systemic treatment with the CaN inhibitors cyclosporin A (CsA) or FK-506, as well as i.c.v. administration of CsA, blocked within-session, but not between-session extinction or initial learning of contextual fear conditioning. Similar effects were found in multiple-session extinction of contextual fear conditioning and in auditory fear conditioning, indicating that CaN is involved in different types of short-term extinction. Meanwhile, inhibition of protein synthesis by cycloheximide (CHX) treatment did not affect within-session extinction, but disrupted fear acquisition and slightly impaired between-session extinction. Our results point to a dissociation of within-and between-session extinction of fear conditioning, with the former being more dependent on CaN activity and the latter on protein synthesis. Moreover, the modulation of within-session extinction did not affect between-session extinction, suggesting that these components are at least partially independent.

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Section: Discussionmentioning

confidence: 99%

Calcineurin inhibition blocks within-, but not between-session fear extinction in mice

et al. 2015

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“…It is also strongly diminished by CaNB (a1) gene KO in forebrain excitatory neurons (Zeng et al 2001). Likewise, depotentiation is blocked by CaN inhibition whether achieved pharmacologically, by neuron-specific expression of a CaN inhibitor in forebrain, or by CaNA (a) KO (Zhuo et al 1999;Jouvenceau et al 2003;Kang-Park et al 2003;Lin et al 2003a;Jouvenceau and Dutar 2006).…”

Section: Basic Properties Of Canmentioning

confidence: 99%

“…It may also explain why LTP is precluded if inhibitory neurotransmission is not specifically blocked during LTP induction (Lu et al 1996). In contrast, when CaN inhibition is restricted to excitatory neurons or occurs during LTP induction, it facilitates LTP and blocks LTD (Hodgkiss and Kelly 1995;Wang and Kelly 1996;Winder et al 1998;Malleret et al 2001;Zeng et al 2001;Jouvenceau et al 2003;Jouvenceau and Dutar 2006).…”

Section: Basic Properties Of Canmentioning

confidence: 99%

Neural functions of calcineurin in synaptic plasticity and memory: Figure 1.

2012

Self Cite

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Major brain functions depend on neuronal processes that favor the plasticity of neuronal circuits while at the same time maintaining their stability. The mechanisms that regulate brain plasticity are complex and engage multiple cascades of molecular components that modulate synaptic efficacy. Protein kinases (PKs) and phosphatases (PPs) are among the most important of these components that act as positive and negative regulators of neuronal signaling and plasticity, respectively. In these cascades, the PP protein phosphatase 2B or calcineurin (CaN) is of particular interest because it is the only Ca 2+ -activated PP in the brain and a major regulator of key proteins essential for synaptic transmission and neuronal excitability. This review describes the primary properties of CaN and illustrates its functions and modes of action by focusing on several representative targets, in particular glutamate receptors, striatal enriched protein phosphatase (STEP), and neuromodulin (GAP43), and their functional significance for synaptic plasticity and memory.

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“…5A), LFS was applied to "naive" inputs. Indeed, many studies have shown that LFS can recruit different signaling cascades depending on the initial state of the stimulated synapses (i.e., naive vs potentiated) (Katsuki et al, 1997;Lee et al, 2000;Jouvenceau et al, 2003).…”

Section: Previous Lfs Does Not Affect Somatic Gene Expression Associamentioning

confidence: 99%

Homosynaptic and Heterosynaptic Inhibition of Synaptic Tagging and Capture of Long-Term Potentiation by Previous Synaptic Activity

Young¹,

Nguyen²

2005

J. Neurosci.

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Long-term potentiation (LTP) is an enhancement of synaptic strength that may contribute to information storage in the mammalian brain. LTP expression can be regulated by previous synaptic activity, a process known as "metaplasticity." Cell-wide occurrence of metaplasticity may regulate synaptic strength. However, few reports have demonstrated metaplasticity at synapses that are silent during activity at converging synaptic inputs. We describe a novel form of cell-wide metaplasticity in hippocampal area CA1. Low-frequency stimulation (LFS) decreased the stability of long-lasting LTP ["late" LTP (L-LTP)] induced later at the same inputs (homosynaptic inhibition) and at other inputs converging on the same postsynaptic cells (heterosynaptic inhibition). Significantly, heterosynaptic inhibition of L-LTP also occurred across basal and apical dendrites ("heterodendritic" inhibition). Because transient early LTP (E-LTP) was not affected by previous LFS, we examined the effects of LFS on the consolidation of E-LTP to L-LTP. The duration of E-LTP induced at one set of inputs can be extended by capturing L-LTP-associated gene products generated by previous activity at other inputs to

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Different phosphatase‐dependent mechanisms mediate long‐term depression and depotentiation of long‐term potentiation in mouse hippocampal CA1 area

Cited by 61 publications

References 32 publications

Calcineurin inhibition blocks within-, but not between-session fear extinction in mice

Calcineurin inhibition blocks within-, but not between-session fear extinction in mice

Neural functions of calcineurin in synaptic plasticity and memory: Figure 1.

Homosynaptic and Heterosynaptic Inhibition of Synaptic Tagging and Capture of Long-Term Potentiation by Previous Synaptic Activity

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