Pub Date : 2021-01-01Epub Date: 2021-11-11DOI: 10.1017/s095252382100016x
Paul J May, Martin O Bohlen, Eddie Perkins, Niping Wang, Susan Warren
A projection by the superior colliculus to the supraoculomotor area (SOA) located dorsal to the oculomotor complex was first described in 1978. This projection's targets have yet to be identified, although the initial study suggested that vertical gaze motoneuron dendrites might receive this input. Defining the tectal targets is complicated by the fact the SOA contains a number of different cell populations. In the present study, we used anterograde tracers to characterize collicular axonal arbors and retrograde tracers to label prospective SOA target populations in macaque monkeys. Close associations were not found with either superior or medial rectus motoneurons whose axons supply singly innervated muscle fibers. S-group motoneurons, which supply superior rectus multiply innervated muscle fibers, appeared to receive a very minor input, but C-group motoneurons, which supply medial rectus multiply innervated muscle fibers, received no input. A number of labeled boutons were observed in close association with SOA neurons projecting to the spinal cord, or the reticular formation in the pons and medulla. These descending output neurons are presumed to be peptidergic cells within the centrally projecting Edinger-Westphal population. It is possible the collicular input provides a signaling function for neurons in this population that serve roles in either stress responses, or in eating and drinking behavior. Finally, a number of close associations were observed between tectal terminals and levator palpebrae superioris motoneurons, suggesting the possibility that the superior colliculus provides a modest direct input for raising the eyelids during upward saccades.
{"title":"Superior colliculus projections to target populations in the supraoculomotor area of the macaque monkey.","authors":"Paul J May, Martin O Bohlen, Eddie Perkins, Niping Wang, Susan Warren","doi":"10.1017/s095252382100016x","DOIUrl":"https://doi.org/10.1017/s095252382100016x","url":null,"abstract":"<p><p>A projection by the superior colliculus to the supraoculomotor area (SOA) located dorsal to the oculomotor complex was first described in 1978. This projection's targets have yet to be identified, although the initial study suggested that vertical gaze motoneuron dendrites might receive this input. Defining the tectal targets is complicated by the fact the SOA contains a number of different cell populations. In the present study, we used anterograde tracers to characterize collicular axonal arbors and retrograde tracers to label prospective SOA target populations in macaque monkeys. Close associations were not found with either superior or medial rectus motoneurons whose axons supply singly innervated muscle fibers. S-group motoneurons, which supply superior rectus multiply innervated muscle fibers, appeared to receive a very minor input, but C-group motoneurons, which supply medial rectus multiply innervated muscle fibers, received no input. A number of labeled boutons were observed in close association with SOA neurons projecting to the spinal cord, or the reticular formation in the pons and medulla. These descending output neurons are presumed to be peptidergic cells within the centrally projecting Edinger-Westphal population. It is possible the collicular input provides a signaling function for neurons in this population that serve roles in either stress responses, or in eating and drinking behavior. Finally, a number of close associations were observed between tectal terminals and levator palpebrae superioris motoneurons, suggesting the possibility that the superior colliculus provides a modest direct input for raising the eyelids during upward saccades.</p>","PeriodicalId":23556,"journal":{"name":"Visual Neuroscience","volume":null,"pages":null},"PeriodicalIF":1.9,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9699455/pdf/nihms-1832882.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40706992","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2020-10-08DOI: 10.1017/S0952523820000103
Jeffry I Fasick, Haya Algrain, Katherine M Serba, Phyllis R Robinson
The pigment reported in the Hara et al. (2018) study, however, is a member of the peropsin family of retinal pigments and was described by the authors as a member of the retinal pigment epitheliumderived rhodopsins, or RRhs, which typically possess lmax values in the blue region of the spectrum between 470–485 nm (Hao & Fong, 1996; Koyanagi et al., 2002). The whale shark RRh sequence from Hara et al. (2018) sorts with other shark RRh opsins (shown in Fig. 3) and is most likely a member of this family of retinal opsins and not an Rh1 opsin.
{"title":"The retinal pigments of the whale shark (Rhincodon typus) and their role in visual foraging ecology-CORRIGENDUM.","authors":"Jeffry I Fasick, Haya Algrain, Katherine M Serba, Phyllis R Robinson","doi":"10.1017/S0952523820000103","DOIUrl":"https://doi.org/10.1017/S0952523820000103","url":null,"abstract":"The pigment reported in the Hara et al. (2018) study, however, is a member of the peropsin family of retinal pigments and was described by the authors as a member of the retinal pigment epitheliumderived rhodopsins, or RRhs, which typically possess lmax values in the blue region of the spectrum between 470–485 nm (Hao & Fong, 1996; Koyanagi et al., 2002). The whale shark RRh sequence from Hara et al. (2018) sorts with other shark RRh opsins (shown in Fig. 3) and is most likely a member of this family of retinal opsins and not an Rh1 opsin.","PeriodicalId":23556,"journal":{"name":"Visual Neuroscience","volume":null,"pages":null},"PeriodicalIF":1.9,"publicationDate":"2020-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1017/S0952523820000103","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38560746","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2020-10-08DOI: 10.1017/S0952523820000085
Jeffry I Fasick, Phyllis R Robinson
In our recent article, Fasick et al. (2019), we examined 18 amino acid positions in the whale shark Rh1 gene that have previously been identified to influence the spectral tuning of Rh1 pigments. Based on this analysis, we established a predicted absorbance value of 496 nm for whale shark Rh1. A recent paper by Hart et al. (2020) confirms the model that we presented by comparing spectral tuning residues between whale shark Rh1 and bamboo shark Rh1. Hart et al. examined 46 spectral tuning positions and concluded that the 2 Rh1 sequences possessed identical residues at all spectral tuning positions involved with the wavelength modulation of normal, wildtype Rh1 pigments. We came to the conclusion that Hara et al. may have expressed whale shark RRh rather than Rh1 based on the fact that RRh pigments typically maximally absorb light <480 nm; only the RRh and not the Rh1 opsin sequence was curated in the Hara et al. supplemental files; and that the current modeling data supported a whale shark Rh1 pigment that maximally absorbs light near 500nm. Given the fact that Hara et al. state that whale shark Rh1 and not RRh was expressed by Hara et al., we acknowledge that they expressed a pigment with an absorbance maximum of 478 nm.
{"title":"Response to Kuraku et al., 2020.","authors":"Jeffry I Fasick, Phyllis R Robinson","doi":"10.1017/S0952523820000085","DOIUrl":"https://doi.org/10.1017/S0952523820000085","url":null,"abstract":"In our recent article, Fasick et al. (2019), we examined 18 amino acid positions in the whale shark Rh1 gene that have previously been identified to influence the spectral tuning of Rh1 pigments. Based on this analysis, we established a predicted absorbance value of 496 nm for whale shark Rh1. A recent paper by Hart et al. (2020) confirms the model that we presented by comparing spectral tuning residues between whale shark Rh1 and bamboo shark Rh1. Hart et al. examined 46 spectral tuning positions and concluded that the 2 Rh1 sequences possessed identical residues at all spectral tuning positions involved with the wavelength modulation of normal, wildtype Rh1 pigments. We came to the conclusion that Hara et al. may have expressed whale shark RRh rather than Rh1 based on the fact that RRh pigments typically maximally absorb light <480 nm; only the RRh and not the Rh1 opsin sequence was curated in the Hara et al. supplemental files; and that the current modeling data supported a whale shark Rh1 pigment that maximally absorbs light near 500nm. Given the fact that Hara et al. state that whale shark Rh1 and not RRh was expressed by Hara et al., we acknowledge that they expressed a pigment with an absorbance maximum of 478 nm.","PeriodicalId":23556,"journal":{"name":"Visual Neuroscience","volume":null,"pages":null},"PeriodicalIF":1.9,"publicationDate":"2020-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1017/S0952523820000085","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38560741","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Fasick et al. (2019) recently reported their analysis on whale shark opsins and claimed, without any firm ground, that our previous study on the whale shark rhodopsin (the product of the RHO gene, sometimes also called an Rh1 gene) (Hara et al., 2018) was not performed on the rhodopsin but on the peropsin (product of RRH gene).We have confirmed that we analyzed the product of the rhodopsin gene (Rhity0007829) that is phylogenetically categorized confidently in the clade of RHO (Supplementary Figure 8a of Hara et al., 2018) as described explicitly in our previous publication.
{"title":"Letter to the editor.","authors":"Shigehiro Kuraku, Kazuaki Yamaguchi, Akihisa Terakita, Mitsumasa Koyanagi","doi":"10.1017/S0952523820000073","DOIUrl":"https://doi.org/10.1017/S0952523820000073","url":null,"abstract":"Fasick et al. (2019) recently reported their analysis on whale shark opsins and claimed, without any firm ground, that our previous study on the whale shark rhodopsin (the product of the RHO gene, sometimes also called an Rh1 gene) (Hara et al., 2018) was not performed on the rhodopsin but on the peropsin (product of RRH gene).We have confirmed that we analyzed the product of the rhodopsin gene (Rhity0007829) that is phylogenetically categorized confidently in the clade of RHO (Supplementary Figure 8a of Hara et al., 2018) as described explicitly in our previous publication.","PeriodicalId":23556,"journal":{"name":"Visual Neuroscience","volume":null,"pages":null},"PeriodicalIF":1.9,"publicationDate":"2020-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1017/S0952523820000073","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38464526","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2020-10-06DOI: 10.1017/S0952523820000097
Silke Becker, Lara S Carroll, Frans Vinberg
Based on clinical findings, diabetic retinopathy (DR) has traditionally been defined as a retinal microvasculopathy. Retinal neuronal dysfunction is now recognized as an early event in the diabetic retina before development of overt DR. While detrimental effects of diabetes on the survival and function of inner retinal cells, such as retinal ganglion cells and amacrine cells, are widely recognized, evidence that photoreceptors in the outer retina undergo early alterations in diabetes has emerged more recently. We review data from preclinical and clinical studies demonstrating a conserved reduction of electrophysiological function in diabetic retinas, as well as evidence for photoreceptor loss. Complementing in vivo studies, we discuss the ex vivo electroretinography technique as a useful method to investigate photoreceptor function in isolated retinas from diabetic animal models. Finally, we consider the possibility that early photoreceptor pathology contributes to the progression of DR, and discuss possible mechanisms of photoreceptor damage in the diabetic retina, such as enhanced production of reactive oxygen species and other inflammatory factors whose detrimental effects may be augmented by phototransduction.
{"title":"Diabetic photoreceptors: Mechanisms underlying changes in structure and function.","authors":"Silke Becker, Lara S Carroll, Frans Vinberg","doi":"10.1017/S0952523820000097","DOIUrl":"https://doi.org/10.1017/S0952523820000097","url":null,"abstract":"<p><p>Based on clinical findings, diabetic retinopathy (DR) has traditionally been defined as a retinal microvasculopathy. Retinal neuronal dysfunction is now recognized as an early event in the diabetic retina before development of overt DR. While detrimental effects of diabetes on the survival and function of inner retinal cells, such as retinal ganglion cells and amacrine cells, are widely recognized, evidence that photoreceptors in the outer retina undergo early alterations in diabetes has emerged more recently. We review data from preclinical and clinical studies demonstrating a conserved reduction of electrophysiological function in diabetic retinas, as well as evidence for photoreceptor loss. Complementing in vivo studies, we discuss the ex vivo electroretinography technique as a useful method to investigate photoreceptor function in isolated retinas from diabetic animal models. Finally, we consider the possibility that early photoreceptor pathology contributes to the progression of DR, and discuss possible mechanisms of photoreceptor damage in the diabetic retina, such as enhanced production of reactive oxygen species and other inflammatory factors whose detrimental effects may be augmented by phototransduction.</p>","PeriodicalId":23556,"journal":{"name":"Visual Neuroscience","volume":null,"pages":null},"PeriodicalIF":1.9,"publicationDate":"2020-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1017/S0952523820000097","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38457997","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2020-09-16DOI: 10.1017/S095252382000005X
Erika D Eggers, Teresia A Carreon
Diabetic retinopathy is now well understood as a neurovascular disease. Significant deficits early in diabetes are found in the inner retina that consists of bipolar cells that receive inputs from rod and cone photoreceptors, ganglion cells that receive inputs from bipolar cells, and amacrine cells that modulate these connections. These functional deficits can be measured in vivo in diabetic humans and animal models using the electroretinogram (ERG) and behavioral visual testing. Early effects of diabetes on both the human and animal model ERGs are changes to the oscillatory potentials that suggest dysfunctional communication between amacrine cells and bipolar cells as well as ERG measures that suggest ganglion cell dysfunction. These are coupled with changes in contrast sensitivity that suggest inner retinal changes. Mechanistic in vitro neuronal studies have suggested that these inner retinal changes are due to decreased inhibition in the retina, potentially due to decreased gamma aminobutyric acid (GABA) release, increased glutamate release, and increased excitation of retinal ganglion cells. Inner retinal deficits in dopamine levels have also been observed that can be reversed to limit inner retinal damage. Inner retinal targets present a promising new avenue for therapies for early-stage diabetic eye disease.
{"title":"The effects of early diabetes on inner retinal neurons.","authors":"Erika D Eggers, Teresia A Carreon","doi":"10.1017/S095252382000005X","DOIUrl":"https://doi.org/10.1017/S095252382000005X","url":null,"abstract":"<p><p>Diabetic retinopathy is now well understood as a neurovascular disease. Significant deficits early in diabetes are found in the inner retina that consists of bipolar cells that receive inputs from rod and cone photoreceptors, ganglion cells that receive inputs from bipolar cells, and amacrine cells that modulate these connections. These functional deficits can be measured in vivo in diabetic humans and animal models using the electroretinogram (ERG) and behavioral visual testing. Early effects of diabetes on both the human and animal model ERGs are changes to the oscillatory potentials that suggest dysfunctional communication between amacrine cells and bipolar cells as well as ERG measures that suggest ganglion cell dysfunction. These are coupled with changes in contrast sensitivity that suggest inner retinal changes. Mechanistic in vitro neuronal studies have suggested that these inner retinal changes are due to decreased inhibition in the retina, potentially due to decreased gamma aminobutyric acid (GABA) release, increased glutamate release, and increased excitation of retinal ganglion cells. Inner retinal deficits in dopamine levels have also been observed that can be reversed to limit inner retinal damage. Inner retinal targets present a promising new avenue for therapies for early-stage diabetic eye disease.</p>","PeriodicalId":23556,"journal":{"name":"Visual Neuroscience","volume":null,"pages":null},"PeriodicalIF":1.9,"publicationDate":"2020-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1017/S095252382000005X","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38384280","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2020-09-14DOI: 10.1017/S0952523820000061
Shahriyar P Majidi, Rithwick Rajagopal
Vision loss, among the most feared complications of diabetes, is primarily caused by diabetic retinopathy, a disease that manifests in well-recognized, characteristic microvascular lesions. The reasons for retinal susceptibility to damage in diabetes are unclear, especially considering that microvascular networks are found in all tissues. However, the unique metabolic demands of retinal neurons could account for their vulnerability in diabetes. Photoreceptors are the first neurons in the visual circuit and are also the most energy-demanding cells of the retina. Here, we review experimental and clinical evidence linking photoreceptors to the development of diabetic retinopathy. We then describe the influence of retinal illumination on photoreceptor metabolism, effects of light modulation on the severity of diabetic retinopathy, and recent clinical trials testing the treatment of diabetic retinopathy with interventions that impact photoreceptor metabolism. Finally, we introduce several possible mechanisms that could link photoreceptor responses to light and the development of retinal vascular disease in diabetes. Collectively, these concepts form the basis for a growing body of investigative efforts aimed at developing novel pharmacologic and nonpharmacologic tools that target photoreceptor physiology to treat a very common cause of blindness across the world.
{"title":"Photoreceptor responses to light in the pathogenesis of diabetic retinopathy.","authors":"Shahriyar P Majidi, Rithwick Rajagopal","doi":"10.1017/S0952523820000061","DOIUrl":"https://doi.org/10.1017/S0952523820000061","url":null,"abstract":"<p><p>Vision loss, among the most feared complications of diabetes, is primarily caused by diabetic retinopathy, a disease that manifests in well-recognized, characteristic microvascular lesions. The reasons for retinal susceptibility to damage in diabetes are unclear, especially considering that microvascular networks are found in all tissues. However, the unique metabolic demands of retinal neurons could account for their vulnerability in diabetes. Photoreceptors are the first neurons in the visual circuit and are also the most energy-demanding cells of the retina. Here, we review experimental and clinical evidence linking photoreceptors to the development of diabetic retinopathy. We then describe the influence of retinal illumination on photoreceptor metabolism, effects of light modulation on the severity of diabetic retinopathy, and recent clinical trials testing the treatment of diabetic retinopathy with interventions that impact photoreceptor metabolism. Finally, we introduce several possible mechanisms that could link photoreceptor responses to light and the development of retinal vascular disease in diabetes. Collectively, these concepts form the basis for a growing body of investigative efforts aimed at developing novel pharmacologic and nonpharmacologic tools that target photoreceptor physiology to treat a very common cause of blindness across the world.</p>","PeriodicalId":23556,"journal":{"name":"Visual Neuroscience","volume":null,"pages":null},"PeriodicalIF":1.9,"publicationDate":"2020-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1017/S0952523820000061","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38471950","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2020-08-11DOI: 10.1017/S0952523820000048
Cyril G Eleftheriou, Elena Ivanova, Botir T Sagdullaev
Diabetic retinopathy (DR) is a frequent complication of diabetes mellitus and an increasingly common cause of visual impairment. Blood vessel damage occurs as the disease progresses, leading to ischemia, neovascularization, blood-retina barrier (BRB) failure and eventual blindness. Although detection and treatment strategies have improved considerably over the past years, there is room for a better understanding of the pathophysiology of the diabetic retina. Indeed, it has been increasingly realized that DR is in fact a disease of the retina's neurovascular unit (NVU), the multi-cellular framework underlying functional hyperemia, coupling neuronal computations to blood flow. The accumulating evidence reveals that both neurochemical (synapses) and electrical (gap junctions) means of communications between retinal cells are affected at the onset of hyperglycemia, warranting a global assessment of cellular interactions and their role in DR. This is further supported by the recent data showing down-regulation of connexin 43 gap junctions along the vascular relay from capillary to feeding arteriole as one of the earliest indicators of experimental DR, with rippling consequences to the anatomical and physiological integrity of the retina. Here, recent advancements in our knowledge of mechanisms controlling the retinal neurovascular unit will be assessed, along with their implications for future treatment and diagnosis of DR.
{"title":"Of neurons and pericytes: The neuro-vascular approach to diabetic retinopathy.","authors":"Cyril G Eleftheriou, Elena Ivanova, Botir T Sagdullaev","doi":"10.1017/S0952523820000048","DOIUrl":"https://doi.org/10.1017/S0952523820000048","url":null,"abstract":"<p><p>Diabetic retinopathy (DR) is a frequent complication of diabetes mellitus and an increasingly common cause of visual impairment. Blood vessel damage occurs as the disease progresses, leading to ischemia, neovascularization, blood-retina barrier (BRB) failure and eventual blindness. Although detection and treatment strategies have improved considerably over the past years, there is room for a better understanding of the pathophysiology of the diabetic retina. Indeed, it has been increasingly realized that DR is in fact a disease of the retina's neurovascular unit (NVU), the multi-cellular framework underlying functional hyperemia, coupling neuronal computations to blood flow. The accumulating evidence reveals that both neurochemical (synapses) and electrical (gap junctions) means of communications between retinal cells are affected at the onset of hyperglycemia, warranting a global assessment of cellular interactions and their role in DR. This is further supported by the recent data showing down-regulation of connexin 43 gap junctions along the vascular relay from capillary to feeding arteriole as one of the earliest indicators of experimental DR, with rippling consequences to the anatomical and physiological integrity of the retina. Here, recent advancements in our knowledge of mechanisms controlling the retinal neurovascular unit will be assessed, along with their implications for future treatment and diagnosis of DR.</p>","PeriodicalId":23556,"journal":{"name":"Visual Neuroscience","volume":null,"pages":null},"PeriodicalIF":1.9,"publicationDate":"2020-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1017/S0952523820000048","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38258787","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2020-07-20DOI: 10.1017/S0952523820000036
Amy R Nippert, Eric A Newman
Blood flow in the retina increases in response to light-evoked neuronal activity, ensuring that retinal neurons receive an adequate supply of oxygen and nutrients as metabolic demands vary. This response, termed "functional hyperemia," is disrupted in diabetic retinopathy. The reduction in functional hyperemia may result in retinal hypoxia and contribute to the development of retinopathy. This review will discuss the neurovascular coupling signaling mechanisms that generate the functional hyperemia response in the retina, the changes to neurovascular coupling that occur in diabetic retinopathy, possible treatments for restoring functional hyperemia and retinal oxygen levels, and changes to functional hyperemia that occur in the diabetic brain.
{"title":"Regulation of blood flow in diabetic retinopathy.","authors":"Amy R Nippert, Eric A Newman","doi":"10.1017/S0952523820000036","DOIUrl":"https://doi.org/10.1017/S0952523820000036","url":null,"abstract":"<p><p>Blood flow in the retina increases in response to light-evoked neuronal activity, ensuring that retinal neurons receive an adequate supply of oxygen and nutrients as metabolic demands vary. This response, termed \"functional hyperemia,\" is disrupted in diabetic retinopathy. The reduction in functional hyperemia may result in retinal hypoxia and contribute to the development of retinopathy. This review will discuss the neurovascular coupling signaling mechanisms that generate the functional hyperemia response in the retina, the changes to neurovascular coupling that occur in diabetic retinopathy, possible treatments for restoring functional hyperemia and retinal oxygen levels, and changes to functional hyperemia that occur in the diabetic brain.</p>","PeriodicalId":23556,"journal":{"name":"Visual Neuroscience","volume":null,"pages":null},"PeriodicalIF":1.9,"publicationDate":"2020-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1017/S0952523820000036","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38176433","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2020-06-17DOI: 10.1017/S0952523820000012
Matthias Schmidt
The nucleus glomerulosus (NG) in paracanthopterygian and acanthopterygian teleost fishes receives afferents from neurons of the nucleus corticalis (NC), whose dendrites extend to the layers, stratum fibrosum et griseum superficiale (SFGS) and stratum griseum centrale (SGC), of the tectum opticum. A re-examination in this study revealed, by means of tracer experiments using biotinylated dextran amine, a separation among both tectal layers, portions of the NC, and target areas in a laminated type of the NG in the South American pufferfish, Colomesus asellus. Neurons of the lateral part of the NC send their dendrites to the SFGS and project to an area located dorsolaterally and centrally in the NG. In contrast, dendrites from neurons of the medial part of the NC run to the SGC, and projections from these neurons terminate in the NG in an area extending from dorsomedial to ventrolateral in the outer portion. Therefore, these two areas in the NG receive input from different sources. The NG in the visual system of tetraodontids may be involved in higher cognitive functions requiring much energy, becoming apparent by its very high level of cytochrome c oxidase activity.
{"title":"Two different areas of the nucleus glomerulosus in the South American pufferfish, <i>Colomesus asellus</i>.","authors":"Matthias Schmidt","doi":"10.1017/S0952523820000012","DOIUrl":"https://doi.org/10.1017/S0952523820000012","url":null,"abstract":"<p><p>The nucleus glomerulosus (NG) in paracanthopterygian and acanthopterygian teleost fishes receives afferents from neurons of the nucleus corticalis (NC), whose dendrites extend to the layers, stratum fibrosum et griseum superficiale (SFGS) and stratum griseum centrale (SGC), of the tectum opticum. A re-examination in this study revealed, by means of tracer experiments using biotinylated dextran amine, a separation among both tectal layers, portions of the NC, and target areas in a laminated type of the NG in the South American pufferfish, Colomesus asellus. Neurons of the lateral part of the NC send their dendrites to the SFGS and project to an area located dorsolaterally and centrally in the NG. In contrast, dendrites from neurons of the medial part of the NC run to the SGC, and projections from these neurons terminate in the NG in an area extending from dorsomedial to ventrolateral in the outer portion. Therefore, these two areas in the NG receive input from different sources. The NG in the visual system of tetraodontids may be involved in higher cognitive functions requiring much energy, becoming apparent by its very high level of cytochrome c oxidase activity.</p>","PeriodicalId":23556,"journal":{"name":"Visual Neuroscience","volume":null,"pages":null},"PeriodicalIF":1.9,"publicationDate":"2020-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1017/S0952523820000012","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38109964","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}