A correlative study of the physiology and morphology of the retinotectal pathway of the perch

1990 ◽  
Vol 4 (4) ◽  
pp. 367-377 ◽  
Author(s):  
D. M. Guthrie ◽  
J. R. Banks

AbstractThe anatomy and physiology of the retinotectal pathway of the perch was investigated using physiological and histological techniques. Massed responses of the optic nerve to single shocks exhibited five distinct peaks. Single-unit responses to shocks indicate two groups of fast fibers correlating well with peaks I and II of the massed response. The flash-evoked response in nerve and tectum has three major phases (PSPI-III), with a marked low-threshold fast component. Patterns of flash-evoked response from single fibers vary, but the responses of fast transient fibers coincide with the timing of PSPI, and longer latency groups with PSPII-III. Units reflexly activated by efferents were also seen, and 12% of units were photically inexcitable.Surprisingly, few fibers responded well to a scanned spot light, unlike tectal cells, and receptive fields were often large (>70 deg). ON/OFF responses, evoked either by whole field or local illumination, were much commoner than pure ON or OFF responses.Effects of electrical stimulation or cautery of the tectum on the flash-evoked response of fiber bundles, via the efferents were marginal, but repetitive stimulation or section of the optic nerve produced clear-cut deficits in the slow components of the flash-evoked response of the nerve. Stimulation of the eighth nerve produced a complex long-latency, large-amplitude response in the optic nerve.The fiber spectrum of the optic nerve taken from electron micrographs revealed the presence of a relatively small group (less than 1%) of thick fibers with diameters between 3 μm and 10 μm that could be correlated with fast responses recorded from the optic nerve, and the remainder with axon diameters down to 0.2 μm providing the slow responses. The distribution of cell-body diameters from sectioned and wholemount material indicated a marked distinction between small and large ganglion cells. The total number of fibers in the nerve was estimated 868,840.

2019 ◽  
Vol 25 (28) ◽  
pp. 3057-3073 ◽  
Author(s):  
Kobra B. Juybari ◽  
Azam Hosseinzadeh ◽  
Habib Ghaznavi ◽  
Mahboobeh Kamali ◽  
Ahad Sedaghat ◽  
...  

Optic neuropathies refer to the dysfunction or degeneration of optic nerve fibers caused by any reasons including ischemia, inflammation, trauma, tumor, mitochondrial dysfunction, toxins, nutritional deficiency, inheritance, etc. Post-mitotic CNS neurons, including retinal ganglion cells (RGCs) intrinsically have a limited capacity for axon growth after either trauma or disease, leading to irreversible vision loss. In recent years, an increasing number of laboratory evidence has evaluated optic nerve injuries, focusing on molecular signaling pathways involved in RGC death. Trophic factor deprivation (TFD), inflammation, oxidative stress, mitochondrial dysfunction, glutamate-induced excitotoxicity, ischemia, hypoxia, etc. have been recognized as important molecular mechanisms leading to RGC apoptosis. Understanding these obstacles provides a better view to find out new strategies against retinal cell damage. Melatonin, as a wide-spectrum antioxidant and powerful freeradical scavenger, has the ability to protect RGCs or other cells against a variety of deleterious conditions such as oxidative/nitrosative stress, hypoxia/ischemia, inflammatory processes, and apoptosis. In this review, we primarily highlight the molecular regenerative and degenerative mechanisms involved in RGC survival/death and then summarize the possible protective effects of melatonin in the process of RGC death in some ocular diseases including optic neuropathies. Based on the information provided in this review, melatonin may act as a promising agent to reduce RGC death in various retinal pathologic conditions.


Biomolecules ◽  
2021 ◽  
Vol 11 (4) ◽  
pp. 496
Author(s):  
Alessandra Maresca ◽  
Valerio Carelli

Inherited neurodegeneration of the optic nerve is a paradigm in neurology, as many forms of isolated or syndromic optic atrophy are encountered in clinical practice. The retinal ganglion cells originate the axons that form the optic nerve. They are particularly vulnerable to mitochondrial dysfunction, as they present a peculiar cellular architecture, with axons that are not myelinated for a long intra-retinal segment, thus, very energy dependent. The genetic landscape of causative mutations and genes greatly enlarged in the last decade, pointing to common pathways. These mostly imply mitochondrial dysfunction, which leads to a similar outcome in terms of neurodegeneration. We here critically review these pathways, which include (1) complex I-related oxidative phosphorylation (OXPHOS) dysfunction, (2) mitochondrial dynamics, and (3) endoplasmic reticulum-mitochondrial inter-organellar crosstalk. These major pathogenic mechanisms are in turn interconnected and represent the target for therapeutic strategies. Thus, their deep understanding is the basis to set and test new effective therapies, an urgent unmet need for these patients. New tools are now available to capture all interlinked mechanistic intricacies for the pathogenesis of optic nerve neurodegeneration, casting hope for innovative therapies to be rapidly transferred into the clinic and effectively cure inherited optic neuropathies.


1989 ◽  
Vol 94 (6) ◽  
pp. 987-995 ◽  
Author(s):  
J B Troy ◽  
C Enroth-Cugell

We examined the dependence of the center radius of X cells on temporal frequency and found that at temporal frequencies above 40 Hz the radius increases in a monotonic fashion, reaching a size approximately 30% larger at 70 Hz. This kind of spatial expansion has been predicted with cable models of receptive fields where inductive elements are included in modeling the neuronal membranes. Hence, the expansion of the center radius is clearly important for modeling X cell receptive fields. On the other hand, we feel that it might be of only minor functional significance, since the responsivity of X cells is attenuated at these high temporal frequencies and the signal-to-noise ratio is considerably worse than at low and midrange temporal frequencies.


2021 ◽  
Vol 51 (6) ◽  
pp. 816-819
Author(s):  
A. T. Aliper ◽  
I. Damjanovic ◽  
A. A. Zaichikova ◽  
E. M. Maximova ◽  
P. V. Maximov

2017 ◽  
Vol 27 (08) ◽  
pp. 1750045 ◽  
Author(s):  
Eduardo Sánchez ◽  
Rubén Ferreiroa ◽  
Adrián Arias ◽  
Luis M. Martínez

The center–surround organization of the receptive fields (RFs) of retinal ganglion cells highlights the presence of local contrast in visual stimuli. As RF of thalamic relay cells follow the same basic functional organization, it is often assumed that they contribute very little to alter the retinal output. However, in many species, thalamic relay cells largely outnumber their retinal inputs, which diverge to contact simultaneously several units at thalamic level. This gain in cell population as well as retinothalamic convergence opens the door to question how information about contrast is transformed at the thalamic stage. Here, we address this question using a realistic dynamic model of the retinothalamic circuit. Our results show that different components of the thalamic RF might implement filters that are analogous to two types of well-known image processing techniques to preserve the quality of a higher resolution version of the image on its way to the primary visual cortex.


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