The Experts below are selected from a list of 123 Experts worldwide ranked by ideXlab platform
Torben Ellegaard Lund - One of the best experts on this subject based on the ideXlab platform.
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Recovery from optic neuritis: an ROI-based analysis of LGN and Visual cortical areas.
Brain, 2007Co-Authors: Kirsten Korsholm, Kristoffer Hougaard Madsen, Jette L. Frederiksen, Arnold Skimminge, Torben Ellegaard LundAbstract:Optic neuritis (ON) is the first clinical manifestation in � 20% of patients with multiple sclerosis (MS). The inflammation and demyelination of the optic nerve are characterized by symptomatic Visual impairment and retrobulbar pain, and associated with decreased Visual acuity, decreased colour and contrast sensitivity, delayed Visual evoked potentials and Visual field defects. Spontaneous recovery of vision typically occurs within weeks or months after onset, depending on the resolution of inflammation, remyelination, restoration of conduction in axons which persist demyelinated and neuronal plasticity in the cortical and Subcortical Visual Pathways. To assess where recovery takes place along the Visual pathway, Visual activation was studied in the lateral geniculate nucleus (LGN), the main thalamic relay nucleus in the Visual pathway and in three areas of the Visual cortex: the lateral occipital complexes (LOC), V1 and V2. We conducted a longitudinal functional magnetic resonance imaging (fMRI) study of regions of interest (ROI) of activation in LGN and Visual cortex in 19 patients with acute ON at onset, 3 and 6 months from presentation. With fMRI we measured the activation in the ROIs and compared activation during monocular stimulation of the affected and unaffected eye. In the acute phase the activation of LGN during Visual stimulation of the affected eye was significantly reduced (P50.01) compared to the unaffected eye. This difference in LGN activation between the affected and unaffected eye diminished during recovery, and after 180 days the difference was no longer significant (P ¼ 0.59). The decreased difference during recovery was mainly due to an increase in the fMRI signal when stimulating the affected eye, but included a component of a decreasing fMRI signal from LGN when stimulating the unaffected eye. In LOC, V1 and V2 activation during Visual stimulation of the affected eye in the acute phase was significantly reduced (P50.01) compared to the unaffected eye, and during recovery the difference diminished with no significant differences left after 180 days. As the pattern of activation in LOC, V1 and V2 resembled the development in LGN we found no evidence of additional cortical adaptive changes. The reduced activation of the LGN to stimulation of the unaffected eye is interpreted as a shift away from early compensatory changes established in the acute phase in LGN and may indicate very early plasticity of the Visual Pathways.
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Recovery from optic neuritis: an ROI-based analysis of LGN and Visual cortical areas.
Brain : a journal of neurology, 2007Co-Authors: Kirsten Korsholm, Kristoffer Hougaard Madsen, Jette L. Frederiksen, Arnold Skimminge, Torben Ellegaard LundAbstract:Optic neuritis (ON) is the first clinical manifestation in approximately 20% of patients with multiple sclerosis (MS). The inflammation and demyelination of the optic nerve are characterized by symptomatic Visual impairment and retrobulbar pain, and associated with decreased Visual acuity, decreased colour and contrast sensitivity, delayed Visual evoked potentials and Visual field defects. Spontaneous recovery of vision typically occurs within weeks or months after onset, depending on the resolution of inflammation, remyelination, restoration of conduction in axons which persist demyelinated and neuronal plasticity in the cortical and Subcortical Visual Pathways. To assess where recovery takes place along the Visual pathway, Visual activation was studied in the lateral geniculate nucleus (LGN), the main thalamic relay nucleus in the Visual pathway and in three areas of the Visual cortex: the lateral occipital complexes (LOC), V1 and V2. We conducted a longitudinal functional magnetic resonance imaging (fMRI) study of regions of interest (ROI) of activation in LGN and Visual cortex in 19 patients with acute ON at onset, 3 and 6 months from presentation. With fMRI we measured the activation in the ROIs and compared activation during monocular stimulation of the affected and unaffected eye. In the acute phase the activation of LGN during Visual stimulation of the affected eye was significantly reduced (P < 0.01) compared to the unaffected eye. This difference in LGN activation between the affected and unaffected eye diminished during recovery, and after 180 days the difference was no longer significant (P = 0.59). The decreased difference during recovery was mainly due to an increase in the fMRI signal when stimulating the affected eye, but included a component of a decreasing fMRI signal from LGN when stimulating the unaffected eye. In LOC, V1 and V2 activation during Visual stimulation of the affected eye in the acute phase was significantly reduced (P < 0.01) compared to the unaffected eye, and during recovery the difference diminished with no significant differences left after 180 days. As the pattern of activation in LOC, V1 and V2 resembled the development in LGN we found no evidence of additional cortical adaptive changes. The reduced activation of the LGN to stimulation of the unaffected eye is interpreted as a shift away from early compensatory changes established in the acute phase in LGN and may indicate very early plasticity of the Visual Pathways.
Matthias Schmidt - One of the best experts on this subject based on the ideXlab platform.
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Contribution of GABA_C receptors to inhibition in the rodent accessory optic system
Experimental Brain Research, 2009Co-Authors: Katja Schlicker, Matthias SchmidtAbstract:The medial terminal nucleus (MTN) of the mammalian accessory optic system controls vertical compensatory eye movements. It consists of two neuronal populations which respond best either to upward or to downward Visual image shifts. The two cell classes are located spatially separate in the dorsal or in the ventral subdivision of the MTN, respectively. Pronounced GABAergic Pathways have been described to exist between neurons in the two MTN subdivisions indicating that inhibitory interactions play a significant role for the generation of MTN cell response properties. Yet, the types of GABA receptors which mediate these inhibitory interactions are unknown. Functionally, it is of particular interest to know whether GABA_C receptors, as in other Subcortical Visual centers, participate in inhibitory mechanisms in MTN neurons. We therefore performed whole-cell patch clamp recordings from MTN neurons in acute mouse midbrain slices. We monitored excitatory and inhibitory postsynaptic responses to afferent stimulation and applied specific GABA receptor agonists and antagonists to identify the GABA receptor types present in MTN neurons. We found that more than 80% of the neurons in both MTN subdivisions express functional GABA_C receptors that can be activated by specific receptor agonists. A blockade of GABA_C receptors, on the other hand, either reduced or enhanced postsynaptic inhibition, indicating that both postsynaptic and presynaptic functions are served by this receptor type. This, together with earlier results, suggests that GABA_C receptors play a general role for the control of neuronal excitability in Subcortical Visual Pathways.
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Contribution of GABAC receptors to inhibition in the rodent accessory optic system
Experimental Brain Research, 2009Co-Authors: Katja Schlicker, Matthias SchmidtAbstract:The medial terminal nucleus (MTN) of the mammalian accessory optic system controls vertical compensatory eye movements. It consists of two neuronal populations which respond best either to upward or to downward Visual image shifts. The two cell classes are located spatially separate in the dorsal or in the ventral subdivision of the MTN, respectively. Pronounced GABAergic Pathways have been described to exist between neurons in the two MTN subdivisions indicating that inhibitory interactions play a significant role for the generation of MTN cell response properties. Yet, the types of GABA receptors which mediate these inhibitory interactions are unknown. Functionally, it is of particular interest to know whether GABAC receptors, as in other Subcortical Visual centers, participate in inhibitory mechanisms in MTN neurons. We therefore performed whole-cell patch clamp recordings from MTN neurons in acute mouse midbrain slices. We monitored excitatory and inhibitory postsynaptic responses to afferent stimulation and applied specific GABA receptor agonists and antagonists to identify the GABA receptor types present in MTN neurons. We found that more than 80% of the neurons in both MTN subdivisions express functional GABAC receptors that can be activated by specific receptor agonists. A blockade of GABAC receptors, on the other hand, either reduced or enhanced postsynaptic inhibition, indicating that both postsynaptic and presynaptic functions are served by this receptor type. This, together with earlier results, suggests that GABAC receptors play a general role for the control of neuronal excitability in Subcortical Visual Pathways.
Paul R. Martin - One of the best experts on this subject based on the ideXlab platform.
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Distribution and specificity of S-cone ("blue cone") signals in Subcortical Visual Pathways.
Visual neuroscience, 2014Co-Authors: Paul R. Martin, Barry B. LeeAbstract:We review here the distribution of S-cone signals and properties of S-cone recipient receptive fields in Subcortical Pathways. Nearly everything we know about S-cone signals in the Subcortical Visual system comes from the study of Visual systems in cats and primates (monkeys); in this review, we concentrate on results from macaque and marmoset monkeys. We discuss segregation of S-cone recipient (blue-on and blue-off) receptive fields in the dorsal lateral geniculate nucleus and describe their receptive field properties. We treat in some detail the question of detecting weak S-cone signals as an introduction for newcomers to the field. Finally, we briefly consider the question on how S-cone signals are distributed among nongeniculate targets.
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Morphology of retinal ganglion cells in a new world monkey, the marmoset Callithrix jacchus.
The Journal of comparative neurology, 1996Co-Authors: Krishna K. Ghosh, Ann K. Goodchild, Ann E. Sefton, Paul R. MartinAbstract:We studied the morphology of retinal ganglion cells in a diurnal New World primate, the marmoset Callithrix jacchus. This species is of interest as a model for primate vision because it has good behavioural Visual acuity, and the retina and Subcortical Visual Pathways are very similar to those of Old World monkeys and humans. Ganglion cells were labelled by placing small crystals of the carbocyanin dye DiI into the optic fibre layer, or by intracellular injection of neurobiotin. Two main classes of ganglion cell were labelled. We call these Group A cells and Group B cells: they are respectively homologous to parasol and midget cell classes. Group A and Group B cells show similar patterns of dye coupling, dendritic stratification and dendritic field size as their counterparts in Old World monkeys and humans. A third group of cells, which we call Group C, is morphologically heterogeneous. Examples corresponding to wide-field ganglion cell types described in Old World primates were encountered. One subgroup of C cells has a morphology very similar to that of the small bistratified (blue-on) cell described in macaque retina, suggesting that this functional pathway is common to all primates. As for other New World monkeys, the marmoset shows a sex-linked polymorphism of cone pigment expression, such that all males are dichromats and the majority of females are trichromats. No systematic differences in Group B cells were seen between male and female retinas, suggesting that trichromacy is not accompanied by specific changes in ganglion cell morphology.
Kirsten Korsholm - One of the best experts on this subject based on the ideXlab platform.
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Recovery from optic neuritis: an ROI-based analysis of LGN and Visual cortical areas.
Brain, 2007Co-Authors: Kirsten Korsholm, Kristoffer Hougaard Madsen, Jette L. Frederiksen, Arnold Skimminge, Torben Ellegaard LundAbstract:Optic neuritis (ON) is the first clinical manifestation in � 20% of patients with multiple sclerosis (MS). The inflammation and demyelination of the optic nerve are characterized by symptomatic Visual impairment and retrobulbar pain, and associated with decreased Visual acuity, decreased colour and contrast sensitivity, delayed Visual evoked potentials and Visual field defects. Spontaneous recovery of vision typically occurs within weeks or months after onset, depending on the resolution of inflammation, remyelination, restoration of conduction in axons which persist demyelinated and neuronal plasticity in the cortical and Subcortical Visual Pathways. To assess where recovery takes place along the Visual pathway, Visual activation was studied in the lateral geniculate nucleus (LGN), the main thalamic relay nucleus in the Visual pathway and in three areas of the Visual cortex: the lateral occipital complexes (LOC), V1 and V2. We conducted a longitudinal functional magnetic resonance imaging (fMRI) study of regions of interest (ROI) of activation in LGN and Visual cortex in 19 patients with acute ON at onset, 3 and 6 months from presentation. With fMRI we measured the activation in the ROIs and compared activation during monocular stimulation of the affected and unaffected eye. In the acute phase the activation of LGN during Visual stimulation of the affected eye was significantly reduced (P50.01) compared to the unaffected eye. This difference in LGN activation between the affected and unaffected eye diminished during recovery, and after 180 days the difference was no longer significant (P ¼ 0.59). The decreased difference during recovery was mainly due to an increase in the fMRI signal when stimulating the affected eye, but included a component of a decreasing fMRI signal from LGN when stimulating the unaffected eye. In LOC, V1 and V2 activation during Visual stimulation of the affected eye in the acute phase was significantly reduced (P50.01) compared to the unaffected eye, and during recovery the difference diminished with no significant differences left after 180 days. As the pattern of activation in LOC, V1 and V2 resembled the development in LGN we found no evidence of additional cortical adaptive changes. The reduced activation of the LGN to stimulation of the unaffected eye is interpreted as a shift away from early compensatory changes established in the acute phase in LGN and may indicate very early plasticity of the Visual Pathways.
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Recovery from optic neuritis: an ROI-based analysis of LGN and Visual cortical areas.
Brain : a journal of neurology, 2007Co-Authors: Kirsten Korsholm, Kristoffer Hougaard Madsen, Jette L. Frederiksen, Arnold Skimminge, Torben Ellegaard LundAbstract:Optic neuritis (ON) is the first clinical manifestation in approximately 20% of patients with multiple sclerosis (MS). The inflammation and demyelination of the optic nerve are characterized by symptomatic Visual impairment and retrobulbar pain, and associated with decreased Visual acuity, decreased colour and contrast sensitivity, delayed Visual evoked potentials and Visual field defects. Spontaneous recovery of vision typically occurs within weeks or months after onset, depending on the resolution of inflammation, remyelination, restoration of conduction in axons which persist demyelinated and neuronal plasticity in the cortical and Subcortical Visual Pathways. To assess where recovery takes place along the Visual pathway, Visual activation was studied in the lateral geniculate nucleus (LGN), the main thalamic relay nucleus in the Visual pathway and in three areas of the Visual cortex: the lateral occipital complexes (LOC), V1 and V2. We conducted a longitudinal functional magnetic resonance imaging (fMRI) study of regions of interest (ROI) of activation in LGN and Visual cortex in 19 patients with acute ON at onset, 3 and 6 months from presentation. With fMRI we measured the activation in the ROIs and compared activation during monocular stimulation of the affected and unaffected eye. In the acute phase the activation of LGN during Visual stimulation of the affected eye was significantly reduced (P < 0.01) compared to the unaffected eye. This difference in LGN activation between the affected and unaffected eye diminished during recovery, and after 180 days the difference was no longer significant (P = 0.59). The decreased difference during recovery was mainly due to an increase in the fMRI signal when stimulating the affected eye, but included a component of a decreasing fMRI signal from LGN when stimulating the unaffected eye. In LOC, V1 and V2 activation during Visual stimulation of the affected eye in the acute phase was significantly reduced (P < 0.01) compared to the unaffected eye, and during recovery the difference diminished with no significant differences left after 180 days. As the pattern of activation in LOC, V1 and V2 resembled the development in LGN we found no evidence of additional cortical adaptive changes. The reduced activation of the LGN to stimulation of the unaffected eye is interpreted as a shift away from early compensatory changes established in the acute phase in LGN and may indicate very early plasticity of the Visual Pathways.
James A. Carr - One of the best experts on this subject based on the ideXlab platform.
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I'll take the low road: The evolutionary underpinnings of Visually triggered fear
Frontiers in neuroscience, 2015Co-Authors: James A. CarrAbstract:Although there is general agreement that the central nucleus of the amygdala (CeA) is critical for triggering the neuroendocrine response to Visual threats, there is uncertainty about the role of Subcortical Visual Pathways in this process. Primates in general appear to depend less on Subcortical Visual Pathways than other mammals. Yet, imaging studies continue to indicate a role for the superior colliculus and pulvinar nucleus in fear activation, despite disconnects in how these brain structures communicate not only with each other but with the amygdala. Studies in fish and amphibians suggest that the neuroendocrine response to Visual threats has remained relatively unchanged for hundreds of millions of years, yet there are still significant data gaps with respect to how Visual information is relayed to telencephalic areas homologous to the CeA, particularly in fish. In fact ray finned fishes may have evolved an entirely different mechanism for relaying Visual information to the telencephalon. In part because they lack a pathway homologous to the lateral geniculate-striate cortex pathway of mammals, amphibians continue to be an excellent model for studying how stress hormones in turn modulate fear activating Visual Pathways. Glucocorticoids, melanocortin peptides, and CRF all appear to play some role in modulating sensorimotor processing in the optic tectum. These observations, coupled with data showing control of the hypothalamus-pituitary-adrenal axis by the superior colliculus, suggest a fear/stress/anxiety neuroendocrine circuit that begins with first order synapses in Subcortical Visual Pathways. Thus, comparative studies shed light not only on how fear triggering Visual Pathways came to be, but how hormones released as a result of this activation modulate these Pathways.
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I'll take the low road: The evolutionary underpinnings of Visually triggered fear.
Frontiers Media S.A., 2015Co-Authors: James A. CarrAbstract:Although there is general agreement that the central nucleus of the amygdala (CeA) is critical for triggering the neuroendocrine response to Visual threats, there is uncertainty about the role of Subcortical Visual Pathways in this process. Primates in general appear to depend less on Subcortical Visual Pathways than other mammals. Yet, imaging studies continue to indicate a role for the superior colliculus and pulvinar nucleus in fear activation, despite disconnects in how these brain structures communicate not only with each other but with the amygdala. Studies in fish and amphibians suggest that the neuroendocrine response to Visual threats has remained relatively unchanged for hundreds of millions of years, yet there are still significant data gaps with respect to how Visual information is relayed to telencephalic areas homologous to the CeA, particularly in fish. In fact ray finned fishes may have evolved an entirely different mechanism for relaying Visual information to the telencephalon. In part because they lack a pathway homologous to the lateral geniculate-striate cortex pathway of mammals, amphibians continue to be an excellent model for studying how stress hormones in turn modulate fear activating Visual Pathways. Glucocorticoids, melanocortin peptides, and CRF all appear to play some role in modulating sensorimotor processing in the optic tectum. These observations, coupled with data showing control of the hypothalamus-pituitary-adrenal axis by the superior colliculus, suggest a fear/stress/anxiety neuroendocrine circuit that begins with first order synapses in Subcortical Visual Pathways. Thus, comparative studies shed light not only on how fear triggering Visual Pathways came to be, but how hormones released as a result of this activation modulate these Pathways
