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Network deficiency exacerbates impairment in a mouse model of retinal degeneration.

Yee CW, Toychiev AH, Sagdullaev BT - Front Syst Neurosci (2012)

Bottom Line: In recording from retina in a mouse model of retinal degeneration (RD), we found that the incidence of oscillatory activity varied across different cell classes, evidence that some retinal networks are more affected by functional changes than others.By stimulating the surviving circuitry at different stages of the neurodegenerative process, we found that this dystrophic oscillator further compromises the function of the retina.These data reveal that retinal remodeling can exacerbate the visual deficit, and that aberrant synaptic activity could be targeted for RD treatment.

View Article: PubMed Central - PubMed

Affiliation: Department of Ophthalmology, Burke Medical Research Institute, Weill Medical College of Cornell University White Plains, NY, USA.

ABSTRACT
Neural oscillations play an important role in normal brain activity, but also manifest during Parkinson's disease, epilepsy, and other pathological conditions. The contribution of these aberrant oscillations to the function of the surviving brain remains unclear. In recording from retina in a mouse model of retinal degeneration (RD), we found that the incidence of oscillatory activity varied across different cell classes, evidence that some retinal networks are more affected by functional changes than others. This aberrant activity was driven by an independent inhibitory amacrine cell oscillator. By stimulating the surviving circuitry at different stages of the neurodegenerative process, we found that this dystrophic oscillator further compromises the function of the retina. These data reveal that retinal remodeling can exacerbate the visual deficit, and that aberrant synaptic activity could be targeted for RD treatment.

No MeSH data available.


Related in: MedlinePlus

Oscillatory activity varies between distinct classes of rd1 GCs. (A) Monostratified clusters significantly differed in their E:I ratios (ANOVA, p < 0.001). As a population, there was a significant correlation between stratification and E:I ratio (Pearson’s r = −0.57, p < 0.001, n = 113). (B) Monostratified clusters with larger dendritic fields had a larger percentage of bursting cells than clusters with smaller dendritic fields (data also in Table 1). This difference was greatest in cells that stratified proximally to the GC layer (∼30%). (C) Monostratified clusters with larger dendritic fields had lower E:I ratios compared to clusters with smaller dendritic fields that stratified similarly (Two-way ANOVA, p = 0.008). Above each group, stratification depths are indicated as IPL percentiles. (D) Bistratified clusters did not differ in their E:I ratio (p = 0.56), but inhibitory oscillations had 316 ± 10% the power of excitatory oscillations (t-test, p < 0.001, n = 53). Data are reported as means ± SEM, except in (B), where percentages within groups are reported.
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Figure 3: Oscillatory activity varies between distinct classes of rd1 GCs. (A) Monostratified clusters significantly differed in their E:I ratios (ANOVA, p < 0.001). As a population, there was a significant correlation between stratification and E:I ratio (Pearson’s r = −0.57, p < 0.001, n = 113). (B) Monostratified clusters with larger dendritic fields had a larger percentage of bursting cells than clusters with smaller dendritic fields (data also in Table 1). This difference was greatest in cells that stratified proximally to the GC layer (∼30%). (C) Monostratified clusters with larger dendritic fields had lower E:I ratios compared to clusters with smaller dendritic fields that stratified similarly (Two-way ANOVA, p = 0.008). Above each group, stratification depths are indicated as IPL percentiles. (D) Bistratified clusters did not differ in their E:I ratio (p = 0.56), but inhibitory oscillations had 316 ± 10% the power of excitatory oscillations (t-test, p < 0.001, n = 53). Data are reported as means ± SEM, except in (B), where percentages within groups are reported.

Mentions: Bursting activity was recorded in ∼70% of rd1 GCs (n = 181), across six monostratified and five bistratified cell clusters (Table 1; Figure 2), which were compared to an earlier classification scheme (Sun et al., 2002) to verify a representative sample of previously identified GCs (Kong et al., 2005; Mazzoni et al., 2008). Monostratified cells varied in bursting probability. Clusters with larger DFs (≥199 μm) were more likely to burst (∼80%) within any given stratum, while those with smaller DFs (<199 μm) were less likely to burst (∼36%) within proximal strata but more likely (approaching 80%) distally (Figure 3B). Overall, cells with larger DFs were more likely to burst (81.8 versus 60.3%).


Network deficiency exacerbates impairment in a mouse model of retinal degeneration.

Yee CW, Toychiev AH, Sagdullaev BT - Front Syst Neurosci (2012)

Oscillatory activity varies between distinct classes of rd1 GCs. (A) Monostratified clusters significantly differed in their E:I ratios (ANOVA, p < 0.001). As a population, there was a significant correlation between stratification and E:I ratio (Pearson’s r = −0.57, p < 0.001, n = 113). (B) Monostratified clusters with larger dendritic fields had a larger percentage of bursting cells than clusters with smaller dendritic fields (data also in Table 1). This difference was greatest in cells that stratified proximally to the GC layer (∼30%). (C) Monostratified clusters with larger dendritic fields had lower E:I ratios compared to clusters with smaller dendritic fields that stratified similarly (Two-way ANOVA, p = 0.008). Above each group, stratification depths are indicated as IPL percentiles. (D) Bistratified clusters did not differ in their E:I ratio (p = 0.56), but inhibitory oscillations had 316 ± 10% the power of excitatory oscillations (t-test, p < 0.001, n = 53). Data are reported as means ± SEM, except in (B), where percentages within groups are reported.
© Copyright Policy - open-access
Related In: Results  -  Collection

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Show All Figures
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Figure 3: Oscillatory activity varies between distinct classes of rd1 GCs. (A) Monostratified clusters significantly differed in their E:I ratios (ANOVA, p < 0.001). As a population, there was a significant correlation between stratification and E:I ratio (Pearson’s r = −0.57, p < 0.001, n = 113). (B) Monostratified clusters with larger dendritic fields had a larger percentage of bursting cells than clusters with smaller dendritic fields (data also in Table 1). This difference was greatest in cells that stratified proximally to the GC layer (∼30%). (C) Monostratified clusters with larger dendritic fields had lower E:I ratios compared to clusters with smaller dendritic fields that stratified similarly (Two-way ANOVA, p = 0.008). Above each group, stratification depths are indicated as IPL percentiles. (D) Bistratified clusters did not differ in their E:I ratio (p = 0.56), but inhibitory oscillations had 316 ± 10% the power of excitatory oscillations (t-test, p < 0.001, n = 53). Data are reported as means ± SEM, except in (B), where percentages within groups are reported.
Mentions: Bursting activity was recorded in ∼70% of rd1 GCs (n = 181), across six monostratified and five bistratified cell clusters (Table 1; Figure 2), which were compared to an earlier classification scheme (Sun et al., 2002) to verify a representative sample of previously identified GCs (Kong et al., 2005; Mazzoni et al., 2008). Monostratified cells varied in bursting probability. Clusters with larger DFs (≥199 μm) were more likely to burst (∼80%) within any given stratum, while those with smaller DFs (<199 μm) were less likely to burst (∼36%) within proximal strata but more likely (approaching 80%) distally (Figure 3B). Overall, cells with larger DFs were more likely to burst (81.8 versus 60.3%).

Bottom Line: In recording from retina in a mouse model of retinal degeneration (RD), we found that the incidence of oscillatory activity varied across different cell classes, evidence that some retinal networks are more affected by functional changes than others.By stimulating the surviving circuitry at different stages of the neurodegenerative process, we found that this dystrophic oscillator further compromises the function of the retina.These data reveal that retinal remodeling can exacerbate the visual deficit, and that aberrant synaptic activity could be targeted for RD treatment.

View Article: PubMed Central - PubMed

Affiliation: Department of Ophthalmology, Burke Medical Research Institute, Weill Medical College of Cornell University White Plains, NY, USA.

ABSTRACT
Neural oscillations play an important role in normal brain activity, but also manifest during Parkinson's disease, epilepsy, and other pathological conditions. The contribution of these aberrant oscillations to the function of the surviving brain remains unclear. In recording from retina in a mouse model of retinal degeneration (RD), we found that the incidence of oscillatory activity varied across different cell classes, evidence that some retinal networks are more affected by functional changes than others. This aberrant activity was driven by an independent inhibitory amacrine cell oscillator. By stimulating the surviving circuitry at different stages of the neurodegenerative process, we found that this dystrophic oscillator further compromises the function of the retina. These data reveal that retinal remodeling can exacerbate the visual deficit, and that aberrant synaptic activity could be targeted for RD treatment.

No MeSH data available.


Related in: MedlinePlus