Dendritic arbor development and synaptogenesis

Cline, Hollis T.

doi:10.1016/s0959-4388(00)00182-3

Cited by 463 publications

(359 citation statements)

References 56 publications

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“…Similar studies in the Fmr1 mutant mouse confirmed these findings, as well as excessive dendritic branching [Comery et al, 1997;Irwin et al, 2002;Galvez et al, 2003]. Given that spines are postsynaptic sites and that dendrites undergo complex alterations during development [Cline, 2001], it is not surprising that a "subtle" morphological change would cause serious functional consequences. The abnormal spine appearance has been interpreted as immaturity or stalled development, possibly due to insufficient pruning [reviewed in Beckel-Mitchener and Greenough, 2004], but it may reflect synaptic loss [Bear et al, 2004].…”

Section: Case In Point: Drosophila Fragile X Mental Retardation 1 (Dfsupporting

confidence: 57%

Mental retardation genes in drosophila: New approaches to understanding and treating developmental brain disorders

Restifo

2005

Ment. Retard. Dev. Disabil. Res. Rev.

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Drosophila melanogaster is emerging as a valuable genetic model system for the study of mental retardation (MR). MR genes are remarkably similar between humans and fruit flies. Cognitive behavioral assays can detect reductions in learning and memory in flies with mutations in MR genes. Neuroanatomical methods, including some at single-neuron resolution, are helping to reveal the cellular bases of faulty brain development caused by MR gene mutations. Drosophila fragile X mental retardation 1 (dfmr1) is the fly counterpart of the human gene whose malfunction causes fragile X syndrome. Research on the fly gene is leading the field in molecular mechanisms of the gene product's biological function and in pharmacological rescue of brain and behavioral phenotypes. Future work holds the promise of using genetic pathway analysis and primary neuronal culture methods in Drosophila as tools for drug discovery for a wide range of MR and related disorders.

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Section: Case In Point: Drosophila Fragile X Mental Retardation 1 (Dfsupporting

confidence: 57%

Mental retardation genes in drosophila: New approaches to understanding and treating developmental brain disorders

Restifo

2005

Ment. Retard. Dev. Disabil. Res. Rev.

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“…Neuronal activity influences the growth of dendrites during development and such activitydependent morphological alterations are likely to have important consequences on the ultimate functioning of the central nervous system (Cline, 2001;Wong and Ghosh, 2002; Van and Cline, 2004). Indeed, dendrites appear to be anatomically plastic (Faherty et al, 2003;Chklovskii et al, 2004;Cooke and Woolley, 2005) and their adaptability is especially prominent during development (Rhin and Claiborne, 1990;Dalva et al, 1994;Lendavi et al, 2000;Hua and Smith, 2004).…”

Section: Introductionmentioning

confidence: 99%

Effects of chronic network hyperexcitability on the growth of hippocampal dendrites

Nishimura

Owens

Swann

2008

Neurobiology of Disease

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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.

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“…During the past few years, a number of studies in several model systems have demonstrated the essential roles of neuronal activity, extracellular cues and intrinsic factors in dendritic morphogenesis (for reviews, see McAllister, 2000;Scott and Luo, 2001;Cline, 2001;Jan and Jan, 2001;Whitford et al, 2002;Wong and Ghosh, 2002;Gao and Bogert, 2003). However, it remains largely unknown what limits the growth of a particular neuron, and in particular, the number and length of dendritic branches during development.…”

Section: Introductionmentioning

confidence: 99%

Control of dendritic development by theDrosophila fragile X-relatedgene involves the small GTPase Rac1

et al. 2003

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Fragile X syndrome is caused by loss-of-function mutations in the fragile X mental retardation 1 gene. How these mutations affect neuronal development and function remains largely elusive. We generated specific point mutations or small deletions in the Drosophila fragile X-related (Fmr1) gene and examined the roles of Fmr1 in dendritic development of dendritic arborization (DA) neurons in Drosophila larvae. We found that Fmr1 could be detected in the cell bodies and proximal dendrites of DA neurons and that Fmr1loss-of-function mutations increased the number of higher-order dendritic branches. Conversely, overexpression of Fmr1 in DA neurons dramatically decreased dendritic branching. In dissecting the mechanisms underlying Fmr1 function in dendrite development, we found that the mRNA encoding small GTPase Rac1 was present in the Fmr1-messenger ribonucleoprotein complexes in vivo. Mosaic analysis with a repressor cell marker (MARCM) and overexpression studies revealed that Rac1 has a cell-autonomous function in promoting dendritic branching of DA neurons. Furthermore, Fmr1 and Rac1 genetically interact with each other in controlling the formation of fine dendritic branches. These findings demonstrate that Fmr1 affects dendritic development and that Rac1 is partially responsible for mediating this effect.

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Dendritic arbor development and synaptogenesis

Cited by 463 publications

References 56 publications

Mental retardation genes in drosophila: New approaches to understanding and treating developmental brain disorders

Mental retardation genes in drosophila: New approaches to understanding and treating developmental brain disorders

Effects of chronic network hyperexcitability on the growth of hippocampal dendrites

Control of dendritic development by theDrosophila fragile X-relatedgene involves the small GTPase Rac1

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