Transient and persistent increases in protein phosphatase activity during long-term depression in the adult hippocampus in vivo

Thiels, Edda; Norman, Eric D.; Barrionuevo, Germán; Klann, Eric

doi:10.1016/s0306-4522(98)00135-3

Cited by 68 publications

(82 citation statements)

References 33 publications

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“…As summarized in Fig. 2, several studies point directly to activation and inactivation of various kinases and phosphatases (44,52,54,55,109,110). Although there have been few reports in neuronal systems, direct oxidative modification of ion channels, including voltage-gated Ca 2+ channels and the ryanodine receptor have been shown to regulate the levels of intracellular Ca 2+ (28,63).…”

Section: Discussionmentioning

confidence: 99%

Sources and Targets of Reactive Oxygen Species in Synaptic Plasticity and Memory

Kishida¹,

Klann²

2006

Antioxidants & Redox Signaling

115

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Increasing evidence suggests that reactive oxygen species (ROS), such as superoxide and hydrogen peroxide, act as necessary signaling molecules in processes underlying cognition. Moreover, ROS have been shown to be necessary in molecular process underlying signal transduction, synaptic plasticity, and memory formation. Research from several laboratories suggests that NADPH oxidase is an important source of superoxide in the brain. Evidence is presented here to show that ROS are in fact important signaling molecules involved in synaptic plasticity and memory formation. Moreover, evidence that the NADPH oxidase complex is a key regulator of ROS generation in synaptic plasticity and memory formation is discussed. Understanding redox signaling in the brain, including the sources and molecular targets of ROS, are important for a full understanding of the signaling pathways that underlie synaptic plasticity and memory. Knowledge of ROS function in the brain also is critical for understanding aging and neurodegenerative diseases of the brain given that several of these disorders, including Alzheimer's disease and Parkinson disease, may be exacerbated by the unregulated generation of ROS.

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Section: Discussionmentioning

confidence: 99%

Sources and Targets of Reactive Oxygen Species in Synaptic Plasticity and Memory

Kishida¹,

Klann²

2006

Antioxidants & Redox Signaling

115

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“…Based on in vitro biochemical studies, unphosphorylated I-2 at T72 is thought to inhibit PP1 by blocking the PP1 active site via the -helix structure on I-2 (Hurley et al, 2007), but in a delayed manner (t 1/2 30 min; Cohen, 1989). It is known that LTD stimulus only results in transient PP1 activation (45 min; Thiels et al, 1998). So our data indicate that NMDA receptor signaling would activate PP1 in the I-2 complex, but at the same time also engage the delayed PP1 inhibitor function of I-2, which could limit the duration of PP1 activation.…”

Section: Pp1 Dephosphorylation At T320 Is Mediated Via Auto-dephosphomentioning

confidence: 99%

“…Early electrophysiological studies showed that PP1 was required for long-term depression (LTD; Mulkey et al, 1993). PP1 is activated during LTD (Thiels et al, 1998), whereas inhibition of PP1 has been suggested to take place during LTP (Blitzer et al, 1998). Studies in mouse models have shown that PP1 regulates the threshold of LTD and LTP induction (Jouvenceau et al, 2006) and that active PP1 suppresses memory formation (Genoux et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

Synaptic NMDA receptor stimulation activates PP1 by inhibiting its phosphorylation by Cdk5

Hou¹,

Sun²,

Siddoway³

et al. 2013

J Gen Physiol

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“…Also, LTD-inducing stimulation in vivo was associated with an increase in protein phosphatase activity (Thiels et al 1998). Although we did not measure hippocampal levels of PP1 and PP2A activity, the blockade of anterograde suppression of L-LTP by two different inhibitors of PP1 and PP2A and the findings of these earlier studies indicate that LFS can engage phosphatases critical for anterograde suppression of L-LTP.…”

Section: How Might Phosphatases Mediate Anterograde Suppression Of L-mentioning

confidence: 99%

“Silent” Metaplasticity of the Late Phase of Long-Term Potentiation Requires Protein Phosphatases

Woo¹,

Nguyen²

2002

Learn. Mem.

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The late phase of long-term potentiation (L-LTP) is correlated with some types of long-term memory, but the mechanisms by which L-LTP is modulated by prior synaptic activity are undefined. Activation of protein phosphatases by low-frequency stimulation (LFS) given before induction of L-LTP may significantly modify L-LTP. Using cellular electrophysiological recording methods in mouse hippocampal slices, we show that LFS given before induction of L-LTP inhibited L-LTP in an activity-dependent manner without affecting either basal synaptic strength or the early phase of LTP (E-LTP). This anterograde inhibitory effect of LFS was persistent, required N-methyl-D-aspartate (NMDA) receptor activation, and was blocked by inhibitors of protein phosphatase 1 (PP1) and protein phosphatase 2A (PP2A). These data indicate that certain patterns of LFS can activate PP1 and/or PP2A, and that long-lasting activation of these phosphatases by prior LFS can suppress the subsequent expression of L-LTP without affecting E-LTP. Because this inhibition of L-LTP is caused by prior synaptic activity that, alone, produced no net effect on synaptic efficacy, we suggest that this is a "silent" form of metaplasticity that may influence long-term information storage by modulating the capacity of synapses to express L-LTP after repeated bouts of activity.

show abstract

Transient and persistent increases in protein phosphatase activity during long-term depression in the adult hippocampus in vivo

Cited by 68 publications

References 33 publications

Sources and Targets of Reactive Oxygen Species in Synaptic Plasticity and Memory

Sources and Targets of Reactive Oxygen Species in Synaptic Plasticity and Memory

Synaptic NMDA receptor stimulation activates PP1 by inhibiting its phosphorylation by Cdk5

“Silent” Metaplasticity of the Late Phase of Long-Term Potentiation Requires Protein Phosphatases

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