Some Forms of cAMP-Mediated Long-Lasting Potentiation Are Associated with Release of BDNF and Nuclear Translocation of Phospho-MAP Kinase

Patterson, Susan L.; Pittenger, Christopher; Morozov, Alexei; Martin, Kelsey C.; Scanlin, Heather; Drake, Carrie T.; Kandel, Eric R.

doi:10.1016/s0896-6273(01)00443-3

Cited by 306 publications

(264 citation statements)

References 70 publications

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“…Another ADR, mycalolide B, also blocked the effect of activin on spine length, and the average spine lengths in neurons treated with activin alone versus neurons treated with activin and 50 nM mycalolide B were 1.59±0.054 m versus 1.50±0.049 m, respectively. The MAP kinase pathway is involved in the effects of activin Because MAP kinase signaling modulates dendritic spine morphology (Wu et al, 2001) and LTP maintenance (Kelleher, 3rd et al, 2004;Patterson et al, 2001), we asked whether the MAP kinase pathway also mediates the activin signaling that alters spinal morphology. When hippocampal primary cultures were treated with activin, phosphorylation of ERK1/2 increased by twofold within 0.5-1 hour (Fig.…”

Section: F-actin-destabilizing Reagents Block the Effects Of Activinmentioning

confidence: 99%

Activin increases the number of synaptic contacts and the length of dendritic spine necks by modulating spinal actin dynamics

Shoji-Kasai

Ageta

Hasegawa

et al. 2007

Journal of Cell Science

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Long-lasting modifications in synaptic transmission depend on de novo gene expression in neurons. The expression of activin, a member of the transforming growth factor β (TGF-β) superfamily, is upregulated during hippocampal long-term potentiation (LTP). Here, we show that activin increased the average number of presynaptic contacts on dendritic spines by increasing the population of spines that were contacted by multiple presynaptic terminals in cultured neurons. Activin also induced spine lengthening, primarily by elongating the neck, resulting in longer mushroom-shaped spines. The number of spines and spine head size were not significantly affected by activin treatment. The effects of activin on spinal filamentous actin (F-actin) morphology were independent of protein and RNA synthesis. Inhibition of cytoskeletal actin dynamics or of the mitogen-activated protein (MAP) kinase pathway blocked not only the activin-induced increase in the number of terminals contacting a spine but also the activin-induced lengthening of spines. These results strongly suggest that activin increases the number of synaptic contacts by modulating actin dynamics in spines, a process that might contribute to the establishment of late-phase LTP.

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Section: F-actin-destabilizing Reagents Block the Effects Of Activinmentioning

confidence: 99%

Activin increases the number of synaptic contacts and the length of dendritic spine necks by modulating spinal actin dynamics

Shoji-Kasai

Ageta

Hasegawa

et al. 2007

Journal of Cell Science

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“…Conversely, in F442A cells, activation of ERK with epidermal growth factor (EGF) increases cAMP by inhibiting a PDE4 isoenzyme (Hoffmann et al, 1999). Consistently, crosstalk exists between cAMP and ERK signaling in the CA1 subregion of the hippocampus (Patterson et al, 2001;Stork and Schmitt, 2002), which is involved in the mediation of synaptic plasticity (Patterson et al, 2001;Roberson et al, 1999) and ERK signalingmediated long-term memory (Blum et al, 1999). Further, PDE4 isoemzymes are phosphorylated and regulated by ERK2.…”

Section: Introductionmentioning

confidence: 96%

Inhibition of the Phosphodiesterase 4 (PDE4) Enzyme Reverses Memory Deficits Produced by Infusion of the MEK Inhibitor U0126 into the CA1 Subregion of the Rat Hippocampus

Zhang

Zhao

Huang

et al. 2004

Neuropsychopharmacol

134

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Cyclic AMP-specific phosphodiesterase 4 (PDE4), which is an integral component of NMDA receptor-mediated cAMP signaling, is involved in the mediation of memory processes. Given that NMDA receptors also mediate MEK/mitogen-activated protein kinase (MAPK, ERK) signaling, which is involved in synaptic plasticity, and that some PDE4 subtypes are phosphorylated and regulated by ERK, it was of interest to determine if PDE4 is involved in MEK/ERK signaling-mediated memory. It was found that rolipram, a PDE4-selective inhibitor, reversed the amnesic effect in the radial-arm maze test of the MEK inhibitor U0126 administered into the CA1 subregion of the rat hippocampus. Consistent with this, rolipram, either by peripheral administration or direct intra-CA1 infusion, enhanced the retrieval of long-term memory impaired by intra-CA1 infusion of U0126 using the step-through inhibitory avoidance test. The same dose of rolipram did not affect U0126-induced reduction of phospho-ERK1/2 levels in the CA1 subregion. However, in primary cultures of rat cerebral cortical neurons, pretreatment with U0126 increased PDE4 activity; this was correlated with the U0126-induced reduction of phospho-ERK1/2 levels. These results suggest that MEK/ERK signaling plays an inhibitory role in regulating PDE4 activity in the brain; this may be a novel mechanism by which MEK/ERK signaling mediates memory. PDE4 is likely to be an important link between the cAMP/PKA and MEK/ERK signaling pathways in the mediation of memory.

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“…Maintenance of HFS-LTP consists of at least two phases: an early, labile phase dependent on covalent modifications of existing proteins; and a late, stable phase requiring new mRNA and protein synthesis (Krug et al, 1984;Matthies et al, 1990;Bliss and Collingridge, 1993;Frey et al, 1996;Nguyen and Kandel, 1996). LTP maintenance is impaired by treatment with antibodies that inhibit activation of the BDNF receptor TrkB, or by deletion of the BDNF or TrkB genes (Figurov et al, 1996;Kang et al, 1997;Korte et al, 1998;Chen et al, 1999;Minichiello et al, 1999;Xu et al, 2000;Kossel et al, 2001;Patterson et al, 2001). Depending on the stimulation parameters used, relatively selective impairment in the ability to generate late, transcription-dependent LTP is seen (Kang et al, 1997;Korte et al, 1998;Minichiello et al, 1999;Patterson et al, 2001).…”

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confidence: 99%

Brain-Derived Neurotrophic Factor Triggers Transcription-Dependent, Late Phase Long-Term PotentiationIn Vivo

et al. 2002

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Acute intrahippocampal infusion of brain-derived neurotrophic factor (BDNF) leads to long-term potentiation (BDNF-LTP) of synaptic transmission at medial perforant path3granule cell synapses in the rat dentate gyrus. Endogenous BDNF is implicated in the maintenance of high-frequency stimulation-induced LTP (HFS-LTP). However, the relationship between exogenous BDNF-LTP and HFS-LTP is unclear. First, we found that BDNF-LTP, like HFS-LTP, is associated with enhancement in both synaptic strength and granule cell excitability (EPSP-spike coupling). Second, treatment with a competitive NMDA receptor (NMDAR) antagonist blocked HFS-LTP but had no effect on the development or magnitude of BDNF-LTP. Thus, NMDAR activation is not required for the induction or expression of BDNF-LTP. Formation of stable, late phase HFS-LTP requires mRNA synthesis and is coupled to upregulation of the immediate early gene activityregulated cytoskeleton-associated protein (Arc). Local infusion of the transcription inhibitor actinomycin D (ACD) 1 hr before or immediately before BDNF infusion inhibited BDNF-LTP and upregulation of Arc protein expression. ACD applied 2 hr after BDNF infusion had no effect, defining a critical time window of transcription-dependent synaptic strengthening. Finally, the functional role of BDNF-LTP was assessed in occlusion experiments with HFS-LTP. HFS-LTP was induced, and BDNF was infused at time points corresponding to early phase (1 hr) or late phase (4 hr) HFS-LTP. BDNF applied during the early phase led to normal BDNF-LTP. In contrast, BDNF-LTP was completely occluded during the late phase. The results strongly support a role for BDNF in triggering transcription-dependent, late phase LTP in the intact adult brain.

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Some Forms of cAMP-Mediated Long-Lasting Potentiation Are Associated with Release of BDNF and Nuclear Translocation of Phospho-MAP Kinase

Cited by 306 publications

References 70 publications

Activin increases the number of synaptic contacts and the length of dendritic spine necks by modulating spinal actin dynamics

Activin increases the number of synaptic contacts and the length of dendritic spine necks by modulating spinal actin dynamics

Inhibition of the Phosphodiesterase 4 (PDE4) Enzyme Reverses Memory Deficits Produced by Infusion of the MEK Inhibitor U0126 into the CA1 Subregion of the Rat Hippocampus

Brain-Derived Neurotrophic Factor Triggers Transcription-Dependent, Late Phase Long-Term PotentiationIn Vivo

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