Characterization of the signaling interactions that promote the survival and growth of developing retinal ganglion cells in culture

Meyer-Franke, Anke; Kaplan, Miriam R.; Pfrieger, Frank W.; Barres, Ben A.

doi:10.1016/0896-6273(95)90172-8

Cited by 770 publications

(637 citation statements)

References 96 publications

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“…One hypothesis to explain these results is that the survival of forebrain neurons in mammalian brain is determined by multiple signaling pathways [such that the removal of one signaling pathway is compensated for by others (Snider, 1994;Meyer-Franke et al, 1995)]. The anatomical basis of redundant trophic signaling may lie in the fact that neuronal populations in the mammalian forebrain generally make and receive a large number of (often reciprocal) synaptic connections with several neuronal populations (Snider, 1994); glial and auto/ paracrine mechanisms of neurotrophin release may also contribute to redundant neurotrophic signaling (Acheson et al, 1995;Yan et al, 1995).…”

Section: Discussionmentioning

confidence: 99%

“…That is, the pattern of Trk receptor and neurotrophin immunohistochemistry indicates that neurotrophins could promote neuron survival in RA by binding to TrkB (and possibly TrkC) receptors after anterograde release from lMAN axons (for BDNF or NT-3) or auto/paracrine release from within RA (for NT-3), or both. In light of evidence that depolarization augments the ability of neurotrophins to promote neuron survival (Ghosh et al, 1994;Meyer-Franke et al, 1995), that exposure to neurotrophins induces dendritic growth and remodeling (McAllister et al, 1995), and that neurotrophins potentiate synaptic transmission (Lohof et al, 1993;Kang and Schuman, 1995), anterograde and auto/paracrine release of neurotrophins would appear to represent important mechanisms for intercellular communication during telencephalic development. Interestingly, a recent study demonstrating anterograde transneuronal transport of neurotrophins in the developing retino-tectal pathway (von Bartheld et al, 1996) suggests that nonretrograde neurotrophic signaling may be a general phenomenon of the CNS that is not…”

Section: Discussionmentioning

confidence: 99%

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Neurotrophins Suppress Apoptosis Induced by Deafferentation of an Avian Motor-Cortical Region

et al. 1997

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Studies of the developing nervous system led to the general view that growth factors promote neuronal survival in a "retrograde" manner. For example, release of NGF from postsynaptic peripheral targets followed by uptake and retrograde transport by presynaptic neurons provided a widely accepted conceptual framework for the action of neurotrophins. In contrast, although presynaptic or "anterograde" influences on the survival of developing neurons have been recognized for some time, the mechanisms by which afferent input regulates the survival of postsynaptic cells have received considerably less attention. In the forebrain network for learned vocal behavior in zebra finches, lesions of a cortical region for song control, the lateral magnocellular nucleus of the anterior neostriatum (lMAN), remove presynaptic input to a motor-cortical song region, the robust nucleus of the archistriatum (RA), and cause massive RA neuron death in young birds that are entering the sensitive period for song learning. Here we report that lesions of lMAN followed by infusions of neurotrophins directly into RA completely suppress neuronal apoptosis in RA. Moreover, we show that lMAN neurons are able to transport neurotrophins in the anterograde direction to RA, that neurotrophin-like immunoreactivity is present in cells in lMAN and RA, and that neurotrophin receptor-like immunoreactivity is present in RA. Expression of neurotrophins in lMAN and RA suggests that lMAN presynaptic input could regulate RA neuron survival by synthesizing, transporting, and releasing neurotrophins anterogradely or by regulating the auto/paracrine release of neurotrophins within RA, or perhaps by both. These data provide the first in vivo demonstration that neurotrophins can prevent the death of deafferented cortical neurons, and they raise the possibility that nonretrograde signaling by neurotrophins may be a common means of promoting neuronal survival in the vertebrate telencephalon. Anterograde and auto/ paracrine neurotrophin signaling, along with the more established view that neurotrophins regulate neuron survival via retrograde mechanisms, suggests multidirectional neurotrophin signaling in the vertebrate telencephalon.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Neurotrophins Suppress Apoptosis Induced by Deafferentation of an Avian Motor-Cortical Region

et al. 1997

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“…Early work with in vitro preparations of neuronal cultures noted that astrocytes were required for proper axon outgrowth, spatial arrangement, and neuron cell survival (Banker, 1980;Noble et al, 1984). The ability to identify astrocyte-specific factors regulating neuron function was achieved with the development of a purified culture of neurons (ie, RGCs), whose survival can be maintained in the absence of glia with the addition of several growth factors (Meyer-Franke et al, 1995). When cultured in isolation, these RGC neurons extend their processes but produce very few functional synapses.…”

Section: Astrocytesmentioning

confidence: 99%

Glial and Neuroimmune Mechanisms as Critical Modulators of Drug Use and Abuse

Lacagnina

Rivera

Bilbo

2016

Neuropsychopharmacol

218

170

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Drugs of abuse cause persistent alterations in synaptic plasticity that may underlie addiction behaviors. Evidence suggests glial cells have an essential and underappreciated role in the development and maintenance of drug abuse by influencing neuronal and synaptic functions in multifaceted ways. Microglia and astrocytes perform critical functions in synapse formation and refinement in the developing brain, and there is growing evidence that disruptions in glial function may be implicated in numerous neurological disorders throughout the lifespan. Linking evidence of function in health and under pathological conditions, this review will outline the glial and neuroimmune mechanisms that may contribute to drug-abuse liability, exploring evidence from opioids, alcohol, and psychostimulants. Drugs of abuse can activate microglia and astrocytes through signaling at innate immune receptors, which in turn influence neuronal function not only through secretion of soluble factors (eg, cytokines and chemokines) but also potentially through direct remodeling of the synapses. In sum, this review will argue that neural-glial interactions represent an important avenue for advancing our understanding of substance abuse disorders.

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“…In contrast, to elicit axon growth from CNS neurons in culture, peptide trophic signals alone are insufficient. For instance, retinal ganglion cells (RGCs) fail to survive in the presence of such trophic signals as BDNF or CNTF unless their cAMP levels are elevated, either pharmacologically or by depolarization (Meyer-Franke et al 1995). cAMP elevation and depolarization do not promote axon growth on their own.…”

Section: Control Of Neuronal Responsiveness To Trophic Peptidesmentioning

confidence: 99%

How does an axon grow?

Goldberg¹

2003

Genes Dev.

203

138

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How do axons grow during development, and why do they fail to regrow when injured? In the complicated mesh of our nervous system, the axon is the information superhighway, carrying all of the data we use to sense our environment and carry out behaviors. To wire up our nervous system properly, neurons must elongate their axons during development to reach their targets. This is no simple task, however. The complex morphology of axons and dendrites puts neurons among the most intricate and beautiful cells in the body. Knowledge of how neurons extend axons and dendrites, elongate at a particular rate, and stop growing at the proper time is critical to understanding the development of our nervous system, yet the regulation of these processes is poorly understood. Considerable attention in recent years has focused on understanding how growth cones are guided and steered through complicated pathways (for review, see Schmidt and Hall 1998;Mueller 1999), and even how neurons initiate new processes (for review, see Da Silva and Dotti 2002), but what mechanisms are involved in elongation itself? Are environmental signals needed to drive axon growth and, if so, what are the intracellular molecular mechanisms by which they induce elongation? What controls the rate of axon growth? How do CNS neurons know whether to extend axons or dendrites? Is the signaling of axon versus dendrite growth attributable to different extracellular signals, different neuronal states, or both? All of these questions bear critically on our understanding of axon growth and here I review recent answers and approaches to the above questions, and highlight their relevance during development, injury, and disease.

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Characterization of the signaling interactions that promote the survival and growth of developing retinal ganglion cells in culture

Cited by 770 publications

References 96 publications

Neurotrophins Suppress Apoptosis Induced by Deafferentation of an Avian Motor-Cortical Region

Neurotrophins Suppress Apoptosis Induced by Deafferentation of an Avian Motor-Cortical Region

Glial and Neuroimmune Mechanisms as Critical Modulators of Drug Use and Abuse

How does an axon grow?

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