Age-Related Changes in the Mouse Outer Retina

Li, Chibo; Cheng, Ming; Yang, Huige; Peachey, Neal S.; Naash, Muna I.

doi:10.1097/00006324-200106000-00015

Cited by 79 publications

(79 citation statements)

References 29 publications

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“…Effects on Control APB mice were much smaller. In previous studies by other investigators, the amplitudes of dark-adapted a-waves and b-wave were found to be reduced as mice aged for both C57BL/6 mice (pigmented mice) and Balb/c mice (albino mice) (Gresh et al, 2003;Li et al, 2001). Between four and 17 months of age, there was a substantial loss of rod photoreceptors (more in the albino mice), which contributed to the reduced ERG amplitudes.…”

Section: Effects Of Aging On the Light-adapted Erg Of Mice Lacking B-mentioning

confidence: 77%

“…Between four and 17 months of age, there was a substantial loss of rod photoreceptors (more in the albino mice), which contributed to the reduced ERG amplitudes. But aging effects have been less obvious for cones, whose counts (middle wavelength) were reduced in aged Balb/c mice, but not in C57BL/6 mice (Gresh et al, 2003;Jacobs and Williams, 2007;Li et al, 2001). Cone-driven flash ERGs were found to be reduced in mice that are a year old, and light-adapted flicker ERG amplitudes were affected, but only mildly in the pigmented mice (Jacobs et al, 2007;Li et al, 2001).…”

Section: Effects Of Aging On the Light-adapted Erg Of Mice Lacking B-mentioning

confidence: 99%

“…But aging effects have been less obvious for cones, whose counts (middle wavelength) were reduced in aged Balb/c mice, but not in C57BL/6 mice (Gresh et al, 2003;Jacobs and Williams, 2007;Li et al, 2001). Cone-driven flash ERGs were found to be reduced in mice that are a year old, and light-adapted flicker ERG amplitudes were affected, but only mildly in the pigmented mice (Jacobs et al, 2007;Li et al, 2001). The findings in the present study for one year old Nob mice versus three to six month old mice show no change in cone photoreceptor driven awaves measured at 6 or 8 ms after a brief flash, and no change in the amplitude of the positive intrusion.…”

Section: Effects Of Aging On the Light-adapted Erg Of Mice Lacking B-mentioning

confidence: 99%

“…This finding raises the possibility that aging effects on postreceptoral elements, and Müller cell function may be more pronounced than on some other retinal elements, particularly in Nob mice. An additional consideration is that the slow negative wave may reflect rod-related signals, and rods are known to be more affected in aging mouse eyes than cones (Gresh et al, 2005;Li et al, 2001). While we cannot completely eliminate this possibility, the backgrounds that we used, have been used in numerous other studies to suppress rod activity.…”

Section: Effects Of Aging On the Light-adapted Erg Of Mice Lacking B-mentioning

confidence: 99%

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Postreceptoral contributions to the light-adapted ERG of mice lacking b-waves

Shirato

Maeda

Miura

et al. 2008

Experimental Eye Research

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The purpose of this study was to determine the contributions of postreceptoral neurons to the lightadapted ERG of the Nob mouse, a model for complete-type congenital stationary night blindness (CSNB1) that lacks a b-wave from depolarizing bipolar cells. Ganzfeld ERGs were recorded from anesthetized adult control mice, control mice injected intravitreally with L-2-amino-4-phosphonobutyric acid (Control APB mice) to remove On pathway activity, and Nob mice. ERGs also were recorded after PDA (cis-2, 3-piperidine-dicarboxylic acid, 3-5 mM) was injected to block transmission to hyperpolarizing (Off) bipolar and horizontal cells, and all 3rd order neurons. Stimuli were brief (< 4 ms, 0.4 -2.5 log sc td s) and long (200 ms, 2.5 -4.6 log sc td) LED flashes (λmax = 513 nm, on a rod suppressing background (2.6 log sc td). Sinusoidal modulation of the LEDs (mean, 2.6 log sc td; contrast, 100%; 3 to 36 Hz) was used to study flicker ERGs.Brief-flash ERGs of Nob mice presented as long-lasting negative waves with a positive-going intrusion that started about 50 ms after the flash and peaked around 120 ms. Control APB mice had similar responses, and in both cases, PDA removed the positive-going intrusion. For long flashes, PDA removed a small, slow "d-wave" after light offset. With sinusoidal stimulation, the fundamental (F1) amplitude of control mice ERG peaked at 8 Hz (~70 μV). For Nob mice the peak was ~20 μV at 6 Hz before PDA and ~10 μV at 3 Hz or lower after PDA. F1 responses were present up to 21 Hz in control and Nob eyes and 15 Hz in Nob eyes after PDA. Between 3 and 6 Hz, F1 phase was 170°-210° more delayed in Nob than control mice; phase was hardly altered by PDA. With vector analysis, a substantial postreceptoral input to the Nob flicker ERG was revealed. In control mice, the second harmonic (F2) response showed peaks of ~10 μV at 3 Hz and 13 Hz. Nob mice showed almost no F2. In summary, in this study it was found that in Nob mice, postreceptoral neurons from the Off pathway make a positive-going contribution to the light-adapted flash ERG, and contribute substantially to sinusoidal flicker ERG.

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Section: Effects Of Aging On the Light-adapted Erg Of Mice Lacking B-mentioning

confidence: 77%

Section: Effects Of Aging On the Light-adapted Erg Of Mice Lacking B-mentioning

confidence: 99%

Section: Effects Of Aging On the Light-adapted Erg Of Mice Lacking B-mentioning

confidence: 99%

Section: Effects Of Aging On the Light-adapted Erg Of Mice Lacking B-mentioning

confidence: 99%

See 2 more Smart Citations

Postreceptoral contributions to the light-adapted ERG of mice lacking b-waves

Shirato

Maeda

Miura

et al. 2008

Experimental Eye Research

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“…Thus, we examined whether the dark-adapted ERG abnormalities of nob2 mice also were stable and recorded ERGs at 3, 7, and 15 months of age. To compensate for the reduction in overall amplitude that occurs in older WT mice (Li et al, 2001), values are expressed as a percentage of the mean for agematched WT mice recorded under the same conditions. At each age tested, the maximum awave amplitude, represented by the Rm P3 values, from nob2 mice were not different from those of WT animals (Fig.…”

Section: Ergs Are Abnormal In Nob2 Micementioning

confidence: 99%

Thenob2mouse, a null mutation inCacna1f: Anatomical and functional abnormalities in the outer retina and their consequences on ganglion cell visual responses

et al. 2006

Self Cite

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Glutamate release from photoreceptor terminals is controlled by voltage-dependent calcium channels (VDCCs). In humans, mutations in the Cacna1f gene, encoding the α 1F subunit of VDCCs, underlie the incomplete form of X-linked congenital stationary night blindness (CSNB2). These mutations impair synaptic transmission from rod and cone photoreceptors to bipolar cells. Here, we report anatomical and functional characterizations of the retina in the nob2 (no b-wave 2) mouse, a naturally occurring mutant caused by a null mutation in Cacna1f. Not surprisingly, the b-waves of both the light-and dark-adapted electroretinogram are abnormal in nob2 mice. The outer plexiform layer (OPL) is disorganized, with extension of ectopic neurites through the outer nuclear layer that originate from rod bipolar and horizontal cells, but not from hyperpolarizing bipolar cells. These ectopic neurites continue to express mGluR6, which is frequently associated with profiles that label with the

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Deafness and retinal degeneration in a novel USH1C knock‐in mouse model

Lentz

Gordon

Farris

et al. 2010

Developmental Neurobiology

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Usher syndrome is the leading cause of combined deaf-blindness, but the molecular mechanisms underlying the auditory and visual impairment are poorly understood. Usher I is characterized by profound congenital hearing loss, vestibular dysfunction and progressive retinitis pigmentosa beginning in early adolescence. Using the c.216G>A cryptic splice site mutation in exon 3 of the USH1C gene found in Acadian Usher I patients in Louisiana, we constructed the first mouse model that develops both deafness and retinal degeneration. The same truncated mRNA transcript found in Usher 1C patients is found in the cochleae and retinas of these knock-in mice. Absent auditory-evoked brainstem responses indicated that the mutant mice are deaf at one month of age. Cochlear histology showed disorganized hair cell rows, abnormal bundles, and loss of both inner and outer hair cells in the middle turns and at the base. Retinal dysfunction as evident by an abnormal electroretinogram was seen as early as 1 month of age, with progressive loss of rod photoreceptors between 6 and 12 months of age. This knock-in mouse reproduces the dual sensory loss of human Usher I, providing a novel resource to study the disease mechanism and the development of therapies.

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Age-Related Changes in the Mouse Outer Retina

Abstract: The amplitude of the mouse ERG declines with age. This change does not appear to reflect a change in the structural integrity of the photoreceptor cells. In functional studies of murine models of late-onset retinal disorders, it will be important to take these changes into consideration.

Cited by 79 publications

References 29 publications

Postreceptoral contributions to the light-adapted ERG of mice lacking b-waves

Postreceptoral contributions to the light-adapted ERG of mice lacking b-waves

Thenob2mouse, a null mutation inCacna1f: Anatomical and functional abnormalities in the outer retina and their consequences on ganglion cell visual responses

Deafness and retinal degeneration in a novel USH1C knock‐in mouse model

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