Eye And Brain[JOURNAL]
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183 papers
Retinopathy of prematurity: the need for prevention.
Liegl R, Hellström A, Smith LE
Eye Brain · 2016 · PMID 28539804 · Full text
More than 450,000 babies are born prematurely in the USA every year. The improved survival of even the most vulnerable low body weight preterm infants has, despite improving health outcomes, led to the resurgence in pret...
More than 450,000 babies are born prematurely in the USA every year. The improved survival of even the most vulnerable low body weight preterm infants has, despite improving health outcomes, led to the resurgence in preterm complications including one of the major causes for blindness in children, retinopathy of prematurity (ROP). The current mainstay in ROP therapy is laser photocoagulation and the injection of vascular endothelial growth factor (VEGF) antibodies in the late stages of the disease after the onset of neovascularization. Both are proven options for ophthalmologists to treat the severe forms of late ROP. However, laser photocoagulation destroys major parts of the retina, and the injection of VEGF antibodies, although rather simple to administer, may cause a systemic suppression of normal vascularization, which has not been studied in sufficient depth. However, the use of neither VEGF antibody nor laser treatment prevents ROP, which should be the long-term goal. It should be possible to prevent ROP by more closely mimicking the intrauterine environment after preterm birth. Such preventive measures include preventing the toxic postbirth influences (eg, oxygen excess) as well as providing the missing intrauterine factors (eg, insulin growth factor 1) and are likely to also reduce other complications of premature birth as well as ROP. This review is meant to summarize the current knowledge on the prevention of ROP with a particular emphasize on the use of insulin growth factor 1 supplementation.
Anti-VEGF therapy in the management of retinopathy of prematurity: what we learn from representative animal models of oxygen-induced retinopathy.
Wang H
Eye Brain · 2016 · PMID 28539803 · Full text
Retinopathy of prematurity (ROP) remains a leading cause of childhood blindness, affecting infants born prematurely. ROP is characterized by the onset of delayed physiological retinal vascular development (PRVD) and foll...
Retinopathy of prematurity (ROP) remains a leading cause of childhood blindness, affecting infants born prematurely. ROP is characterized by the onset of delayed physiological retinal vascular development (PRVD) and followed by pathologic neovascularization into the vitreous instead of the retina, called intravitreal neovascularization (IVNV). Therefore, the therapeutic strategy for treating ROP is to promote PRVD and inhibit or prevent IVNV. Vascular endothelial growth factor (VEGF) plays an important role in the pathogenesis of ROP. There is a growing body of studies testing the use of anti-VEGF agents as a treatment for ROP. Intravitreal anti-VEGF treatment for ROP has potential advantages compared with laser photocoagulation, the gold standard for the treatment of severe ROP; however, intravitreal anti-VEGF treatment has been associated with reactivation of ROP and suppression of systemic VEGF that may affect body growth and organ development in preterm infants. Therefore, it is important to understand the role of VEGF in PRVD and IVNV. This review includes the current knowledge of anti-VEGF treatment for ROP from animal models of oxygen-induced retinopathy (OIR), highlighting the importance of VEGF inhibition by targeting retinal Müller cells, which inhibits IVNV and permits PRVD. The signaling events involved in mediating VEGF expression and promoting VEGF-mediated angiogenesis, including hypoxia-dependent signaling, erythropoietin/erythropoietin receptor-, oxidative stress-, beta-adrenergic receptor-, integrin-, Notch/Delta-like ligand 4- and exon guidance molecules-mediated signaling pathways, are also discussed.
Targeting VEGF in canine oxygen-induced retinopathy - a model for human retinopathy of prematurity.
McLeod DS, Lutty GA
Eye Brain · 2016 · PMID 28539802 · Full text
Development of the dog superficial retinal vasculature is similar to the mechanism of human retinal vasculature development; they both develop by vasculogenesis, differentiation, and assembly of vascular precursors calle...
Development of the dog superficial retinal vasculature is similar to the mechanism of human retinal vasculature development; they both develop by vasculogenesis, differentiation, and assembly of vascular precursors called angioblasts. Canine oxygen-induced retinopathy (OIR) was first developed by Arnall Patz in an effort to experimentally determine the effects of hyperoxia on the development of the retinal vasculature. The canine OIR model has many characteristics in common with human retinopathy of prematurity. Exposure of 1-day-old dogs to hyperoxia for 4 days causes a vaso-obliteration throughout the retina. Vasoproliferation, after the animals have returned to room air, is robust. The initial small preretinal neovascular formations anastomose to form large preretinal membranes that eventually cause tractional retinal folds. The end-stage pathology of the canine model is similar to stage IV human retinopathy of prematurity. Therefore, canine OIR is an excellent forum to evaluate the response to drugs targeting VEGF and its receptors. Evaluation of an antibody to VEGF-R2 and the VEGF-Trap demonstrated that doses should be titered down so that preretinal neovascularization is inhibited but retinal revascularization is able to proceed, vascularizing peripheral retina and preventing it from being a source of VEGF.
Impact of improved neonatal care on the profile of retinopathy of prematurity in rural neonatal centers in India over a 4-year period.
Vinekar A, Jayadev C, Kumar S … +4 more , Mangalesh S, Dogra MR, Bauer NJ, Shetty B
Eye Brain · 2016 · PMID 28539801 · Full text
PURPOSE: To report the reduction in the incidence and severity of retinopathy of prematurity (ROP) in rural India over a 4-year period following the introduction of improved neonatal care practices. METHODS: The Karnatak...
PURPOSE: To report the reduction in the incidence and severity of retinopathy of prematurity (ROP) in rural India over a 4-year period following the introduction of improved neonatal care practices. METHODS: The Karnataka Internet Diagnosis of Retinopathy of Prematurity program (KIDROP), is a tele-medicine network that screens for ROP in different zones of Karnataka state in rural India. North Karnataka is the most underdeveloped and remote zone of this program and did not have any ROP screening programs before the intervention of the KIDROP in 2011. Six government and eleven private neonatal centers in this zone were screened weekly. Specific neonatal guidelines for ROP were developed and introduced in these centers. They included awareness about risk factors, oxygen regulation protocols, use of pulse oxymetry, monitoring postnatal weight gain, nutritional best practices, and management of sepsis. The incidence and severity of ROP were compared before the guidelines were introduced (Jan 2011 to Dec 2012) and after the guidelines were introduced (July 2013 to June 2015). RESULTS: During this 4-year period, 4,167 infants were screened over 11,390 imaging sessions. The number of enrolled infants increased from 1,825 to 2,342 between the two periods (<0.001). The overall incidence of any stage ROP reduced significantly from 26.8% to 22.4% (<0.001). The incidence of treatment-requiring ROP reduced from 20.7% to 16% (=0.06), and of the treated disease, aggressive posterior ROP reduced from 20.8% to 13.1% (=0.23) following introduction of the guidelines. DISCUSSION: Rural neonatal centers in middle-income countries have a large, unscreened burden of ROP. Improving neonatal care in these centers can positively impact the incidence and severity of ROP even in a relatively short period. A combined approach of a robust ROP screening program and improved neonatal care practices is required to address the challenge.
Current screening and treatments in retinopathy of prematurity in the US.
Suelves AM, Shulman JP
Eye Brain · 2016 · PMID 28539800 · Full text
Retinopathy of prematurity (ROP) is a complex disease characterized by an aberrant developmental retinal angiogenesis in preterm infants and can carry significant visual morbidity, including retinal detachment and blindn...
Retinopathy of prematurity (ROP) is a complex disease characterized by an aberrant developmental retinal angiogenesis in preterm infants and can carry significant visual morbidity, including retinal detachment and blindness. Though large scale, randomized clinical trials have improved our understanding of the pathophysiology and progression of the disease, the management of ROP remains a challenge for ophthalmologists. This review addresses the up-to-date screening approach, diagnosis, and treatment guidelines for ROP in the US.
Retinopathy of prematurity blindness worldwide: phenotypes in the third epidemic.
Quinn GE
Eye Brain · 2016 · PMID 28539799 · Full text
Blindness due to retinopathy of prematurity (ROP) is an increasing problem worldwide as improved levels of neonatal care are provided in countries with developing neonatal intensive care units. The occurrence of ROP blin...
Blindness due to retinopathy of prematurity (ROP) is an increasing problem worldwide as improved levels of neonatal care are provided in countries with developing neonatal intensive care units. The occurrence of ROP blindness varies dramatically with the socioeconomic development of a country. In regions with high levels of neonatal care and adequate resources, ROP blindness is largely restricted to premature infants with very low birth weight and low gestational age while in middle- and low-income countries with regional variation in technology and capacity, limited health resources may well limit the care of the premature newborn.
Progress in the clinical development and utilization of vision prostheses: an update.
Brandli A, Luu CD, Guymer RH … +1 more , Ayton LN
Eye Brain · 2016 · PMID 28539798 · Full text
Vision prostheses, or "bionic eyes", are implantable medical bionic devices with the potential to restore rudimentary sight to people with profound vision loss or blindness. In the past two decades, this field has rapidl...
Vision prostheses, or "bionic eyes", are implantable medical bionic devices with the potential to restore rudimentary sight to people with profound vision loss or blindness. In the past two decades, this field has rapidly progressed, and there are now two commercially available retinal prostheses in the US and Europe, and a number of next-generation devices in development. This review provides an update on the development of these devices and a discussion on the future directions for the field.
Advances in diagnosis, clinical care, research, and treatment in retinopathy of prematurity.
Hartnett ME, Capone A
Eye Brain · 2016 · PMID 27795669 · Full text
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Revisiting the mouse model of oxygen-induced retinopathy.
Kim CB, D'Amore PA, Connor KM
Eye Brain · 2016 · PMID 27499653 · Full text
Abnormal blood vessel growth in the retina is a hallmark of many retinal diseases, such as retinopathy of prematurity (ROP), proliferative diabetic retinopathy, and the wet form of age-related macular degeneration. In pa...
Abnormal blood vessel growth in the retina is a hallmark of many retinal diseases, such as retinopathy of prematurity (ROP), proliferative diabetic retinopathy, and the wet form of age-related macular degeneration. In particular, ROP has been an important health concern for physicians since the advent of routine supplemental oxygen therapy for premature neonates more than 70 years ago. Since then, researchers have explored several animal models to better understand ROP and retinal vascular development. Of these models, the mouse model of oxygen-induced retinopathy (OIR) has become the most widely used, and has played a pivotal role in our understanding of retinal angiogenesis and ocular immunology, as well as in the development of groundbreaking therapeutics such as anti-vascular endothelial growth factor injections for wet age-related macular degeneration. Numerous refinements to the model have been made since its inception in the 1950s, and technological advancements have expanded the use of the model across multiple scientific fields. In this review, we explore the historical developments that have led to the mouse OIR model utilized today, essential concepts of OIR, limitations of the model, and a representative selection of key findings from OIR, with particular emphasis on current research progress.
Clinical biomarkers and molecular basis for optimized treatment of diabetic retinopathy: current status and future prospects.
Saxena R, Singh D, Saklani R … +1 more , Gupta SK
Eye Brain · 2016 · PMID 28539797 · Full text
Diabetic retinopathy is a highly specific microvascular complication of diabetes and a leading cause of blindness worldwide. It is triggered by hyperglycemia which causes increased oxidative stress leading to an adaptive...
Diabetic retinopathy is a highly specific microvascular complication of diabetes and a leading cause of blindness worldwide. It is triggered by hyperglycemia which causes increased oxidative stress leading to an adaptive inflammatory assault to the neuroretinal tissue and microvasculature. Prolonged hyperglycemia causes increased polyol pathway flux, increased formation of advanced glycation end-products, abnormal activation of signaling cascades such as activation of protein kinase C (PKC) pathway, increased hexosamine pathway flux, and peripheral nerve damage. All these changes lead to increased oxidative stress and inflammatory assault to the retina resulting in structural and functional changes. In addition, neuroretinal alterations affect diabetes progression. The most effective way to manage diabetic retinopathy is by primary prevention such as hyperglycemia control. While the current mainstay for the management of severe and proliferative diabetic retinopathy is laser photocoagulation, its role is diminishing with the development of newer drugs including corticosteroids, antioxidants, and antiangiogenic and anti-VEGF agents which work as an adjunct to laser therapy or independently. The current pharmacotherapy of diabetic retinopathy is incomplete as a sole treatment option in view of limited efficacy and short-term effect. There is a definite clinical need to develop new pharmacological therapies for diabetic retinopathy, particularly ones which would be effective through the oral route and help recover lost vision. The increasing understanding of the mechanisms of diabetic retinopathy and its biomarkers is likely to help generate better and more effective medications.
How bees distinguish patterns by green and blue modulation.
Horridge A
Eye Brain · 2015 · PMID 28539796 · Full text
In the 1920s, Mathilde Hertz found that trained bees discriminated between shapes or patterns of similar size by something related to total length of contrasting contours. This input is now interpreted as modulation in g...
In the 1920s, Mathilde Hertz found that trained bees discriminated between shapes or patterns of similar size by something related to total length of contrasting contours. This input is now interpreted as modulation in green and blue receptor channels as flying bees scan in the horizontal plane. Modulation is defined as total contrast irrespective of sign multiplied by length of edge displaying that contrast, projected to vertical, therefore, combining structure and contrast in a single input. Contrast is outside the eye; modulation is a phasic response in receptor pathways inside. In recent experiments, bees trained to distinguish color detected, located, and measured three independent inputs and the angles between them. They are the tonic response of the blue receptor pathway and modulation of small-field green or (less preferred) blue receptor pathways. Green and blue channels interacted intimately at a peripheral level. This study explores in more detail how various patterns are discriminated by these cues. The direction of contrast at a boundary was not detected. Instead, bees located and measured total modulation generated by horizontal scanning of contrasts, irrespective of pattern. They also located the positions of isolated vertical edges relative to other landmarks and distinguished the angular widths between vertical edges by green or blue modulation alone. The preferred inputs were the strongest green modulation signal and angular width between outside edges, irrespective of color. In the absence of green modulation, the remaining cue was a measure and location of blue modulation at edges. In the presence of green modulation, blue modulation was inhibited. Black/white patterns were distinguished by the same inputs in blue and green receptor channels. Left-right polarity and mirror images could be discriminated by retinotopic green modulation alone. Colors in areas bounded by strong green contrast were distinguished as more or less blue than the background. The blue content could also be summed over the whole target. There were no achromatic patterns for bees and no evidence that they detected black, white, or gray levels apart from the differences in blue content or modulation at edges. Most of these cues would be sensitive to background color but some were influenced by changes in illumination. The bees usually learned only to avoid the unrewarded target. Exactly the same preferences of the same inputs were used in the detection of single targets as in discrimination between two targets.
Infectious optic neuropathies: a clinical update.
Kahloun R, Abroug N, Ksiaa I … +4 more , Mahmoud A, Zeghidi H, Zaouali S, Khairallah M
Eye Brain · 2015 · PMID 28539795 · Full text
Different forms of optic neuropathy causing visual impairment of varying severity have been reported in association with a wide variety of infectious agents. Proper clinical diagnosis of any of these infectious condition...
Different forms of optic neuropathy causing visual impairment of varying severity have been reported in association with a wide variety of infectious agents. Proper clinical diagnosis of any of these infectious conditions is based on epidemiological data, history, systemic symptoms and signs, and the pattern of ocular findings. Diagnosis is confirmed by serologic testing and polymerase chain reaction in selected cases. Treatment of infectious optic neuropathies involves the use of specific anti-infectious drugs and corticosteroids to suppress the associated inflammatory reaction. The visual prognosis is generally good, but persistent severe vision loss with optic atrophy can occur. This review presents optic neuropathies caused by specific viral, bacterial, parasitic, and fungal diseases.
Papilledema: epidemiology, etiology, and clinical management.
Rigi M, Almarzouqi SJ, Morgan ML … +1 more , Lee AG
Eye Brain · 2015 · PMID 28539794 · Full text
Papilledema is optic disc swelling due to high intracranial pressure. Possible conditions causing high intracranial pressure and papilledema include intracerebral mass lesions, cerebral hemorrhage, head trauma, meningiti...
Papilledema is optic disc swelling due to high intracranial pressure. Possible conditions causing high intracranial pressure and papilledema include intracerebral mass lesions, cerebral hemorrhage, head trauma, meningitis, hydrocephalus, spinal cord lesions, impairment of cerebral sinus drainage, anomalies of the cranium, and idiopathic intracranial hypertension (IIH). Irrespective of the cause, visual loss is the feared morbidity of papilledema, and the main mechanism of optic nerve damage is intraneuronal ischemia secondary to axoplasmic flow stasis. Treatment is directed at correcting the underlying cause. In cases where there is no other identifiable cause for intracranial hypertension (ie, IIH) the available options include both medical and surgical modalities. Weight loss and diuretics remain the mainstays for treatment of IIH, and surgery is typically reserved for patients who fail, are intolerant to, or non-compliant with maximum medical therapy.
Patchy distributions of myelin and vesicular glutamate transporter 2 align with cytochrome oxidase blobs and interblobs in the superficial layers of the primary visual cortex.
Rockoff EC, Balaram P, Kaas JH
Eye Brain · 2014 Sep · PMID 26097384 · Full text
Blobs are a modular component of the primary visual cortex (area 17) of all primates, but not of other mammals closely related to primates. They are characterized as an even distribution of patches, puffs, or blobs of de...
Blobs are a modular component of the primary visual cortex (area 17) of all primates, but not of other mammals closely related to primates. They are characterized as an even distribution of patches, puffs, or blobs of dense cytochrome oxidase (CO) expression in layer III of area 17, and are now known to differ from surrounding, nonblob cortex in thalamic, intrinsic, and extrastriate connections. Previous studies have also recognized a blob-like pattern of myelin-dense patches in layer III of area 17 of primates, and more recently the vesicular glutamate transporter (VGLUT)-2 isoform of the VGLUT family has been found to selectively distribute to layer III patches in a similar blob-like pattern. Here, we sought to determine if the blob-like patterns all identify the same modular structures in area 17 of primates by staining alternate brain sections cut parallel to the surface of area 17 of a prosimian primate () for CO, myelin, and VGLUT2. By aligning the sections from the three preparations, we provide clear evidence that the three preparations all identify the same modular blob structures. The results provide a further understanding of the functional nature of the blobs by demonstrating that their higher level of CO activity is related to thalamic inputs from the lateral geniculate nucleus that use VGLUT2 as their main glutamate transporter, and via myelinated axons.
Distinct patterns of corticogeniculate feedback to different layers of the lateral geniculate nucleus.
Ichida JM, Mavity-Hudson JA, Casagrande VA
Eye Brain · 2014 Sep · PMID 25892906 · Full text
In primates, feedforward visual pathways from retina to lateral geniculate nucleus (LGN) are segregated to different layers. These layers also receive strong reciprocal feedback pathways from cortex. The degree to which...
In primates, feedforward visual pathways from retina to lateral geniculate nucleus (LGN) are segregated to different layers. These layers also receive strong reciprocal feedback pathways from cortex. The degree to which feedforward streams in primates are segregated from feedback streams remains unclear. Here, we asked whether corticogeniculate cells that innervate the magnocellular (M), parvocellular (P), and koniocellular (K) layers of the LGN in the prosimian primate bush baby () can be distinguished based on either the laminar distribution or morphological characteristics of their axons and synaptic contacts in LGN, or on their cell body position, size, and dendritic distribution in cortex. Corticogeniculate axons and synapses were labeled anterogradely with biotinylated dextran injections in layer 6 of cortex. Corticogeniculate cell bodies were first labeled with fluorescent dextran injections limited to individual M, P, or K LGN layers and then filled with biotinylated Lucifer yellow. Results showed that feedback to the M or P LGN layers arises from cells with dendrites primarily confined to cortical layer 6 and axons restricted to either M or P LGN layers, but not both. Feedback to K LGN layers arises from cells: 1) whose dendrites distribute rather evenly across cortical layers 5 and 6; 2) whose dendrites always extend into layer 4; and 3) whose axons are never confined to K layers but always overlap with either P or M layers. Corticogeniculate axons also showed distributions that were retinotopically precise based on known receptive field sizes of layer 6 cells, and these axons mainly made synapses with glutamatergic projection neurons in the LGN in all layers. Taken together with prior physiological results, we argue that the morphological differences between the three corticogeniculate pathways show that the M and P feedback pathways could rapidly and specifically enhance local LGN activity, while we speculate that the K feedback pathway is organized to temporally synchronize activity between LGN and cortex.
Horner syndrome: clinical perspectives.
Kanagalingam S, Miller NR
Eye Brain · 2015 · PMID 28539793 · Full text
Horner syndrome consists of unilateral ptosis, an ipsilateral miotic but normally reactive pupil, and in some cases, ipsilateral facial anhidrosis, all resulting from damage to the ipsilateral oculosympathetic pathway. H...
Horner syndrome consists of unilateral ptosis, an ipsilateral miotic but normally reactive pupil, and in some cases, ipsilateral facial anhidrosis, all resulting from damage to the ipsilateral oculosympathetic pathway. Herein, we review the clinical signs and symptoms that can aid in the diagnosis and localization of a Horner syndrome as well as the causes of the condition. We emphasize that pharmacologic testing can confirm its presence and direct further testing and management.
Histological features of layers and sublayers in cortical visual areas V1 and V2 of chimpanzees, macaque monkeys, and humans.
Balaram P, Young NA, Kaas JH
Eye Brain · 2014 Sep · PMID 25788835 · Full text
The layers and sublayers of primary visual cortex, or V1, in primates are easily distinguishable compared to those in other cortical areas, and are especially distinct in anthropoid primates - monkeys, apes, and humans -...
The layers and sublayers of primary visual cortex, or V1, in primates are easily distinguishable compared to those in other cortical areas, and are especially distinct in anthropoid primates - monkeys, apes, and humans - where they also vary in histological appearance. This variation in primate-specific specialization has led to a longstanding confusion over the identity of layer 4 and its proposed sublayers in V1. As the application of different histological markers relate to the issue of defining and identifying layers and sublayers, we applied four traditional and four more recent histological markers to brain sections of V1 and adjoining secondary visual cortex (V2) in macaque monkeys, chimpanzees, and humans in order to compare identifiable layers and sublayers in both cortical areas across these species. The use of Nissl, neuronal nuclear antigen (NeuN), Gallyas myelin, cytochrome oxidase (CO), acetylcholinesterase (AChE), nonphosphorylated neurofilament H (SMI-32), parvalbumin (PV), and vesicular glutamate transporter 2 (VGLUT2) preparations support the conclusion that the most popular scheme of V1 lamination, that of Brodmann, misidentifies sublayers of layer 3 (3Bβ and 3C) as sublayers of layer 4 (4A and 4B), and that the specialized sublayer of layer 3 in monkeys, 3Bβ, is not present in humans. These differences in interpretation are important as they relate to the proposed functions of layer 4 in primate species, where layer 4 of V1 is a layer that receives and processes information from the visual thalamus, and layer 3 is a layer that transforms and distributes information to other cortical areas.
Metabotropic glutamate receptor 5 shows different patterns of localization within the parallel visual pathways in macaque and squirrel monkeys.
Shostak Y, Wenger A, Mavity-Hudson J … +1 more , Casagrande VA
Eye Brain · 2014 Sep · PMID 25774086 · Full text
Glutamate is used as an excitatory neurotransmitter by the koniocellular (K), magnocellular (M), and parvocellular (P) pathways to transfer signals from the primate lateral geniculate nucleus (LGN) to primary visual cort...
Glutamate is used as an excitatory neurotransmitter by the koniocellular (K), magnocellular (M), and parvocellular (P) pathways to transfer signals from the primate lateral geniculate nucleus (LGN) to primary visual cortex (V1). Glutamate acts through both fast ionotropic receptors, which appear to carry the main sensory message, and slower, modulatory metabotropic receptors (mGluRs). In this study, we asked whether mGluR5 relates in distinct ways to the K, M, and P LGN axons in V1. To answer this question, we used light microscopic immunocytochemistry and preembedding electron microscopic immunogold labeling to determine the localization of mGluR5 within the layers of V1 in relation to the K, M, and P pathways in macaque and squirrel monkeys. These pathways were labeled separately via wheat germ agglutinin-horseradish peroxidase (WGA-HRP) injections targeting the LGN layers. mGluR5 is of interest because it: 1) has been shown to be expressed in the thalamic input layers; 2) appears to be responsible for some types of oscillatory firing, which could be important in the binding of visual features; and 3) has been associated with a number of sensory-motor gating-related pathologies, including schizophrenia and autism. Our results demonstrated the presence of mGluR5 in the neuropil of all V1 layers. This protein was lowest in IVCα (M input) and the infragranular layers. In layer IVC, mGluR5 also was found postsynaptic to about 30% of labeled axons, but the distribution was uneven, such that postsynaptic mGluR5 label tended to occur opposite smaller (presumed P), and not larger (presumed M) axon terminals. Only in the K pathway in layer IIIB, however, was mGluR5 always found in the axon terminals themselves. The presence of mGluR5 in K axons and not in M and P axons, and the presence of mGluR5 postsynaptic mainly to smaller P and not larger M axons suggest that the response to the release of glutamate is modulated in distinct ways within and between the parallel visual pathways of primates.
How bees distinguish colors.
Horridge A
Eye Brain · 2015 · PMID 28539792 · Full text
Behind each facet of the compound eye, bees have photoreceptors for ultraviolet, green, and blue wavelengths that are excited by sunlight reflected from the surrounding panorama. In experiments that excluded ultraviolet,...
Behind each facet of the compound eye, bees have photoreceptors for ultraviolet, green, and blue wavelengths that are excited by sunlight reflected from the surrounding panorama. In experiments that excluded ultraviolet, bees learned to distinguish between black, gray, white, and various colors. To distinguish two targets of differing color, bees detected, learned, and later recognized the strongest preferred inputs, irrespective of which target displayed them. First preference was the position and measure of blue reflected from white or colored areas. They also learned the positions and a measure of the green receptor modulation at vertical edges that displayed the strongest green contrast. Modulation is the receptor response to contrast and was summed over the length of a contrasting vertical edge. This also gave them a measure of angular width between outer vertical edges. Third preference was position and a measure of blue modulation. When they returned for more reward, bees recognized the familiar coincidence of these inputs at that place. They cared nothing for colors, layout of patterns, or direction of contrast, even at black/white edges. The mechanism is a new kind of color vision in which a large-field tonic blue input must coincide in time with small-field phasic modulations caused by scanning vertical edges displaying green or blue contrast. This is the kind of system to expect in medium-lowly vision, as found in insects; the next steps are fresh looks at old observations and quantitative models.
Distribution of cortical neurons projecting to the superior colliculus in macaque monkeys.
Cerkevich CM, Lyon DC, Balaram P … +1 more , Kaas JH
Eye Brain · 2014 Sep · PMID 25663799 · Full text
To better reveal the pattern of corticotectal projections to the superficial layers of the superior colliculus (SC), we made a total of ten retrograde tracer injections into the SC of three macaque monkeys (). The majori...
To better reveal the pattern of corticotectal projections to the superficial layers of the superior colliculus (SC), we made a total of ten retrograde tracer injections into the SC of three macaque monkeys (). The majority of these injections were in the superficial layers of the SC, which process visual information. To isolate inputs to the purely visual layers in the superficial SC from those inputs to the motor and multisensory layers deeper in the SC, two injections were placed to include the intermediate and deep layers of the SC. In another case, an injection was placed in the medial pulvinar, a nucleus not known to be strongly connected with visual cortex, to identify possible projections from tracer spread past the lateral boundary of the SC. Four conclusions are supported by the results: 1) all early visual areas of cortex, including V1, V2, V3, and the middle temporal area, project to the superficial layers of the SC; 2) with the possible exception of the frontal eye field, few areas of cortex outside of the early visual areas project to the superficial SC, although many do, however, project to the intermediate and deep layers of the SC; 3) roughly matching retinotopy is conserved in the projections of visual areas to the SC; and 4) the projections from different visual areas are similarly dense, although projections from early visual areas appear somewhat denser than those of higher order visual areas in macaque cortex.
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