Ganglion cell death during normal retinal development in the chick: Comparisons with cell death induced by early target field destruction

Hughes, William F.; McLoon, Steven C.

doi:10.1016/0014-4886(79)90204-8

Cited by 190 publications

(81 citation statements)

References 27 publications

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“…An unresolved issue is whether a more prolonged blockade of axonal transport can result in a substantial decrease of surviving RGC s. It seems likely that a longer perturbation would affect a larger proportion of RGCs, consistent with previous experiments (Hughes and McLoon, 1979;Carpenter et al, 1986;Vanselow et al, 1990) designed to induce a protracted loss of target support. The kinetics of this process have never been analyzed in detail; however, the present results together with the available literature (Carpenter et al, 1986;Cui and Harvey, 1995) suggest that the massive and almost synchronous loss of RGCs after a lesion is a rapid process quite unlike deprivation-induced death.…”

Section: Effects Of Injury and Trophic Deprivation On Rgc Survivalmentioning

confidence: 54%

Axonal Transport Blockade in the Neonatal Rat Optic Nerve Induces Limited Retinal Ganglion Cell Death

et al. 1997

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Optic nerve section in the newborn rat results in a rapid apoptotic degeneration of most axotomized retinal ganglion cells (RGCs). This massive process of neuronal death has been ascribed mainly to the interruption of a trophic factor supply from target structures rather than to the axonal damage per se. To distinguish between these two possibilities, we induced a reversible axonal transport blockade in the developing optic nerve by topical application of a local anesthetic (lidocaine). Light and electron microscopy showed no alterations in the fine structure of treated optic nerves. Retinae of treated and control rats were stained with cresyl violet and examined at different times after surgery. We found that axonal transport blockade induced only a limited number of pyknotic RGCs. Degeneration of these cells was completely prevented by inhibiting protein synthesis during lidocaine application. We conclude that the rapid degeneration of RGCs after axotomy can be ascribed only partly to the loss of retrogradely transported trophic factors.Key words: neuronal death; axonal transport; retinal ganglion cells; apoptosis; rat optic nerve; retrograde degenerationRetinal ganglion cells (RGC s), as well as other mammalian CNS neurons, eventually die as a result of axonal injury (Grafstein and Ingoglia, 1982;Bregman and Reier, 1986;Hefti, 1986; VillegasPerez et al., 1993). Transection of the optic nerve is known to induce massive RGC death by an apoptotic process in both developing (Rabacchi et al., 1994a) and adult rats (Berkelaar et al., 1994;Garcia-Valenzuela et al., 1994). The molecular nature of the signal triggering the loss of axotomized neurons is largely unknown. According to the trophic theory, the effects of axotomy can be ascribed to the disconnection of neurons from their targets, resulting in the sudden loss of retrogradely transported trophic molecules (Oppenheim, 1991;Snider et al., 1992;Johnson and Deckwerth, 1993). An alternative hypothesis is that axonal injury per se can induce cell death. In particular, acute alterations in cellular homeostasis and ionic imbalances subsequent to plasmalemmal leakage, such as C a 2ϩ deregulation, have been implicated (Choi, 1992;Snider et al., 1992).Especially in the neonate, a lack of target-derived trophic signals is proposed as the main cause of death for axotomized RGC s. It is known that trophic factors, such as NGF and BDNF, are synthesized in the major retinal projection fields, the optic tectum (Hofer et al., 1990;Maisonpierre et al., 1990;Friedman et al., 1991) and the dorsal lateral geniculate nucleus (dLGN) (Schoups et al., 1995). E xogenous administration of NGF and BDN F, as well as other growth factors, can partly prevent RGC death after optic nerve lesion (C armignoto et al., 1989;Mey and Thanos, 1993;Cohen et al., 1994;Mansour-Robaey et al., 1994;Rabacchi et al., 1994b). Moreover, the survival of highly purified RGCs in culture can be enhanced by both tectal cells (McCaffery et al., 1982;Armson and Bennett, 1983) and soluble tectal factors (Meyer-Fran...

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Section: Effects Of Injury and Trophic Deprivation On Rgc Survivalmentioning

confidence: 54%

Axonal Transport Blockade in the Neonatal Rat Optic Nerve Induces Limited Retinal Ganglion Cell Death

et al. 1997

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“…This idea of an intraretinal determination of the maturational processes of the retina (discussed also in Rapaport and Stone, , 1983 is an alternative to the suggestion made in several studies (Rager and Rager, 1976;Hinds and Hinds, 1978;Hughes and McLoon, 1979;Stone et al, 1982) that the maturation of the retina and, in particular, of the ganglion cell layer, is determined by a competition among the axons of ganglion cells for synaptic space in the visual centers of the brain, It should be noted, however, that the two ideas are not mutually exclusive.…”

Section: Mechanisms Of Maturationmentioning

confidence: 94%

The topography of cytogenesis in the developing retina of the cat

Rapaport¹,

Stone²

1983

J. Neurosci.

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We have studied the pattern of cytogenesis in the developing retina of the cat, by observing mitotic cells in sections and whole mounts of the retinae of animals between the ages of E (embryonic day) 29 and P (postnatal day) 20. The whole mounts were prepared with the mitotic or ventricular layer uppermost; all of the mitotic cells in this layer could then be surveyed. In retinae from animals up to E46, mitotic cells were present in the ventricular layer at densities of 1000 to 3000 cells/mm2, and their density did not vary consistently with position in the retina. Thus cell division occurs throughout the retina at these ages, with an approximately constant spatial density. By E50, cytogenesis begins to cease and there is a significant pattern to the cessation. Initially, mitotic activity ceases over a small region of retina at the site of the developing area centralis. The nonmitotic area then increases with age, comprising the central 30 to 50% of the retina at birth and the whole of the retina by PlO. The pattern of cessation of cytogenesis is closely coincident in space and time with the development of the outer plexiform layer and the maturation of the ganglion cell layer described in previous studies. These patterns presumably contribute to the regional variations in structure apparent in the adult retina.

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“…5) and partially overlaps with the period of RGC neurogenesis, differentiation and migration (García-Porrero and Ojeda, 1979;Cuadros and Ríos, 1988). The later wave occurs between E10 and E14, when RGCs become dependent on trophic support from their targets (Hughes and La Velle, 1975;Rager and Rager, 1978;Hughes and McLoon, 1979). In the INL, pyknotic cells appear during embryonic day 8.…”

Section: Birdsmentioning

confidence: 99%

Cell death in the developing vertebrate retina

Vecino¹,

Hernández²,

Garcı́a³

2004

Int. J. Dev. Biol.

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Programmed cell death occurs naturally, as a physiological process, during the embryonic development of multicellular organisms. In the retina, which belongs to the central nervous system, at least two phases of cell death have been reported to occur during development. An early phase takes place concomitant with the processes of neurogenesis, cell migration and cell differentiation. A later phase affecting mainly neurons occurs when connections are established and synapses are formed, resulting in selective elimination of inappropriate connections. This pattern of cell death in the developing retina is common among different vertebrates. However, the timing and magnitude of retinal cell death varies among species. In addition, a precise regulation of apoptosis during retinal development has been described. Factors such as neurotrophins, among many others, and electrical activity influence the survival of retinal cells during the course of development. In this paper, we present a summary of these different aspects of programmed cell death during retinal development, and examine how these differ among different species.

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Ganglion cell death during normal retinal development in the chick: Comparisons with cell death induced by early target field destruction

Cited by 190 publications

References 27 publications

Axonal Transport Blockade in the Neonatal Rat Optic Nerve Induces Limited Retinal Ganglion Cell Death

Axonal Transport Blockade in the Neonatal Rat Optic Nerve Induces Limited Retinal Ganglion Cell Death

The topography of cytogenesis in the developing retina of the cat

Cell death in the developing vertebrate retina

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