Flicker assessment of rod and cone function in a model of retinal degeneration

Rubin, G. R.; Kraft, Timothy W.

doi:10.1007/s10633-007-9066-9

Cited by 17 publications

(19 citation statements)

References 37 publications

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“…Cone survival in P23H rats depends on the mutation (Machida et al, 2000) and previous studies have documented cone degeneration from P21 in P23H-1 rats (Machida et al, 2000; Cuenca et al, 2004; Pinilla et al, 2005a; García-Ayuso et al, 2013), but also long term cone survival for P23H-3 rats (Chrysostomou et al, 2009; Lu et al, 2013; Fernández-Sánchez et al, 2015). In the RCS strain, previous electrophysiological and morphological studies have indicated that cone cell death may begin before P30 (Pinilla et al, 2005b; Rubin and Kraft, 2007; Huang et al, 2011). …”

Section: Discussionmentioning

confidence: 94%

Early Events in Retinal Degeneration Caused by Rhodopsin Mutation or Pigment Epithelium Malfunction: Differences and Similarities

et al. 2017

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To study the course of photoreceptor cell death and macro and microglial reactivity in two rat models of retinal degeneration with different etiologies. Retinas from P23H-1 (rhodopsin mutation) and Royal College of Surgeon (RCS, pigment epithelium malfunction) rats and age-matched control animals (Sprague-Dawley and Pievald Viro Glaxo, respectively) were cross-sectioned at different postnatal ages (from P10 to P60) and rhodopsin, L/M- and S-opsin, ionized calcium-binding adapter molecule 1 (Iba1), glial fibrillary acid protein (GFAP), and proliferating cell nuclear antigen (PCNA) proteins were immunodetected. Photoreceptor nuclei rows and microglial cells in the different retinal layers were quantified. Photoreceptor degeneration starts earlier and progresses quicker in P23H-1 than in RCS rats. In both models, microglial cell activation occurs simultaneously with the initiation of photoreceptor death while GFAP over-expression starts later. As degeneration progresses, the numbers of microglial cells increase in the retina, but decreasing in the inner retina and increasing in the outer retina, more markedly in RCS rats. Interestingly, and in contrast with healthy animals, microglial cells reach the outer nuclei and outer segment layers. The higher number of microglial cells in dystrophic retinas cannot be fully accounted by intraretinal migration and PCNA immunodetection revealed microglial proliferation in both models but more importantly in RCS rats. The etiology of retinal degeneration determines the initiation and pattern of photoreceptor cell death and simultaneously there is microglial activation and migration, while the macroglial response is delayed. The actions of microglial cells in the degeneration cannot be explained only in the basis of photoreceptor death because they participate more actively in the RCS model. Thus, the retinal degeneration caused by pigment epithelium malfunction is more inflammatory and would probably respond better to interventions by inhibiting microglial cells.

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Section: Discussionmentioning

confidence: 94%

Early Events in Retinal Degeneration Caused by Rhodopsin Mutation or Pigment Epithelium Malfunction: Differences and Similarities

et al. 2017

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“…Humans as well as cats can decode up to ϳ70 Hz of flickering visual stimuli. However, in rats, even though the critical flicker frequency (CFF) of electroretinogram responses could be as high as 50 Hz (Rubin and Kraft, 2007), the CFF of the cells in the visual cortex was found to be ϳ20 Hz (Wells et al, 2001). Evolutional merit of the features found at this synapse may exist for rats, and, as all visual information must pass through the LGN before it reaches the visual cortex, this synapse would be an ideal location for signal filtering optimized for each species.…”

Section: Discussionmentioning

confidence: 99%

Mechanisms Underlying Signal Filtering at a Multisynapse Contact

Budisantoso¹,

Matsui²,

Kamasawa³

et al. 2012

J. Neurosci.

111

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Visual information must be relayed through the lateral geniculate nucleus before it reaches the visual cortex. However, not all spikes created in the retina lead to postsynaptic spikes and properties of the retinogeniculate synapse contribute to this filtering. To understand the mechanisms underlying this filtering process, we conducted electrophysiology to assess the properties of signal transmission in the Long-Evans rat. We also performed SDS-digested freeze-fracture replica labeling to quantify the receptor and transporter distribution, as well as EM reconstruction to describe the 3D structure. To analyze the impact of transmitter diffusion on the activity of the receptors, simulations were integrated. We identified that a large contributor to the filtering is the marked paired-pulse depression at this synapse, which was intensified by the morphological characteristics of the contacts. The broad presynaptic and postsynaptic contact area restricts transmitter diffusion two dimensionally. Additionally, the presence of multiple closely arranged release sites invites intersynaptic spillover, which causes desensitization of AMPA receptors. The presence of AMPA receptors that slowly recover from desensitization along with the high presynaptic release probability and multivesicular release at each synapse also contribute to the depression. These features contrast with many other synapses where spatiotemporal spread of transmitter is limited by rapid transmitter clearance allowing synapses to operate more independently. We propose that the micrometer-order structure can ultimately affect the visual information processing.

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“…The normal morphology of P21 RCS rats seen here is consistent with previously reported functional changes in RCS rats. Cone function, evaluated using the amplitude of cone-driven critical fl icker frequency 25 and threshold multiunit responses recorded from the superior colliculus in light-adapted rats, were nearly normal at P21-25 in RCS rats. 8 An implication of this fi nding for therapeutic strategies is that, to achieve preservation of cone function, therapies should be performed prior to the completion of cone development.…”

Section: Discussionmentioning

confidence: 99%