Nerve Cells and Fibers in the Optic Lobe Cortex of Octopus

Author(s):  
Norman M. Case ◽  
E. G. Gray

Montages of electron micrographs from the outer portion of the cortex of the optic lobe of Octopus are shown. Sheets of dark cytoplasm which originate from glial cells in the outer granular layer form a basement layer separating the outer granular layer from the deeper plexiform layer.Optic nerve fibers from the retina entering the optic lobe around its periphery must pass between the amacrine cells composing the bulk of the outer granular layer. Here they are the darker of the two fiber types that can be identified. Passing through the basement layer they expand into large “carrot” shaped terminal endings easily identified by their dark appearance caused by the extremely high content of synaptic vesicles they contain.Fibers in the neuropil press tightly against and indent the “carrots” and occasionally make synaptic contact with them. Some fibers penetrate deeply into the “carrots” where they branch and terminate in grape-like clusters that show many synaptic contacts with the enveloping bag.

The synaptic contacts in the inner and outer plexiform layers of the frog retina have been identified and studied by electron microscopy. In the inner plexiform layer, two types of synaptic contact were recognized. One type, believed to be the synaptic contact of the bipolar terminals, is characterized by a synaptic ribbon in the presynaptic cytoplasm. At such ribbon contacts, there are ordinarily two postsynaptic elements, both of which usually contain numerous synaptic vesicles and appear morphologically identical. The second type of synaptic contact in the inner plexiform layer has a more conventional morpho­logy and is observed very much more frequently than are the ribbon contacts. It is characterized by a dense aggregation of synaptic vesicles clustered close to the presynaptic membrane and is thought to be the synaptic contact of the amacrine processes. The conventional synapses are presynaptic to ribbon-containing processes, ganglion cell dendrites, and other amacrine cell processes. Reciprocal contacts between processes making ribbon synapses, and processes making conventional synapses are often observed. Serial synapses between morphologically identical processes, presumably amacrine processes, are frequently seen; and up to four synapses in series between five adjacent processes have been observed. These findings suggest that in the inner plexiform layer of the frog: (1) bipolar terminals synapse primarily with amacrine processes; (2) amacrine processes synapse extensively with the processes of other amacrine cells; and (3) ganglion cells are driven primarily by the amacrine cells. In the outer plexiform layer, processes penetrate into invaginations in the bases of the receptor terminals and lie in close proximity to the synaptic ribbons of the terminals, where the processes presumably receive synaptic input from the receptors. Elsewhere in the outer plexiform layer, knob-like processes, probably from horizontal cells, make conventional synaptic contacts with other horizontal cell processes and probably with bipolar dendrites.


1971 ◽  
Vol 19 (2) ◽  
pp. 85-96 ◽  
Author(s):  
E. REALE ◽  
L. LUCIANO ◽  
M. SPITZNAS

In the rabbit retina acetylcholinesterase activity is localized in the perinuclear cisterna, in the cisternae of the rough surfaced endoplasmic reticulum and in the Golgi apparatus of ganglion cells and amacrine cells. The histochemical reaction is positive also in the rough surfaced endoplasmic reticulum of some horizontal cells. The highest activity is seen in the internal plexiform layer; because of artifacts caused by the diffusion of the enzyme, a clear demonstration of relation of the positivity to one or the other regular components of this layer, however, is not possible. Myelinated fibers which exhibit acetylcholinesterase activity and are most probably efferent are found in the internal plexiform layer. In the retinal nerve fiber layer and in the optic nerve only a few fibers show a positive reaction.


Each optic nerve contains several bundles of axons. The axons have their surface membranes directly apposed and the bundles lie in troughs of the elongated Schwann cells. The axons have pronounced varicosities along their length. The axons enter the optic lobe and run between the granule cells to synapse in the plexiform zone. The granule cells are small neurons. Their cytoplasmic organelles include endoplasmic reticulum, ribosomes, agranular reticulum and of special interest, oval or spherical bodies with a lamellated cortex and granular medulla. The elongated varicose presynaptic bags of the optic axons contain mitochondria in the proximal region, numerous synaptic vesicles and, sometimes, neurofilaments. Below the mitochondrial zone, synaptic contacts are made with small spines invaginated into the bags. The spines probably originate from the trunks of the granule cells. Tunnel fibres that are probably trunks of the outer granule cells, run through channels in the synaptic bags.


The optic lobes provide a system for coding the visual input, for storing a record of it and for decoding to produce particular motor responses. There are at least three types of optic nerve fibre, ending at different depths in the layered dendritic systems of the plexiform zone. Here the optic nerve fibres meet the branches of at least four types of cell. (1) Centripetal cells passing excitation inwards. The dendrites of these are very long, with fields orientated more often in horizontal and vertical than in other directions. (2) Numerous amacrine cells, with cone-shaped dendritic fields but no determinable axon. (3) Centrifugal cells conducting back to the retina. (4) Commissural fibres from the opposite optic lobe, and other afferents. After section of the optic nerves the plexiform layer of the corresponding part of the optic lobe becomes reduced, but the tangential layers of dendrites remain. There is a reduction in the thickness of the layers of amacrine and other cells and a shrinkage of the whole lobe. Conversely the tangential layers can be degenerated, leaving the optic nerve fibres, by severing the arteries to the optic lobe. The centre of the optic lobe contains cells with spreading dendritic trees of many forms. Some run mainly tangentially, others are radial cones. Those towards the centre send axons to the optic tract. Small multipolar cells accompany the large neurons of the cell islands. About 2 x 10 7 optic nerve fibres visible with the light microscope enter the lobes but only 0-5 x 106, or less, leave in the optic tract, these being distributed to some ten centres in the supraoesophageal lobes. It is suggested that the variety of shapes of the dendritic trees within the optic lobes provides the elements of the coding system by which visual input is classified.


PLoS ONE ◽  
2021 ◽  
Vol 16 (2) ◽  
pp. e0247401
Author(s):  
Rukiye Aydın ◽  
Mine Barış ◽  
Ceren Durmaz-Engin ◽  
Lama A. Al-Aswad ◽  
Dana M. Blumberg ◽  
...  

Glaucoma is a chronic neurodegenerative disease of the optic nerve and a leading cause of irreversible blindness, worldwide. While the experimental research using animal models provides growing information about cellular and molecular processes, parallel analysis of the clinical presentation of glaucoma accelerates the translational progress towards improved understanding, treatment, and clinical testing of glaucoma. Optic nerve axon injury triggers early alterations of retinal ganglion cell (RGC) synapses with function deficits prior to manifest RGC loss in animal models of glaucoma. For testing the clinical relevance of experimental observations, this study analyzed the functional correlation of localized alterations in the inner plexiform layer (IPL), where RGCs establish synaptic connections with retinal bipolar and amacrine cells. Participants of the study included a retrospective cohort of 36 eyes with glaucoma and a control group of 18 non-glaucomatous subjects followed for two-years. The IPL was analyzed on consecutively collected macular SD-OCT scans, and functional correlations with corresponding 10–2 visual field scores were tested using generalized estimating equations (GEE) models. The GEE-estimated rate of decrease in IPL thickness (R = 0.36, P<0.001) and IPL density (R = 0.36, P<0.001), as opposed to unchanged or increased IPL thickness or density, was significantly associated with visual field worsening at corresponding analysis locations. Based on multivariate logistic regression analysis, this association was independent from the patients’ age, the baseline visual field scores, or the baseline thickness or alterations of retinal nerve fiber or RGC layers (P>0.05). These findings support early localized IPL alterations in correlation with progressing visual field defects in glaucomatous eyes. Considering the experimental data, glaucoma-related increase in IPL thickness/density might reflect dendritic remodeling, mitochondrial redistribution, and glial responses for synapse maintenance, but decreased IPL thickness/density might correspond to dendrite atrophy. The bridging of experimental data with clinical findings encourages further research along the translational path.


1999 ◽  
Vol 16 (3) ◽  
pp. 475-481 ◽  
Author(s):  
HAI-BIAO LI ◽  
KWOK-FAI SO ◽  
WAH CHEUK

Light-microscopic immunocytochemistry was utilized to localize the different populations of substance P-immunoreactive (SP-IR) neurons in the hamster retina. Based on observation of 2505 SP-IR neurons in transverse sections, 34% were amacrine cells whose pear-shaped or round cell bodies (7–8 μm) were situated in the inner half of the inner nuclear layer (INL) or in the inner plexiform layer (IPL), while 66% of SP-IR somata (6–20 μm) were located in the ganglion cell layer (GCL) which were interpreted to be displaced amacrine cells and retinal ganglion cells (RGCs). At least three types of SP-IR amacrine cells were identified. The SP-IR processes were distributed in strata 1, 3, and 5 with the densest plexus in stratum 5 of the inner plexiform layer. In the wholemounted retina, the SP-IR cells were found to be distributed throughout the entire retina and their mean number was estimated to be 4224 ± 76. Two experiments were performed to clarify whether any of the SP-IR neurons in the GCL were RGCs. The first experiment demonstrated the presence of SP-IR RGCs by retrogradely labeling the RGCs and subsequently staining the SP-IR cells in the retina using immunocytochemistry. The second experiment identified SP-IR central projections of RGCs to the contralateral dorsal lateral geniculate nucleus. This projection disappeared following removal of the contralateral eye. The number of SP-IR RGCs was estimated following optic nerve section. At 2 months after sectioning the optic nerve, the total number of SP-IR neurons in the GCL reduced from 4224 ± 76 to a mean of 1192 ± 139. Assuming that all SP-IR neurons in the GCL which disappeared after nerve section were RGCs, the number of SP-IR RGCs was estimated to be 3032, representing 3–4% of the total RGCs. In summary, findings of the present study provide evidence for the existence of SP-IR RGCs in the hamster retina.


The optic nerve fibres project on to the optic lobe in a regular manner, being precisely re-assorted after passing through a chiasma. In the outer plexiform zone the optic nerve fibres end in contact with the dendrites of second-order visual cells. These presumably serve to classify the visual input and four types can be recognized anatomically: (1) The smallest have minute circular dendritic fields, in contact with one or few optic nerve fibres. (2) There are also larger circular fields. (3) Many cells have very elongated narrow dendritic fields each running straight in one direction and thus perhaps sensitive to edges. (4) The largest second-order visual cells have enormous oval dendritic fields, several millimetres long, orientated in the long axis of the lobe. Each type of field occupies a different level, producing the characteristic layering of the outer plexiform zone. Numerous amacrine cell processes end in the outer plexiform layer, some are very small with restricted branches, others have wide trees with fibres passing first inwards then outwards several times. There are thus possibilities of establishing uniform conditions of excitation or inhibition over small or large areas of the visual field. The dendrites of the centrifugal cells with axons passing to the retina spread in the various layers of the plexiform zone. They could serve to project information of the areas excited, or inhibited, out to the retina. The axons of the second-order visual cells form radial columns in the outer part of the medulla of the optic lobe. Those with the smaller dendritic fields end more superficially, the largest ones about half-way through the lobe. Each column contains fibres and neuropil at its centre, surrounded by multipolar and bipolar amacrine cells, whose branches enter the neuropil among the endings of the second-order visual cells. Horizontal multipolar cells of various sizes link the columns. Third-order visual cells send dendrites into these columns and axons deeper into the lobe, some directly to the optic tract. The giant cells of the magnocellular lobe can thus be activated by a visual pathway involving only two previous synapses (as well as by a direct static pathway involving none). Central to the zone of radial columns is a zone where many of the connexions are tangential. There is an increasing number of large cells passing centrally, many being presumably fourth-order visual neurons. They send axons either elsewhere within the lobe or to the optic tract. Fibres reaching the lobe from the central brain or opposite lobe are distributed in this region and also reach out into the radial columns. In many of the tracts leaving the optic lobes for other centres the fibres maintain precise topographical relations, as also do those of the optic commissure. This regularity is especially clear in the bundles that pass to the motor centres (peduncle lobes and anterior basal lobes) but may be present in others. There is thus a regular mapping of the visual field throughout much of the system. Other pathways show complex interweaving, for instance those for colour control, where the response pattern is not topographically related to the visual input.


Author(s):  
Charles A. Stirling

The lateral giant (LG) to motor giant (MoG) synapses in crayfish (Procambarus clarkii) abdominal ganglia are the classic electrotonic synapses. They have previously been described as having synaptic vesicles and as having them on both the pre- and postsynaptic sides of symmetrical synaptic junctions. This positioning of vesicles would make these very atypical synapses, but in the present work on the crayfish Astacus pallipes the motor giant has never been found to contain any type of vesicle at its synapses with the lateral giant fiber.The lateral to motor giant fiber synapses all occur on short branches off the main giant fibers. Closely associated with these giant fiber synapses are two small presynaptic nerves which make synaptic contact with both of the giant fibers and with their small branches.


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.


Biology ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 169
Author(s):  
Jacqueline Reinhard ◽  
Susanne Wiemann ◽  
Sebastian Hildebrandt ◽  
Andreas Faissner

Glaucoma is a neurodegenerative disease that is characterized by the loss of retinal ganglion cells (RGC) and optic nerve fibers. Increased age and intraocular pressure (IOP) elevation are the main risk factors for developing glaucoma. Mice that are heterozygous (HET) for the mega-karyocyte protein tyrosine phosphatase 2 (PTP-Meg2) show chronic and progressive IOP elevation, severe RGCs loss, and optic nerve damage, and represent a valuable model for IOP-dependent primary open-angle glaucoma (POAG). Previously, evidence accumulated suggesting that glaucomatous neurodegeneration is associated with the extensive remodeling of extracellular matrix (ECM) molecules. Unfortunately, little is known about the exact ECM changes in the glaucomatous retina and optic nerve. Hence, the goal of the present study was to comparatively explore ECM alterations in glaucomatous PTP-Meg2 HET and control wild type (WT) mice. Due to their potential relevance in glaucomatous neurodegeneration, we specifically analyzed the expression pattern of the ECM glycoproteins fibronectin, laminin, tenascin-C, and tenascin-R as well as the proteoglycans aggrecan, brevican, and members of the receptor protein tyrosine phosphatase beta/zeta (RPTPβ/ζ) family. The analyses were carried out in the retina and optic nerve of glaucomatous PTP-Meg2 HET and WT mice using quantitative real-time PCR (RT-qPCR), immunohistochemistry, and Western blot. Interestingly, we observed increased fibronectin and laminin levels in the glaucomatous HET retina and optic nerve compared to the WT group. RT-qPCR analyses of the laminins α4, β2 and γ3 showed an altered isoform-specific regulation in the HET retina and optic nerve. In addition, an upregulation of tenascin-C and its interaction partner RPTPβ/ζ/phosphacan was found in glaucomatous tissue. However, comparable protein and mRNA levels for tenascin-R as well as aggrecan and brevican were observed in both groups. Overall, our study showed a remodeling of various ECM components in the glaucomatous retina and optic nerve of PTP-Meg2 HET mice. This dysregulation could be responsible for pathological processes such as neovascularization, inflammation, and reactive gliosis in glaucomatous neurodegeneration.


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