Randomized retinal ganglion cell axon routing at the optic chiasm of GAP-43-deficient mice: association with midline recrossing and lack of normal ipsilateral axon turning

During mammalian development, retinal ganglion cell (RGC) axons from nasal retina cross the optic chiasm midline, whereas temporal retina axons do not and grow ipsilaterally, resulting in a projection of part of the visual world onto one side of the brain while the remaining part is represented on the opposite side. Previous studies have shown that RGC axons in GAP-43-deficient mice initially fail to grow from the optic chiasm to form optic tracts and are delayed temporarily in the midline region. Here we show that this delayed RGC axon exit from the chiasm is characterized by abnormal randomized axon routing into the ipsilateral and contralateral optic tracts, leading to duplicated representations of the visual world in both sides of the brain. Within the chiasm, individual contralaterally projecting axons grow in unusual semicircular trajectories, and the normal ipsilateral turning of ventral temporal axons is absent. These effects on both axon populations suggest that GAP-43 does not mediate pathfinding specifically for one or the other axon population but is more consistent with a model in which the initial pathfinding defect at the chiasm/tract transition zone leads to axons backing up into the chiasm, resulting in circular trajectories and eventual random axon exit into one or the other optic tract. Unusual RGC axon trajectories include chiasm midline recrossing similar to abnormal CNS midline recrossing in invertebrate "roundabout" mutants and Drosophila with altered calmodulin function. This resemblance and the fact that GAP-43 also has been proposed to regulate calmodulin availability raise the possibility that calmodulin function is involved in CNS midline axon guidance in both vertebrates and invertebrates.     

Neurite outgrowth stimulated by neural cell adhesion molecules requires growth-associated protein-43 (GAP-43) function and is associated with GAP-43 phosphorylation in growth cones

The mechanisms whereby cell adhesion molecules (CAMs) promote axonal growth and synaptic plasticity are poorly understood. Here we show that the neurite outgrowth stimulated by NCAM-mediated fibroblast growth factor (FGF) receptor activation in cerebellar granule cells is associated with increased GAP-43 phosphorylation on serine-41. In contrast, neither NCAM nor FGF was able to stimulate neurite outgrowth in similar neurons from mice in which the GAP-43 gene had been deleted by homologous recombination. Integrin-mediated neurite outgrowth was unaffected by GAP-43 deletion. Both neurite outgrowth and rapid phosphorylation of GAP-43 in isolated growth cones required the first three Ig domains of a NCAM-Fc chimera and were stimulated maximally at 5 micrograms/ml (approximately 50 nM). Likewise, GAP-43 phosphorylation in isolated growth cones also was stimulated by an L1-Fc chimera. Both neurite outgrowth and NCAM-stimulated GAP-43 phosphorylation were inhibited by antibodies to the FGF receptor and a diacylglycerol lipase inhibitor (RHC80267) that blocks the production of arachidonic acid in response to activation of the FGF receptor. Direct activation of the FGF receptor and the arachidonic acid cascade with either basic FGF or melittin also resulted in increased GAP-43 phosphorylation. These data suggest that the stimulation of neurite outgrowth by NCAM requires GAP-43 function and that GAP-43 phosphorylation in isolated growth cones occurs via an FGF receptor-dependent increase in arachidonic acid.     

Retinal ganglion cell layer and visual function in a patient with optic disc drusen

BACKGROUND: To correlate the retinal ganglion cell pattern to visual acuity and visual field data in a patient with bilateral optic disc drusen, a quantitative clinicopathological study was carried out. METHODS: Both retinae of a patient with optic drusen were whole-mounted. Retinal ganglion cell counts were made using a sampling scheme covering the whole retina and compared to the findings in 10 normal retinae. Relative ganglion cell reduction in the drusen retinae was correlated to clinical data. RESULTS: The total retinal ganglion cell count was reduced from 1244858+/-98736 in normal retinae to 305319 on the right and 527571 on the left eye with optic disc drusen. Large ganglion cells had a better chance of survival. Parafoveal ganglion cell loss was 57% for the right and 36% for the left eye, while visual acuity was 0.8 and 1.0 respectively. The mean light sensitivity loss increased from the centre (6.2 dB) to paracentral (9.9 dB), mid-peripheral (13.7 dB) and outer peripheral (15.0 dB) retina, while ganglion cell losses were smallest in outer peripheral retina (21.9%), followed by central (53.0%), mid-peripheral (70.9%) and paracentral retina (87.7%). CONCLUSION: These data validate Frisén's theory on central retinal resolution and provide the structural basis for the clinical rule that low visual acuity should not be attributed to disc drusen. Automated light sense perimetry gives an inadequate picture of retinal damage caused by optic disc drusen.     

Inhibition of protein tyrosine kinases impairs axon extension in the embryonic optic tract

The role of protein tyrosine kinase (PTK) activity in the development of the retinal projection was examined in vivo by applying inhibitors of cytoplasmic PTKs, herbimycin A and lavendustin A, to intact brain preparations of Xenopus embryos. The inhibitors were present during the period when retinal ganglion cell axons first navigate through the optic tract to reach their target, the optic tectum. A majority of inhibitor-treated retinal axons stalled at the beginning of the optic tract, leading to an 80% reduction in projection length at the highest doses. All inhibitor-treated axons that did extend into the optic tract exhibited normal pathfinding behavior. Tyrosine kinase assays of inhibitor-treated brains demonstrated that at doses at which retinal axon extension was severely impaired, PTK activity, including that of src family proteins, was reduced by 50-60%. Consistent with the in vivo findings, PTK inhibitors reduced neurite outgrowth from cultured retinal neurons by 70-80%. This contrasts with the strong enhancement of outgrowth induced by the same inhibitors in cultured chick ciliary ganglion neurons and suggests that the mediation of outgrowth by PTK activity may vary in different neuronal types. Inhibitor-treated growth cones cultured on laminin were larger than normal, suggesting that tyrosine phosphorylation can modulate growth cone-substrate adhesive interactions. Our results in vivo and in vitro provide complementary evidence that retinal axon outgrowth is inhibited by pharmacological blockers of PTK activity and indicate that inhibitor-sensitive PTKs normally play a role in promoting retinal neurite extension.     

Domains of regulatory gene expression and the developing optic chiasm: correspondence with retinal axon paths and candidate signaling cells

In mammals, some axons from each retina cross at the optic chiasm, whereas others do not. Although several loci have been identified within the chiasmatic region that appear to provide guidance cues to the retinal axons, the underlying molecular mechanisms that regulate this process are poorly understood. Here we investigate whether the earliest retinal axon trajectories and a cellular population (CD44 and stage-specific embryonic antigen 1 [SSEA] neurons), previously implicated in directing axon growth in the developing chiasm (reviewed in Mason and Sretavan [1997] Curr. Op. Neurobiol. 7:647-653), correlate with the expression patterns of several regulatory genes (BF-1, BF-2, Dlx-2, Nkx-2.1, Nkx-2.2, and Shh). These studies demonstrate that gene expression patterns in the chiasmatic region reflect the longitudinal subdivisions of the forebrain in that axon tracts in this region generally are aligned parallel to these subdivisions. Moreover, zones defined by overlapping domains of regulatory gene expression coincide with sites implicated in providing guidance information for retinal axon growth in the developing optic chiasm. Together, these data support the hypothesis that molecularly distinct, longitudinally aligned domains in the forebrain regulate the pattern of retinal axon projections in the developing hypothalamus.     

Changes in the retinal ganglion cell layer and optic nerve of rats exposed neonatally to cocaine

In a study of 452 ex-prisoners in England in 1990, 66 people reported that they were tested for HIV antibodies when last in prison. The circumstances under which many of those who were tested were difficult: 36% found it an unpleasant experience, 17% had not taken the test voluntarily and 55% said they received no counselling. Further information was gathered about the experiences of those who were HIV positive or assumed to be. Most were accommodated in a 'special location', not allowed to associate with other prisoners and denied access to work or recreational facilities. These data highlight the difficulties arising from the policy of Viral Infectivity Restrictions, a set of regulations applied to the management of prisoners with HIV in English prisons. This policy created a distressing situation for those tested for HIV or identified as being HIV positive in prison. For the prison environment, these conditions may create a vicious circle reinforcing inaccurate beliefs and anxieties.     

Sexually dimorphic development of the mammalian reproductive tract requires Wnt-7a

An important feature of mammalian development is the generation of sexually dimorphic reproductive tracts from the Müllerian and Wolffian ducts. In females, Müllerian ducts develop into the oviduct, uterus, cervix and upper vagina, whereas Wolffian ducts regress. In males, testosterone promotes differentiation of Wolffian ducts into the epididymis, vas deferens and seminal vesicle. The Sertoli cells of the testes produce Müllerian-inhibiting substance, which stimulates Müllerian duct regression in males. The receptor for Müllerian-inhibiting substance is expressed by mesenchymal cells underlying the Müllerian duct that are thought to mediate regression of the duct. Mutations that inactivate either Müllerian-inhibiting substance or its receptor allow development of the female reproductive tract in males. These pseudohermaphrodites are frequently infertile because sperm passage is blocked by the presence of the female reproductive system. Here we show that male mice lacking the signalling molecule Wnt-7a fail to undergo regression of the Müllerian duct as a result of the absence of the receptor for Müllerian-inhibiting substance. Wnt7a-deficient females are infertile because of abnormal development of the oviduct and uterus, both of which are Müllerian duct derivatives. Therefore, we propose that signalling by Wnt-7a allows sexually dimorphic development of the Müllerian ducts.     

Directed expression of the growth-associated protein B-50/GAP-43 to olfactory neurons in transgenic mice results in changes in axon morphology and extraglomerular fiber growth

B-50/GAP-43, a neural growth-associated phosphoprotein, is thought to play a role in neuronal plasticity and nerve fiber formation since it is expressed at high levels in developing and regenerating neurons and in growth cones. Using a construct containing the coding sequence of B-50/GAP-43 under the control of regulatory elements of the olfactory marker protein (OMP) gene, transgenic mice were generated to study the effect of directed expression of B-50/GAP-43 in a class of neurons that does not normally express B-50/GAP-43, namely, mature OMP-positive olfactory neurons. Olfactory neurons have a limited lifespan and are replaced throughout adulthood by new neurons that migrate into the upper compartment of the epithelium following their formation from stem cells in the basal portion of this neuroepithelium. Thus, the primary olfactory pathway is exquisitely suited to examine a role of B-50/GAP-43 in neuronal migration, lifespan, and nerve fiber growth. We find that B-50/GAP-43 expression in adult olfactory neurons results in numerous primary olfactory axons with enlarged endings preferentially located at the rim of individual glomeruli. Furthermore, ectopic olfactory nerve fibers in between the juxtaglomerular neurons or in close approximation to blood vessels were frequently observed. This suggests that expression of B-50/GAP-43 in mature olfactory neurons alters their response to signals in the bulb. Other parameters examined, that is, migration and lifespan of olfactory neurons are normal in B-50/GAP-43 transgenic mice. These observations provide direct in vivo evidence for a role of B-50/GAP-43 in nerve fiber formation and in the determination of the morphology of axons.     

Ion channel redistribution and function during development of the myelinated axon

The development of myelinated axons represents one of the most complex interactions among different cell types in the nervous system. Striking changes occur in both morphology and function in the early postnatal period. Myelination effectively isolates electrically most of the axolemma and dramatically alters the pathways for current flow that are required for rapid, reliable, and efficient conduction. Correspondingly, ion channels must be directed to and stabilized at their required sites. In the case of Na+ channels, this requires a 25-fold increase in density within nodes of Ranvier, and, in mammalian fibers, a virtually complete spatial separation from voltage-dependent K+ channels. Nodes must also be properly spaced to ensure a high conduction velocity and energy efficiency without compromising the safety factor for reliable propagation. In this review, we consider the events responsible for axon development, emphasizing the involvement of ion channels. We discuss the current state of research in this area, including some controversies regarding mechanisms of neuron-glial communication.     

Retinal ganglion cell depletion alters the phenotypic expression of GABA and GAD in the rat retina

We have looked at the phenotypic expression of gamma-aminobutyric acid (GABA) and the two isoforms of its synthetic enzyme [glutamic acid decarboxylase (GAD)-65 and -67] in adult rat retinas that had the superior colliculus, pretectum and optic tract lesioned unilaterally at birth. It has been shown previously that this type of manipulation induces retrograde degeneration of retinal ganglion cells presumably without affecting other intraretinal neurons. We present evidence that GABAergic amacrine cells are affected by such manipulation. The number of cells immunoreactive for GABA, GAD-65 and GAD-67 decreased in the inner nuclear layer. In the retinal ganglion cell layer, however, the number of GABA- and GAD-65-labelled cells increased, while the number of GAD-67-labelled cells did not change. Biochemical assay showed that overall GAD activity was not altered in retinas of lesioned animals. Our results support the notion that, while neonatal lesion reorganizes the expression of GABA and GAD in the retina, enzyme activity is maintained within normal levels.     

GAP-43 expression in the medulla of macaque monkeys: changes during postnatal development and the effects of early median nerve repair

Expression of GAP-43, a neuronal specific growth associated phosphoprotein, has been highly correlated with the growth and remodeling of the nervous system during development and regeneration. As part of an effort to understand mechanisms of developmental plasticity in the somatosensory system, we determined how the expression of GAP-43 is affected by prenatal and early postnatal nerve cut and repair in macaque monkeys. We also observed normal developmental changes in the expression of GAP-43 during early postnatal life in macaque monkeys. The normal cuneate nucleus, as well as other nuclei of the ascending somatosensory pathways, had low levels of GAP-43 at birth that increased by 3 months and declined thereafter to reach adult levels between 8 and 15 months of age. Fiber tracts expressed low levels of GAP-43 at all postnatal ages, except the pyramidal tract which demonstrated high levels a birth that decreased over the first year. These observations suggest a gradual but differential synaptic maturation in lower brain stem nuclei as macaque monkeys mature. Greatly increased levels of GAP-43 were observed at the time of birth in the cuneate nucleus of two macaque monkeys with prenatal (E94 and El 14) nerve repair. Such an increase was not found after prenatal nerve repair with a postnatal survival time of 15 months, or after early postnatal nerve repair with short (80 days) or long (20 months) survivals. The results suggest that reorganization mechanisms at central terminals of peripheral nerves are very different following prenatal than postnatal nerve damage.     

Medial cell mixing during axial morphogenesis of the amphibian embryo requires cadherin function

A truncated form of Xenopus E-cadherin (deltaE-cad) comprising the cytoplasmic and transmembrane domains was overexpressed generating a dominant negative mutation in the urodelan amphibian embryo Pleurodeles waltl. deltaE-cad mRNA and rhodamine-lysinated-dextran (RLDx) cell lineage tracer were microinjected into 32-cell stage blastomeres which contribute principally to the notochord and central nervous system. deltaE-cad expression causes defects in forebrain and hindbrain formation coupled with the development of supernumerary vesicles. Duplication of the notochord also occurs due to the retardation of medial cell intercalation with correlated duplications of spinal cord and somites. These results emphasize the role of cadherins in mediating cell-cell adhesion in early amphibian embryogenesis. They extend to Pleurodeles the observations made in Xenopus, illustrating that despite differences in morphogenetic processes, the molecular mechanisms are conserved in these two species.     

Regulated binding of the protein kinase C substrate GAP-43 to the V0/C2 region of protein kinase C-delta

The interaction between protein kinase C-delta and its neuronal substrate, GAP-43, was studied. Two forms of protein kinase C-delta were isolated from COS cells and characterized by differences in gel mobility, GAP-43 binding, and specific GAP-43 and histone kinase activities. A slow migrating, low specific activity form of protein kinase C-delta bound directly to immobilized GAP-43. Binding was abolished in the presence of EGTA, suggesting Ca2+ dependence of the interaction. The free catalytic domain of protein kinase C-delta did not bind GAP-43, suggesting the existence of a binding site in the regulatory domain. Glutathione S-transferase-protein kinase C-delta regulatory domain fusion proteins were generated and tested for binding to GAP-43. The V0/C2-like amino-terminal domain was defined as the GAP-43-binding site. GAP-43 binding to this region is inhibited by EGTA and regulated at Ca2+ levels between 10(-7) and 10(-6) M. The interaction between protein kinase C-delta and GAP-43 was studied in intact cells by coexpression of the two proteins in human embryonic kidney cells followed by immunoprecipitation. Complex formation occurred only after treatment of the cells with the Ca2+ ionophore ionomycin, indicating that elevation of intracellular Ca2+ is required for interaction in vivo. It is concluded that protein kinase C-delta interacts with GAP-43 through the V0/C2-like domain, outside the catalytic site, and that this interaction is modulated by intracellular Ca2+.     

Up-regulation of Bax protein in degenerating retinal ganglion cells precedes apoptotic cell death after optic nerve lesion in the rat

Retrograde degeneration of retinal ganglion cells as a consequence of optic nerve lesion has been shown to fulfil the criteria of apoptosis. In the present study, we investigated the time course of ganglion cell apoptosis following intraorbital crushing of the optic nerve in adult rats using morphological criteria and applying a terminal transferase technique (TUNEL) for in situ detection of DNA strand breaks. In addition, we examined expression patterns of the anti-apoptotic proteins Bcl-2 and Bcl-X and the cell death-promoting protein Bax in retinae after crushing the optic nerve. Apoptotic nuclei were detected in the ganglion cell layer in the first 3 weeks after optic nerve crush, with a peak after 6 days. Bcl-2 and Bcl-X proteins were expressed in ganglion cells at low levels. Expression of Bcl-2 decreased further during the days following crush. Bcl-X expression was initially increased, followed by a decline over the following days. In contrast, Bax protein, which was expressed in most ganglion cells at moderate baseline levels, was sharply increased as early as 30 min after crush, reached peak levels after 3 days, and remained up-regulated for at least 1 week thereafter. Double labelling for Bax and TUNEL in retinal sections, however, did not reveal colocalization of the two signals in individual retinal ganglion cells, consistent with the idea that increases in Bax precede apoptosis after optic nerve lesion. Thus, retinal ganglion cell death might be prevented by ablation of Bax protein in these cells, or by up-regulation of Bax-antagonists such as Bcl-2 or Bcl-X.     

从主位功能及其推进模式看语篇的阅读理解

主位功能及其推进模式的研究对语篇的阅读理解有很强的实践价值.小句主位的定义和分类,高位主位的定义和确认,主位发展在语篇阅读理解中的功能和作用,主位链或述位链和标记性主位的功能和作用,与宏现主位相呼应的的回应主位的功能和作用以及主述位发展变化与语篇结构等与语篇的阅读理解的研究紧密联系.     

Temporal changes in beta-tubulin and neurofilament mRNA levels after transection of adult rat retinal ganglion cell axons in the optic nerve

Axons of adult mammalian retinal ganglion cells (RGCs) do not regenerate spontaneously after injury in the optic nerve and show a persistent decrease in the rate of transport of tubulin and neurofilament proteins. To investigate further the expression of cytoskeletal proteins in these axotomized CNS neurons, mRNA levels of beta-tubulin and the 150 kDa neurofilament subunit (NF-M) were measured after interrupting the optic nerve 9 mm from the eye. Northern blots of RNA extracted from whole retinas after optic nerve transection showed that the total level of both of these mRNAs fell after injury. To determine if this decrease was a result of the death of axotomized RGCs or reflected changes in individual neurons, RNA probes were hybridized to radial cryostat sections of normal and axotomized retinas from 1 d to 6 months after injury. Grain counts revealed two trends of tubulin expression in RGCs. An early increase in tubulin mRNAs in the axotomized RGCs was followed by a later decrease. Such an increase in tubulin mRNA levels has been correlated with regenerative growth in other neurons. By 1 week after injury, the beta-tubulin mRNA levels decreased to 70% of the control value. Moreover, the time of this fall coincided with the onset of a marked slowing of cytoskeletal transport that follows injury in the optic nerve. In contrast, NF-M mRNA levels dropped immediately after axotomy, and remained at 80% of the control level. It is suggested that the transient increase in tubulin mRNAs may reflect an early regenerative response whose persistence depends on further growth cone interactions with the substrate.     

Expression of beta-amyloid precursor protein immunoreactivity in the retina of the rat during normal development and after neonatal optic tract lesion

Immunoreactivity to beta-amyloid precursor protein (APP) was present in the inner plexiform, ganglion cell and optic fibre layers, as well as in blood vessels, at birth in normally developing rat retinas. In the inner plexiform layer immunoreactivity disappeared by postnatal day (P) 14. A small population of ganglion cells was immunoreactive at birth, but none were visible at P7. From P14 onwards, however, there was weak immunoreactivity in ganglion cells again, and strong staining in Müller glia. Retinas affected by neonatal optic tract lesions contained more immunoreactive ganglion cells at P4 than did controls, but by P14 there was a severe loss of ganglion cells. These observations are consistent with APP being involved in retinal differentiation, including maturation of glia and neurones, synaptogenesis and possibly neuronal survival.     

Quantitative relations in the retinal ganglion cell layer of the rat: neurons, glia and capillaries before and after optic nerve section

The severity of pulmonary fibrosis is the main prognostic factor for survival of patients with interstitial lung diseases (ILD). Unfortunately, lung biopsy, which is the best method to assess fibrosis quantitatively, is done only once during the evolution of the disease. In this study we analyzed the relationship between the degree of fibrosis and the exponential constant k, derived from the lung pressure-volume curve (LPVC) in 33 patients with chronic ILD, 19 with pigeon breeder's disease (PBD), and 14 with idiopathic pulmonary fibrosis (IPF). Pulmonary function tests, including the LPVC, were obtained before biopsy. A semiquantitative histologic assessment of the severity of fibrosis was performed on lung tissues. All patients showed a decrease of total lung capacity, residual volume, compliance, and Pao2. The mean value of the constant k was 0.08 +/- 0.06. When expressed as a percent of normal values, 25 patients exhibited values of k lower than 70% of predicted; of the remaining 8 patients whose values were above 70% of predicted, 7 had PBD and only one IPF. On morphologic analysis, 19 patients displayed more than 50% fibrosis. No significant correlations were found between the extent of the lesion or severity of lung fibrosis and the conventional pulmonary function tests. By contrast, a moderate but significant correlation was found between k and the severity of lung fibrosis (r = -0.38, p < 0.05). These findings show that the shape of the LPVC, represented by the constant k, predicts the degree of lung fibrosis and could be useful in the clinical assessment and follow-up of patients with ILD.     

Astrocyte progression from G1 to S phase of the cell cycle depends upon multiple protein interaction

The proliferation of cultured astrocytes is positively and negatively regulated, respectively, by the endogenous neuropeptides, endothelin-3 (ET-3) and atrial natriuretic peptide (ANP). Here, we determined the important steps for the modulation by ET and ANP of G1 to S phase cell cycle progression. ET-3 stimulated an increased number of fetal rat diencephalic astrocytes to progress through G1/S, and this was blocked significantly by ANP. ET augmented the gene expression and/or protein production of D-type, A and E cyclins, whereas ANP inhibited these events significantly. ET also stimulated the activation of the cyclin-dependent kinases Cdk2, Cdk4, and Cdk6, directed against the retinoblastoma protein pRb, and this was inhibited by as much as 80% by ANP. As an additional mechanism of cell cycle restraint, ANP stimulated the production of multiple cyclin-dependent kinase inhibitory (CKI) proteins, including p16, p27, and p57. This was critical because antisense oligonucleotides to each CKI reversed ANP-induced inhibition of ET-stimulated DNA synthesis by as much as 85%. CKI antisense oligonucleotides also reversed the ANP inhibition of Cdk phosphorylation of pRb. In turn, ET inhibited ANP-stimulated production of the CKIs, thereby promoting cell cycle progression. Specific and changing associations of the CKI with Cdk2 and Cdk4 were stimulated by ANP and inhibited by ET. Our findings identify several mechanisms by which endogenous modulators of astrocyte proliferation can control the G1-S progression and indicate that multiple CKIs are necessary to restrain cell cycle progression in these cells.     

Dendritic field development of retinal ganglion cells in the cat following neonatal damage to visual cortex: evidence for cell class specific interactions

A well-known feature of the mammalian retina is the inverse relation that exists in central and peripheral retina between the density of retinal ganglion cells and their dendritic field sizes. Functionally, this inverse relation is thought to represent a means by which retinal coverage is maintained, despite significant changes in ganglion cell density. While it is generally agreed that the dendritic fields of mature retinal ganglion cells reflect, in part, competitive interactions that occur during development, the issue of whether these interactions are cell class specific remains unclear. In order to examine this question, we used intracellular staining techniques and an in vitro, living retina preparation to compare the soma and dendritic field sizes of alpha and beta ganglion cells from normal retinae with those of cells located in matched areas of retinae in which the density of beta ganglion cells had been reduced selectively by neonatal removal of visual cortex areas 17, 18, and 19. Our intracellular data show that while an early, selective, reduction in beta cell density has little or no effect on the cell body and dendritic field sizes of mature alpha cells, it results in a 13% increase in the mean soma area and an 83% increase in the mean dendritic field area of surviving beta cells. This differential effect suggests that the soma and dendritic field sizes of alpha and beta ganglion cells in the mature cat retina result primarily from competitive interactions during development that are cell class specific.