Stabilization of Dendritic Arbor Structure in Vivo by CaMKII

Wu, Gang; Cline, Hollis T.

doi:10.1126/science.279.5348.222

Cited by 353 publications

(299 citation statements)

References 42 publications

(5 reference statements)

Supporting

Mentioning

275

Contrasting

Unclassified

Order By: Relevance

“…Activation of NMDA receptors has been shown to result in activation of CREB by phosphorylation at Ser 133 (Hardingham et al, 2002;Wayman et al, 2006). Numerous upstream signaling cascades can impinge on CREB to influence gene expression and dendrite growth (Wu and Cline, 1998;Wu et al, 2001;Redmond et al, 2002;Vaillant et al, 2002;Wayman et al, 2006). Our studies suggest that following chronic bicuculline treatment the level of pCREB in hippocampal neurons is decreased while the levels of CREB itself remain unaltered.…”

Section: Suppression Of Dendrite Growth: Roles For Nmda Receptors Andmentioning

confidence: 48%

Effects of chronic network hyperexcitability on the growth of hippocampal dendrites

Nishimura

Owens

Swann

2008

Neurobiology of Disease

View full text Add to dashboard Cite

Experiments reported here were motivated by studies in both human epilepsy and animal models in which stunted dendritic arbors are observed. Our goal was to determine if chronic network hyperexcitability alters dendritic growth. Experiments were conducted in hippocampal slice cultures obtained from infant mice that express the fluorescent protein YFP in CA1 hippocampal pyramidal cells. Results showed that 4 days of GABAa receptor blockade produced a 40% decrease in basilar dendritic length. When dendritic growth was followed over this 4 day interval, dendrites in untreated slices doubled in length, however dendrites in bicuculline treated cultures failed to grow. These effects were suppressed by APV -suggesting a dependence on NMDA receptor activation. Activation of the transcription factor CREB was also decreased by chronic network hyperexcitability -pointing to possible molecular events underlying the observed suppression of growth. Taken together, our results suggest that chronic hippocampal network hyperexcitability limits dendritic growth.

show abstract

Section: Suppression Of Dendrite Growth: Roles For Nmda Receptors Andmentioning

confidence: 48%

Effects of chronic network hyperexcitability on the growth of hippocampal dendrites

Nishimura

Owens

Swann

2008

Neurobiology of Disease

View full text Add to dashboard Cite

show abstract

“…As neurons elaborate a complex dendritic arbor, they also form and strengthen glutamatergic retinotectal synapses by mechanisms that are enhanced by visual stimulation (31) and require NMDA receptor and CaMKII activity (22,32). Furthermore, AMPA receptor-and NMDA receptor-mediated transmission is required for normal dendritic arbor development (20,33).…”

Section: Delcpeb Expression Reduces the Strength Of Glutamatergic Synmentioning

confidence: 99%

The RNA binding protein CPEB regulates dendrite morphogenesis and neuronal circuit assembly in vivo

Bestman

Cline

2008

Proc. Natl. Acad. Sci. U.S.A.

Self Cite

View full text Add to dashboard Cite

Visual system development requires experience-dependent mechanisms that regulate neuronal structure and function, including dendritic arbor growth, synapse formation, and stabilization. Although RNA binding proteins have been shown to affect some forms of synaptic plasticity in adult animals, their role in the development of neuronal structure and functional circuitry is not clear. Using two-photon time-lapse in vivo imaging and electrophysiology combined with morpholino-mediated knockdown and expression of functional deletion mutants, we demonstrate that the mRNA binding protein, cytoplasmic polyadenylation element binding protein1 (CPEB1), affects experience-dependent neuronal development and circuit formation in the visual system of Xenopus laevis. These data indicate that sensory experience controls circuit development by regulating translational activity of mRNAs.circuit integration ͉ experience-dependent plasticity ͉ in vivo imaging ͉ visual system ͉ whole-cell recording D uring CNS development, neuronal structure, synaptic connections, and circuit functions change in response to sensory input. Although the regulation of mRNA translation and new protein synthesis have been implicated in some forms of neuronal plasticity in adult animals (1, 2), their role in experience-dependent sensory system plasticity has not been addressed (3). In the brain, the translation of many mRNAs is regulated by their association with ribonucleoprotein (RNP) granules, which are composed of core RNA binding proteins, translational machinery, and mRNAs (4). RNA binding proteins package specific mRNAs within RNP granules, regulate their transport into dendrites, and in principle, could temporally and spatially govern their translation in response to synaptic activity (4). Because of these features, mRNA binding proteins are in a unique position to control developmental events through the coordinated translation of a functionally related cohort of mRNAs (5, 6). Indeed, local protein synthesis affords neurons the ability to stabilize changes in synaptic connections and alter neuronal output (7). Recent studies indicate that cytoplasmic polyadenylation element binding protein 1 (CPEB1) is among a handful of RNA binding proteins that regulate dendritic protein synthesis and synaptic plasticity in vitro (8). Although studies in mutant mice implicate CPEB1 in some forms of synaptic and spine plasticity and in memory extinction (9-11), no studies have examined the potential role of CPEB1 in dendritic arbor development, experience-dependent structural plasticity, or the integration of neurons into a functional circuit in an intact animal.CPEB1 (Orb in D. melanogaster) is a member of an evolutionarily conserved family of RNA binding proteins that is expressed in the brain (in vertebrates, CPEB1-4). While all members are defined by the presence of RNA recognition motifs in their carboxy-terminals, CPEB1 is the only member that targets mRNAs containing cytoplasmic polyadenylation elements (CPEs) in their 3Ј untranslated regions (12). Origina...

show abstract

“…For example, the calcium-calmodulin-dependent protein kinase II (CaMK II) is involved in stabilizing structural rearrangements. 81 Chronic, but not acute treatment with tianeptine caused increased phosphorylation of the CaMK II-PKC site (Ser831) on GluR1 subunit of AMPA receptors in the hippocampus (CA3 and dentate gyrus) and cerebral cortex of mice. Although there was a trend for an increase, the PKA site (Ser845) was not significantly affected by tianeptine.…”

Section: Neurobiological Properties Of Tianeptinementioning

confidence: 93%

Neurobiology of mood, anxiety, and emotions as revealed by studies of a unique antidepressant: tianeptine

McEwen

Olie

2005

Mol Psychiatry

View full text Add to dashboard Cite

Recent studies have provided evidence that structural remodeling of certain brain regions is a feature of depressive illness, and the postulated underlying mechanisms contribute to the idea that there is more to antidepressant actions that can be explained exclusively by a monoaminergic hypothesis. This review summarizes recent neurobiological studies on the antidepressant, tianeptine (S-1574, [3-chloro-6-methyl-5,5-dioxo-6,11-dihydro-(c,f)-dibenzo-(1,2-thiazepine)-11-yl) amino]-7 heptanoic acid, sodium salt), a compound with structural similarities to the tricyclic antidepressant agents, the efficacy and good tolerance of which have been clearly established. These studies have revealed that the neurobiological properties of tianeptine involve the dynamic interplay between numerous neurotransmitter systems, as well as a critical role of structural and functional plasticity in the brain regions that permit the full expression of emotional learning. Although the story is far from complete, the schema underlying the effect of tianeptine on central plasticity is the most thoroughly studied of any antidepressants. Effects of tianeptine on neuronal excitability, neuroprotection, anxiety, and memory have also been found. Together with clinical data on the efficacy of tianeptine as an antidepressant, these actions offer insights into how compounds like tianeptine may be useful in the treatment of neurobiological features of depressive disorders. Molecular Psychiatry (2005) 10, 525-537.

show abstract

Stabilization of Dendritic Arbor Structure in Vivo by CaMKII

Cited by 353 publications

References 42 publications

Effects of chronic network hyperexcitability on the growth of hippocampal dendrites

Effects of chronic network hyperexcitability on the growth of hippocampal dendrites

The RNA binding protein CPEB regulates dendrite morphogenesis and neuronal circuit assembly in vivo

Neurobiology of mood, anxiety, and emotions as revealed by studies of a unique antidepressant: tianeptine

Contact Info

Product

Resources

About