Anatomical Specializations Related to Foraging in the Visual System of a Nocturnal Insectivorous Bird, the Band-Winged Nightjar (Aves: Caprimulgiformes)

2019 ◽  
Vol 94 (Suppl. 1-4) ◽  
pp. 27-36 ◽  
Author(s):  
Juan Esteban Salazar ◽  
Daniel Severin ◽  
Tomas Vega-Zuniga ◽  
Pedro Fernández-Aburto ◽  
Alfonso Deichler ◽  
...  

Nocturnal animals that rely on their visual system for foraging, mating, and navigation usually exhibit specific traits associated with living in scotopic conditions. Most nocturnal birds have several visual specializations, such as enlarged eyes and an increased orbital convergence. However, the actual role of binocular vision in nocturnal foraging is still debated. Nightjars (Aves: Caprimulgidae) are predators that actively pursue and capture flying insects in crepuscular and nocturnal environments, mainly using a conspicuous “sit-and-wait” tactic on which pursuit begins with an insect flying over the bird that sits on the ground. In this study, we describe the visual system of the band-winged nightjar (Systellura longirostris), with emphasis on anatomical features previously described as relevant for nocturnal birds. Orbit convergence, determined by 3D scanning of the skull, was 73.28°. The visual field, determined by ophthalmoscopic reflex, exhibits an area of maximum binocular overlap of 42°, and it is dorsally oriented. The eyes showed a nocturnal-like normalized corneal aperture/axial length index. Retinal ganglion cells (RGCs) were relatively scant, and distributed in an unusual oblique-band pattern, with higher concentrations in the ventrotemporal quadrant. Together, these results indicate that the band-winged nightjar exhibits a retinal specialization associated with the binocular area of their dorsal visual field, a relevant area for pursuit triggering and prey attacks. The RGC distribution observed is unusual among birds, but similar to that of some visually dependent insectivorous bats, suggesting that those features might be convergent in relation to feeding strategies.

Author(s):  
Shadi Rajabi ◽  
Craig A. Simmons ◽  
C. Ross Ethier

Glaucoma, a chronic optic neuropathy, is the second most common cause of blindness, affecting 67 million people worldwide. The damage in glaucoma occurs at the optic nerve head (ONH), where the axons of the retinal ganglion cells leave the eye posteriorly. Glaucoma is frequently associated with elevated intraocular pressure (IOP), and visual field loss can be prevented by significant lowering of IOP. Hence, the role of pressure in glaucoma is important. Unfortunately, the mechanism by which pressure leads to vision loss in glaucoma is very poorly understood.


Development ◽  
1994 ◽  
Vol 120 (6) ◽  
pp. 1643-1649 ◽  
Author(s):  
K.H. Herzog ◽  
K. Bailey ◽  
Y.A. Barde

Using a sensitive and quantitative method, the mRNA levels of brain-derived neurotrophic factor (BDNF) were determined during the development of the chick visual system. Low copy numbers were detected, and BDNF was found to be expressed in the optic tectum already 2 days before the arrival of the first retinal ganglion cell axons, suggesting an early role of BDNF in tectal development. After the beginning of tectal innervation, BDNF mRNA levels markedly increased, and optic stalk transection at day 4 (which prevents subsequent tectal innervation) was found to reduce the contralateral tectal levels of BDNF mRNA. Comparable reductions were obtained after injection of tetrodotoxin into one eye, indicating that, already during the earliest stages of target encounter in the CNS, the degree of BDNF gene expression is influenced by activity-dependent mechanisms. BDNF mRNA was also detected in the retina itself and at levels comparable to those found in the tectum. Together with previous findings indicating that BDNF prevents the death of cultured chick retinal ganglion cells, these results support the idea that the tightly controlled expression of the BDNF gene might be important in the co-ordinated development of the visual system.


2011 ◽  
Vol 52 (8) ◽  
pp. 5515 ◽  
Author(s):  
Preethi S. Ganapathy ◽  
Richard E. White ◽  
Yonju Ha ◽  
B. Renee Bozard ◽  
Paul L. McNeil ◽  
...  

2019 ◽  
Vol 16 (1) ◽  
Author(s):  
Barakat Alrashdi ◽  
Bassel Dawod ◽  
Andrea Schampel ◽  
Sabine Tacke ◽  
Stefanie Kuerten ◽  
...  

Abstract Background In multiple sclerosis (MS) and in the experimental autoimmune encephalomyelitis (EAE) model of MS, the Nav1.6 voltage-gated sodium (Nav) channel isoform has been implicated as a primary contributor to axonal degeneration. Following demyelination Nav1.6, which is normally co-localized with the Na+/Ca2+ exchanger (NCX) at the nodes of Ranvier, associates with β-APP, a marker of neural injury. The persistent influx of sodium through Nav1.6 is believed to reverse the function of NCX, resulting in an increased influx of damaging Ca2+ ions. However, direct evidence for the role of Nav1.6 in axonal degeneration is lacking. Methods In mice floxed for Scn8a, the gene that encodes the α subunit of Nav1.6, subjected to EAE we examined the effect of eliminating Nav1.6 from retinal ganglion cells (RGC) in one eye using an AAV vector harboring Cre and GFP, while using the contralateral either injected with AAV vector harboring GFP alone or non-targeted eye as control. Results In retinas, the expression of Rbpms, a marker for retinal ganglion cells, was found to be inversely correlated to the expression of Scn8a. Furthermore, the gene expression of the pro-inflammatory cytokines Il6 (IL-6) and Ifng (IFN-γ), and of the reactive gliosis marker Gfap (GFAP) were found to be reduced in targeted retinas. Optic nerves from targeted eyes were shown to have reduced macrophage infiltration and improved axonal health. Conclusion Taken together, our results are consistent with Nav1.6 promoting inflammation and contributing to axonal degeneration following demyelination.


Redox Biology ◽  
2019 ◽  
Vol 24 ◽  
pp. 101199 ◽  
Author(s):  
Soumya Navneet ◽  
Jing Zhao ◽  
Jing Wang ◽  
Barbara Mysona ◽  
Shannon Barwick ◽  
...  

PLoS ONE ◽  
2013 ◽  
Vol 8 (10) ◽  
pp. e76590 ◽  
Author(s):  
Amir H. Marvasti ◽  
Andrew J. Tatham ◽  
Linda M. Zangwill ◽  
Christopher A. Girkin ◽  
Jeffrey M. Liebmann ◽  
...  

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