Expression of Neurotrophin-3 (NT-3) and Anterograde Axonal Transport of Endogenous NT-3 by Retinal Ganglion Cells in Chick Embryos

Bartheld, Christopher S. von; Butowt, Rafał

doi:10.1523/jneurosci.20-02-00736.2000

Cited by 48 publications

(26 citation statements)

References 85 publications

(137 reference statements)

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“…GAD-65 mRNA was detected in only 2.5% of the CB neurons, and 8% of the PV neurons confirming the predominantly excitatory nature of these cell classes (Mize, 1996;Lane et al, 1997). TrkA mRNA is not expressed in SC (Sobreviela et al, 1994) and the low-affinity neurotrophin receptor p75 is largely confined to retinal afferents (VonBartheld and Butowt, 2000), although some p75 staining seems associated with superficial tectal cells (Harvey, 1994).…”

Section: Superior Colliculus Neurons Grow In Response To Cortically Imentioning

confidence: 80%

Differential effects of cortical neurotrophic factors on development of lateral geniculate nucleus and superior colliculus neurons: anterograde and retrograde actions

Wahle

Cristo²,

Schwerdtfeger

et al. 2003

Development

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Neurotrophins strongly affect visual system development and plasticity. However, the mode of delivery and targets of neurotrophin action are still under debate. For instance, cortical NT-4/5 (neurotrophin 4/5; Ntf4/5) was shown to rescue lateral geniculate nucleus (LGN) neurons from monocular deprivation-induced atrophy suggesting a retrograde action on thalamic afferents. It is still unclear whether LGN neurons respond to NT-4/5 and other neurotrophins during development in animals with normal vision. We now show that infusions of NT-4/5 and NGF (nerve growth factor) into visual cortex at the onset and the peak of the critical period accelerated LGN neuron growth. BDNF (brain-derived neurotrophic factor) was ineffective. The effects of neurotrophin on LGN development were clearly dissociated from the effects at cortical level because soma growth of cortical layer IV and VI neurons was strongly promoted by BDNF. NT-4/5 was only effective at the onset, but no longer at the peak of the critical period suggesting a switch in neurotrophin dependency for these cortical cell classes. To dissociate retrograde and anterograde effects of the TrkB ligands, we analyzed the stratum griseum superficiale (SGS) of the superior colliculus, a target of visual cortical efferents. Indeed, TrkB-expressing inhibitory SGS neurons responded to cortical NT-4/5 infusion with somatic growth. Strikingly, the TrkB-expressing excitatory tectothalamic calbindin neurons in the SGS did not respond. This demonstrated for the first time a selective cell type-specific anterograde action of NT-4/5 and suggested for the LGN that anterograde as well as retrograde effects contribute to soma size regulation. Strikingly, cortical infusion of the cytokine LIF, which affects development of visual cortex neurochemical architecture, transiently inhibited growth of neurons in LGN,cortical layer IV and VI and SGS. In summary, the study presents three important results. First, central neurons regulate soma size development in an age-and ligand-specific fashion. Second, NT-4/5 and NGF accelerate LGN development in rats with normal vision while LIF delays growth. Third,anterogradely transported NT-4/5 effectively promotes neuronal maturation. These differential actions on subcortical neurons may contribute to the different effects of neurotrophins on visual system development and plasticity.

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Section: Superior Colliculus Neurons Grow In Response To Cortically Imentioning

confidence: 80%

Differential effects of cortical neurotrophic factors on development of lateral geniculate nucleus and superior colliculus neurons: anterograde and retrograde actions

Wahle

Cristo²,

Schwerdtfeger

et al. 2003

Development

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“…They were obtained with a very relevant model system: the rat retinotectal pathway which allows to assay for transcytosis via optic nerve section and use of RGC-specific markers (von Bartheld et al, 1996;Caleo et al, 2000Caleo et al, , 2009von Bartheld and Butowt, 2000). In the rat, virtually all RGCs send a unidirectional projection to the superior colliculus, with 97% of the axons crossing at the chiasm and innervating the contralateral tectum (Cowey and Perry, 1979).…”

Section: Discussionmentioning

confidence: 99%

“…In the rat, virtually all RGCs send a unidirectional projection to the superior colliculus, with 97% of the axons crossing at the chiasm and innervating the contralateral tectum (Cowey and Perry, 1979). Cell bodies of RGCs can be easily exposed to exogenous ligands by injections into the vitreous humor, and the optic nerve is amenable to surgical manipulation (Manning et al, 1990;von Bartheld et al, 1996;Caleo et al, 2000Caleo et al, , 2009von Bartheld and Butowt, 2000). This model system has been extensively used for studies of anterograde transport and transcytosis (von Bartheld et al, 2001;Caleo and Cenni, 2004;von Bartheld, 2004).…”

Section: Discussionmentioning

confidence: 99%

“…Certain neurotrophic factors can also be anterogradely transported and transcytosed. For example, in developing chick brain, NT-3 is transported in the anterograde direction, from cell bodies to the axon terminals, and the intact neurotrophin is released after anterograde transport, taken up and used by second-order visual neurons (von Bartheld et al, 1996;von Bartheld and Butowt, 2000). BDNF travels in an anterograde direction along the rat optic nerve and has rapid effects on retinal target neurons in the superior colliculus and lateral geniculate nucleus of the brain (Caleo et al, 2000.…”

Section: Discussionmentioning

confidence: 99%

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Evidence for Anterograde Transport and Transcytosis of Botulinum Neurotoxin A (BoNT/A)

Restani¹,

Antonucci²,

et al. 2011

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“…Traditionally, neurotrophins were believed to be derived by retrograde axonal transport from target cells, but recent studies revealed that neurotrophins are also transported anterogradely along axons (von Bartheld et al, 1996;Zhou and Rush, 1996;Altar et al, 1997;Conner et al, 1997;Heymach and Barres, 1997;Smith et al, 1997;Yan et al, 1997;Fawcett et al, 2000;von Bartheld and Butowt, 2000) and may act as extremely potent excitatory neurotransmitters (Kafitz et al, 1999). Anterograde signals provide trophic support from afferents (Linden, 1994;von Bartheld et al, 1996;Altar et al, 1997), may mediate fast, local effects at synaptic sites (Lohof et al, 1993;Kang and Schuman, 1995;Thoenen, 1995;Kafitz et al, 1999;Poo, 2001), and regulate dendritic growth, neuronal cytoarchitecture, and phenotypes (Altar et al, 1997;McAllister et al, 1999;Fawcett et al, 2000).…”

Section: Abstract: Neurotrophic Factors; Secretion; Presynaptic Termmentioning

confidence: 99%

Mechanisms of the Release of Anterogradely Transported Neurotrophin-3 from Axon Terminals

et al. 2002

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Neurotrophins have profound effects on synaptic function and structure. They can be derived from presynaptic, as well as postsynaptic, sites. To date, it has not been possible to measure the release of neurotrophins from axon terminals in intact tissue. We implemented a novel, extremely sensitive assay for the release and transfer of anterogradely transported neurotrophin-3 (NT-3) from a presynaptic to a postsynaptic location that uses synaptosomal fractionation after introduction of radiolabeled NT-3 into the retinotectal projection of chick embryos. Release of the anterogradely transported NT-3 in intact tissue was assessed by measuring the amount remaining in synaptosomal preparations after treatment of whole tecta with pharmacological agents. Use of this assay reveals that release of NT-3 from axon terminals is increased by depolarization, calcium influx via N-type calcium channels, and cAMP analogs, and release is most profoundly increased by excitation with kainic acid or mobilization of calcium from intracellular stores. NT-3 release depends on extracellular sodium, CaM kinase II activity, and requires intact microtubules and microfilaments. Dantrolene inhibits the high potassium-induced release of NT-3, indicating that release of calcium from intracellular stores is required. Tetanus toxin also inhibits NT-3 release, suggesting that intact synaptobrevin or synaptobrevin-like molecules are required for exocytosis. Ultrastructural autoradiography and immunolabel indicate that NT-3 is packaged in presumptive large dense-core vesicles. These data show that release of NT-3 from axon terminals depends on multiple regulatory proteins and ions, including the mobilization of local calcium. The data provide insight in the mechanisms of anterograde neurotrophins as synaptic modulators. ; presynaptic terminals; calcium; axonal transport; neurotrophin; synapse; synaptic transmission Neurotrophins are important regulators of neuronal differentiation and synaptic plasticity (Lohof et al., 1993;Snider, 1994;Kang and Schuman, 1995;Thoenen, 1995;McAllister et al., 1999;Poo, 2001). Traditionally, neurotrophins were believed to be derived by retrograde axonal transport from target cells, but recent studies revealed that neurotrophins are also transported anterogradely along axons (von Bartheld et al Key words: neurotrophic factors; secretion

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Expression of Neurotrophin-3 (NT-3) and Anterograde Axonal Transport of Endogenous NT-3 by Retinal Ganglion Cells in Chick Embryos

Cited by 48 publications

References 85 publications

Differential effects of cortical neurotrophic factors on development of lateral geniculate nucleus and superior colliculus neurons: anterograde and retrograde actions

Differential effects of cortical neurotrophic factors on development of lateral geniculate nucleus and superior colliculus neurons: anterograde and retrograde actions

Evidence for Anterograde Transport and Transcytosis of Botulinum Neurotoxin A (BoNT/A)

Mechanisms of the Release of Anterogradely Transported Neurotrophin-3 from Axon Terminals

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