Melanopsin and non-melanopsin expressing retinal ganglion cells innervate the hypothalamic suprachiasmatic nucleus

2003 ◽  
Vol 20 (6) ◽  
pp. 601-610 ◽  
Author(s):  
PATRICIA J. SOLLARS ◽  
CYNTHIA A. SMERASKI ◽  
JESSICA D. KAUFMAN ◽  
MALCOLM D. OGILVIE ◽  
IGNACIO PROVENCIO ◽  
...  
Keyword(s):  
Retinal Ganglion Cells ◽  
Suprachiasmatic Nucleus ◽  
Pseudorabies Virus ◽  
Fluorescent Protein ◽  
Ganglion Cells ◽  
Optic Tract ◽  
Retrograde Transport ◽  
Lateral Geniculate Body ◽  
Retinal Ganglion ◽  
Green Fluorescent

Retinal input to the hypothalamic suprachiasmatic nucleus (SCN) synchronizes the SCN circadian oscillator to the external day/night cycle. Retinal ganglion cells that innervate the SCN via the retinohypothalamic tract are intrinsically light sensitive and express melanopsin. In this study, we provide data indicating that not all SCN-projecting retinal ganglion cells express melanopsin. To determine the proportion of ganglion cells afferent to the SCN that express melanopsin, ganglion cells were labeled following transsynaptic retrograde transport of a recombinant of the Bartha strain of pseudorabies virus (PRV152) constructed to express the enhanced green fluorescent protein (EGFP). PRV152 injected into the anterior chamber of the eye retrogradely infects four retinorecipient nuclei in the brain via autonomic circuits to the eye, resulting in transneuronally labeled ganglion cells in the contralateral retina 96 h after intraocular infection. In animals with large bilateral lesions of the lateral geniculate body/optic tract, ganglion cells labeled with PRV152 are retrogradely infected from only the SCN. In these animals, most PRV152-infected ganglion cells were immunoreactive for melanopsin. However, a significant percentage (10–20%) of EGFP-labeled ganglion cells did not express melanopsin. These data suggest that in addition to the intrinsically light-sensitive melanopsin-expressing ganglion cells, conventional ganglion cells also innervate the SCN. Thus, it appears that the rod/cone system of photoreceptors may provide signals to the SCN circadian system independent of intrinsically light-sensitive melanopsin ganglion cells.

Pathways of regenerated retinotectal axons in goldfish

Development ◽  
1986 ◽  
Vol 93 (1) ◽  
pp. 1-28
Author(s):  
Claudia A. O. Stuermer
Keyword(s):  
Optic Nerve ◽  
Retinal Ganglion Cells ◽  
Normal Development ◽  
Ganglion Cells ◽  
Optic Tract ◽  
Spatiotemporal Pattern ◽  
Retinal Ganglion ◽  
Retinal Axons ◽  
Age Related ◽  
Regenerated Fibres

This study investigates the order of regenerating retinal axons in the goldfish. The spatiotemporal pattern of axon regrowth was assessed by applying horseradish peroxidase (HRP) to regenerating axons in the optic tract at various times after optic nerve section and by analysing the distribution of retrogradely labelled ganglion cells in retina. At all regeneration stages labelled ganglion cells were widely distributed over the retina. There was no hint that axons from central (older) ganglion cells might regrow earlier, and peripheral (younger) ganglion cells later, as occurs in normal development. The absence of an age-related ordering in the regenerated optic nerve was demonstrated by labelling a few axon bundles intraorbitally with HRP (Easter, Rusoff & Kish, 1981) caudal to the previous cut. The retrogradely labelled cells in retina were randomly distributed in regenerates andnot clustered in annuli as in normals. Tracing regenerating axons which were stained anterogradelyfrom intraretinal HRP applications or retrogradely from single labelled tectal fascicles illustrated the fact that the regenerating axons coursed in abnormal routes in the optic nerve and tract. On the surface of the tectum regenerated fibres re-established a fascicle fan. The retinal origin of tectal fascicles was assessed by labelling individual peripheral, intermediate and rostral fascicles with HRP. The retrogradely labelled ganglion cells in the retina were often more widely distributed than in normals, but were mostly found in peripheral, intermediate and central retina, respectively. The order of fibre departure from each tectal fascicle was revealed by placing HRP either on the fascicle's proximal or on its distal half. With proximal labelling sites labelled ganglion cells were found in the temporal and nasal retina, and with distal labelling sites labelled ganglion cells were confined to nasal retina only. Further, the axonal trajectories of anterogradely labelled dorsotemporal retinal ganglion cells were compared to those of dorsonasal retinal ganglion cells in tectal whole mounts. Dorsotemporal axons were confined to the rostral tectal half, whereas dorsonasal axons followed fascicular routes into the fascicles' distal end and reached into caudal tectum. This suggests that the fibres exited along their fascicle's course in a temporonasal sequence. Thus in the tectum, fibres in fascicles restore a gross spatial and age-related order and tend to follow their normal temporonasal sequence of exit.

Abnormally high variability in the uncrossed retinofugal pathway of mice with albino mosaicism

Development ◽  
1987 ◽  
Vol 101 (4) ◽  
pp. 857-867 ◽  
Author(s):  
R.W. Guillery ◽  
G. Jeffery ◽  
B.M. Cattanach
Keyword(s):  
Retinal Ganglion Cells ◽  
Ganglion Cells ◽  
Gene Dosage ◽  
Optic Tract ◽  
High Variability ◽  
Retinal Ganglion ◽  
Rare Occurrence ◽  
Autosome Translocation ◽  
Open Question ◽  
The Relationship

Female mice showing albino mosaicism due to an X-autosome translocation [Is(In7;X)Ct] have been studied in order to investigate the relationship between the distribution of melanin and the formation, early in development, of the abnormally small uncrossed retinofugal pathway characteristically found in all albino mammals. Earlier evidence indicates that cells normally bearing melanin play a role in producing the abnormality. In the mosaic mice, the albino gene is expressed in only about half of the cells due to random X-inactivation and the patches of normal and albino cells are extremely small relative to total retinal size (less than 1/50). We argued that if all the cells that would normally bear melanin play a role in producing the albino abnormality then the mosaic mice would have a pathway abnormality, about half the size of that in the albino mice. If, however, only a small patch of these cells plays a role, as has been proposed in earlier studies, then one would expect the size of the uncrossed pathway to be highly variable in the mosaic mice. The size of the uncrossed pathway was assessed by placing horseradish peroxidase in the region of the optic tract and lateral geniculate nucleus unilaterally and then counting the number of retrogradely labelled retinal ganglion cells on the same side. The mosaic mice showed a highly variable uncrossed pathway. In some of the mosaic mice, it was the same size as in the albinos and, in others, it was the same size as in normally pigmented mice. Surprisingly, in a small number of mosaic mice, the uncrossed pathway was larger than normal. Whether this relatively rare occurrence of a supernormal uncrossed pathway is due to the higher gene dosage or to the translocation itself remains an open question.

scholarly journals Target-Derived Neurotrophic Factor Deprivation Puts Retinal Ganglion Cells on Death Row: Cold Hard Evidence and Caveats

2019 ◽  
Vol 20 (17) ◽  
pp. 4314 ◽  
Author(s):  
Marie Claes ◽  
Lies De Groef ◽  
Lieve Moons
Keyword(s):  
Animal Models ◽  
Disease Progression ◽  
Retinal Ganglion Cells ◽  
Neurotrophic Factors ◽  
Neurotrophic Factor ◽  
Ganglion Cells ◽  
Retrograde Transport ◽  
Retinal Ganglion ◽  
Hard Evidence ◽  
Glaucoma Treatment

Glaucoma and other optic neuropathies are characterized by axonal transport deficits. Axonal cargo travels back and forth between the soma and the axon terminus, a mechanism ensuring homeostasis and the viability of a neuron. An example of vital molecules in the axonal cargo are neurotrophic factors (NTFs). Hindered retrograde transport can cause a scarcity of those factors in the retina, which in turn can tilt the fate of retinal ganglion cells (RGCs) towards apoptosis. This postulation is one of the most widely recognized theories to explain RGC death in the disease progression of glaucoma and is known as the NTF deprivation theory. For several decades, research has been focused on the use of NTFs as a novel neuroprotective glaucoma treatment. Until now, results in animal models have been promising, but translation to the clinic has been highly disappointing. Are we lacking important knowledge to lever NTF therapies towards the therapeutic armamentarium? Or did we get the wrong end of the stick regarding the NTF deprivation theory? In this review, we will tackle the existing evidence and caveats advocating for and against the target-derived NTF deprivation theory in glaucoma, whilst digging into associated therapy efforts.

The effect of retinal growth on the postnatal development and distribution of displaced retinal ganglion cells in the retina of the chameleon (squamata)

2003 ◽  
Vol 20 (3) ◽  
pp. 273-283 ◽  
Author(s):  
MATTHIAS OTT ◽  
BRENO BELLINTANI-GUARDIA
Keyword(s):  
Retinal Ganglion Cells ◽  
Ganglion Cells ◽  
Retrograde Transport ◽  
Dendritic Arbor ◽  
Adult Size ◽  
Retinal Ganglion ◽  
Accessory Optic System ◽  
Dendritic Field ◽  
Eye Size ◽  
Retinal Growth

Retinal ganglion cells (RGCs) usually increase their dendritic field area with postnatal retinal growth. The mechanisms that regulate the postnatal shape of dendritic arbors in the growing retina are not well understood. Quantitative studies suffer from the difficulty of labeling specific subpopulations of RGCs selectively including their dendritic processes. In this study, we labeled displaced retinal ganglion cells (DGC) that are known to project to the accessory optic system (AOS) in juvenile and adult chameleons by retrograde transport of dextran amines. The complete population of DGCs was quantitatively screened for the effects of postnatal retinal growth on cell morphology, dendritic field coverage, and dendritic arbor size. The adult eye contained 2000 DGCs/retina. This number was already present at birth. The smaller size of the hatchling eye (approximately 1/3 of the adult size) led to higher densities of DGCs. The greatest accumulation of juvenile DGCs (two-fold higher compared to the adult) was found in the periphery of the retina where the greatest surface expansion was observed. DGC dendritic field areas were adjusted proportionally to this expansion in order to maintain a constant dendritic coverage. The increase of dendritic fields was mediated by two putative passive mechanisms: First, an elongation of individual dendrites similar to previous reports of postnatal RGC development in the retina of goldfish and chicks. Second, and more prominent, we observed that neighboring dendrites were pulled apart from each other. This resulted in a looser spacing of the initially tightly packed dendrites of each dendritic arbor. This dispersal of dendrites over a larger area was, due to its passive nature, proportional to the increase of the retinal surface and preserved a constant dendritic coverage irrespective of the animal's age and eye size.

scholarly journals Rat's Nucleus of the Optic Tract and Retinal Ganglion Cells

1991 ◽  
Vol 1991 (Supplement51) ◽  
pp. 10-17
Author(s):  
Isao Kato ◽  
Tomoyuki Okada ◽  
Shoji Watanabe ◽  
Shigeki Sato ◽  
Isamu Takeyama
Keyword(s):  
Retinal Ganglion Cells ◽  
Ganglion Cells ◽  
Optic Tract ◽  
Retinal Ganglion
Sign in / Sign up

Export Citation Format

Share Document