TrkB Signaling Modulates Spine Density and Morphology Independent of Dendrite Structure in Cultured Neonatal Purkinje Cells

Shimada, Atsuyoshi; Mason, Carol A.; Morrison, Mary E.

doi:10.1523/jneurosci.18-21-08559.1998

Cited by 162 publications

(122 citation statements)

References 106 publications

(127 reference statements)

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“…Local protein synthesis triggered by BDNF may stabilize efficacy changes by stimulating more activity-dependent phosphorylation of ␣-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors and assisting in remodeling of the postsynaptic element into a more efficacious configuration. In accord with the latter idea, stabilization of LTP requires expression of Arc during a period (27) when the structural modifications associated with LTP are beginning to emerge (47), and BDNF signaling has been shown to have profound effects on synaptic density (48,49), the thickness of the postsynaptic density (50), and the length of the active zone at asymmetric synapses (38).…”

Section: Discussionmentioning

confidence: 89%

The brain-derived neurotrophic factor enhances synthesis of Arc in synaptoneurosomes

Yin

Edelman²,

Vanderklish³

2002

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

246

189

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Protein synthesis in neurons is essential for the consolidation of memory and for the stabilization of activity-dependent forms of synaptic plasticity such as long-term potentiation (LTP). Activitydependent translation of dendritically localized mRNAs has been proposed to be a critical source of new proteins necessary for synaptic change. mRNA for the activity-regulated cytoskeletal protein, Arc, is transcribed during LTP and learning, and disruption of its translation gives rise to deficits in both. We have found that selective translation of Arc in a synaptoneurosomal preparation is induced by the brain-derived neurotrophic factor, a neurotrophin that is released during high-frequency stimulation patterns used to elicit LTP. This effect involves signaling through the TrkB receptor and is blocked by the N-methyl-D-aspartate-type glutamate receptor antagonist, MK801. The results suggest there is a synergy between neurotrophic and ionotropic mechanisms that may influence the specificity and duration of changes in synaptic efficacy at glutamatergic synapses.T he brain-derived neurotrophic factor (BDNF), a member of the nerve growth factor (NGF) superfamily of neurotrophins (1, 2), influences the differentiation and survival of neurons and the maintenance of their arborizations (3-6). Other data suggest that BDNF is also involved in both short-and long-term plasticity of glutamatergic synapses (7,8). BDNF signaling enhances synaptic maturation and increases synaptic density in the hippocampus (9), and in the adult the synthesis and secretion of BDNF continue to be regulated by activity (10-12). Exogenous application of BDNF induces a rapid and persistent enhancement of synaptic transmission in hippocampal and cortical preparations (13,14) and facilitates the induction of long-term potentiation (LTP) in slices from young animals (15). Stimulation patterns used to elicit LTP also result in release of the BDNF protein from presynaptic terminals (16,17).Local protein synthesis may influence changes in synaptic efficacy induced by BDNF. Early and reversible effects of BDNF involve pre-and postsynaptic changes that do not require protein synthesis. For example, application of BDNF enhances evoked glutamate release (18) and increases the probability that the N-methyl-D-aspartate (NMDA) receptor channel will be open (19). Longer-term influences on synaptic efficacy, however, may require BDNF-induced local protein synthesis. BDNF-induced synaptic potentiation in hippocampal slices is blocked by inhibitors of protein synthesis (20). Potentiation induced by BDNF can be obtained in slices in which synapses have been severed from cell bodies, suggesting that synthesis of the required protein(s) is dendritically localized (20). In accord with this possibility, it has been shown that BDNF specifically induces the expression of transfected c-myc in dissected dendrites (21), and the dendritic synthesis of a reporter protein construct flanked by the 5Ј and 3Ј untranslated regions of ␣-calmodulin-dependent protein kinase II ]. These ...

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Section: Discussionmentioning

confidence: 89%

The brain-derived neurotrophic factor enhances synthesis of Arc in synaptoneurosomes

Yin

Edelman²,

Vanderklish³

2002

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

246

189

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“…5). In the postnatal stage, BDNF-TrkB signaling regulates dendritic spine density but not dendritic outgrowth (Shimada et al, 1998). Other CRMP family members, CRMP1 and CRMP3, have shown to positively regulate dendritic spine density (Yamashita et al, 2006;Quach et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

CRMP5 (Collapsin Response Mediator Protein 5) Regulates Dendritic Development and Synaptic Plasticity in the Cerebellar Purkinje Cells

Yamashita¹,

Mosinger²,

Roy³

et al. 2011

J. Neurosci.

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Collapsin response mediator protein 5 (CRMP5) is one of the CRMP members that expresses abundantly in the developing brain. To examine the in vivo function of CRMP5, we generated crmp5-deficient (crmp5 Ϫ/Ϫ ) mice. Anti-calbindin immunofluorescence studies of crmp5 Ϫ/Ϫ mice revealed aberrant dendrite morphology; specifically, a decrease in the size of soma and diameter of primary dendrite of the cerebellar Purkinje cells at postnatal day 21 (P21) and P28, but not at P14. Coincidentally, CRMP5 is detected in Purkinje cells at P21 and P28 from crmp5 ϩ/Ϫ mice. In cerebellar slices of crmp5 Ϫ/Ϫ mice, the induction of long-term depression of excitatory synaptic transmission between parallel fibers and Purkinje cells was deficient. Given that brain-derived neurotrophic factor (BDNF) plays major roles in dendritic development, we tried to elucidate the possible roles of CRMP5 in BDNF signaling. The effect of BDNF to induce dendritic branching was markedly attenuated in cultured crmp5 Ϫ/Ϫ neurons. Furthermore, CRMP5 was tyrosine phosphorylated when coexpressed with neurotrophic tyrosine kinase receptor type 2 (TrkB), a receptor for BDNF, in HEK293T cells. These findings suggest that CRMP5 is involved in the development, maintenance and synaptic plasticity of Purkinje cells.

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“…Accordingly, cortical pyramidal neurons of TrkB mutant mice are characterized by thinner and less complex dendrites than those in WT mice (Xu et al, 2000). Moreover, the increase in spine numbers both in Purkinje cells and in hippocampal neurons was blocked by inhibiting TrkB signaling (Shimada et al, 1998;Tyler and Pozzo-Miller, 2001). Overall, these results suggest that positive structural changes are induced via the activation of Trk receptors.…”

Section: Discussionmentioning

confidence: 99%

The p75 Neurotrophin Receptor Negatively Modulates Dendrite Complexity and Spine Density in Hippocampal Neurons

Zagrebelsky¹,

Holz²,

Dechant³

et al. 2005

J. Neurosci.

260

236

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The correlation between functional and structural neuronal plasticity is by now well documented. However, the molecular mechanisms translating patterns of neuronal activity into specific changes in the structure of neurons remain unclear. Neurotrophins can be released in an activity-dependent manner, and they are capable of controlling both neuronal morphology and functional synaptic changes. They are thus attractive molecules to be studied in the context of synaptic plasticity. In the CNS, most of the work so far has focused on the role of BDNF and of its tyrosine kinase B receptor (

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TrkB Signaling Modulates Spine Density and Morphology Independent of Dendrite Structure in Cultured Neonatal Purkinje Cells

Cited by 162 publications

References 106 publications

The brain-derived neurotrophic factor enhances synthesis of Arc in synaptoneurosomes

The brain-derived neurotrophic factor enhances synthesis of Arc in synaptoneurosomes

CRMP5 (Collapsin Response Mediator Protein 5) Regulates Dendritic Development and Synaptic Plasticity in the Cerebellar Purkinje Cells

The p75 Neurotrophin Receptor Negatively Modulates Dendrite Complexity and Spine Density in Hippocampal Neurons

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