RGS9-1 is required for normal inactivation of mouse cone phototransduction

A. L. Lyubarsky, C. K. Chen, F. Naarendorp, X. Zhang, T. Wensel, M. I. Simon, Edward N Pugh Jr

Research output: Contribution to journalArticle

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Abstract

Purpose: To test the hypothesis that Regulator of G-protein Signaling 9 (RGS9-1) is necessary for the normal inactivation of retinal cones. Methods: Mice having the gene RGS9-1 inactivated in both alleles (RGS9-1 -/-) were tested between the ages 8-10 weeks with electroretinographic (ERG) protocols that isolate cone-driven responses. Immunohistochemistry was performed with a primary antibody against RGS9-1 (anti-RGS9-1c), with the secondary conjugated to fluorescein isothiocyanate, and with rhodamine-conjugated peanut agglutinin. Results: (1) Immunohistochemistry showed RGS9-1 to be strongly expressed in the cones of wildtype (WT is C57BL/6) mice, but absent from the cones of RGS9-1 mice. (2) Cone-driven b-wave responses of dark-adapted RGS9-1 -/- mice had saturating amplitudes and sensitivities in the midwave and UV regions of the spectrum equal to or slightly greater than those of WT (C57BL/6) mice. (3) Cone-driven b-wave and a-wave responses of RGS9-1 -/- mice recovered much more slowly than those of WT after a strong conditioning flash: for a flash estimated to isomerize 1.2% of the M-cone pigment and 0.9% of the UV-cone pigment, recovery of 50% saturating amplitude was approximately 60-fold slower than in WT. Conclusions: (1) The amplitudes and sensitivities of the cone-driven responses indicate that cones and cone-driven neurons in RGS9-1 -/- mice have normal generator currents. (2) The greatly retarded recovery of cone-driven responses of RGS9-1 -/- mice relative to those of WT mice establishes that RGS9-1 is required for normal inactivation of the cone phototransduction cascades of both UV- and M-cones.

Original languageEnglish (US)
Pages (from-to)71-78
Number of pages8
JournalMolecular Vision
Volume7
StatePublished - 2001
Externally publishedYes

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Light Signal Transduction
Inbred C57BL Mouse
Immunohistochemistry
GTP-Binding Protein Regulators
Peanut Agglutinin
Retinal Cone Photoreceptor Cells
Fluorescein
Alleles
Neurons
Antibodies

ASJC Scopus subject areas

  • Ophthalmology

Cite this

Lyubarsky, A. L., Chen, C. K., Naarendorp, F., Zhang, X., Wensel, T., Simon, M. I., & Pugh Jr, E. N. (2001). RGS9-1 is required for normal inactivation of mouse cone phototransduction. Molecular Vision, 7, 71-78.

RGS9-1 is required for normal inactivation of mouse cone phototransduction. / Lyubarsky, A. L.; Chen, C. K.; Naarendorp, F.; Zhang, X.; Wensel, T.; Simon, M. I.; Pugh Jr, Edward N.

In: Molecular Vision, Vol. 7, 2001, p. 71-78.

Research output: Contribution to journalArticle

Lyubarsky, AL, Chen, CK, Naarendorp, F, Zhang, X, Wensel, T, Simon, MI & Pugh Jr, EN 2001, 'RGS9-1 is required for normal inactivation of mouse cone phototransduction', Molecular Vision, vol. 7, pp. 71-78.
Lyubarsky AL, Chen CK, Naarendorp F, Zhang X, Wensel T, Simon MI et al. RGS9-1 is required for normal inactivation of mouse cone phototransduction. Molecular Vision. 2001;7:71-78.
Lyubarsky, A. L. ; Chen, C. K. ; Naarendorp, F. ; Zhang, X. ; Wensel, T. ; Simon, M. I. ; Pugh Jr, Edward N. / RGS9-1 is required for normal inactivation of mouse cone phototransduction. In: Molecular Vision. 2001 ; Vol. 7. pp. 71-78.
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T1 - RGS9-1 is required for normal inactivation of mouse cone phototransduction

AU - Lyubarsky, A. L.

AU - Chen, C. K.

AU - Naarendorp, F.

AU - Zhang, X.

AU - Wensel, T.

AU - Simon, M. I.

AU - Pugh Jr, Edward N

PY - 2001

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N2 - Purpose: To test the hypothesis that Regulator of G-protein Signaling 9 (RGS9-1) is necessary for the normal inactivation of retinal cones. Methods: Mice having the gene RGS9-1 inactivated in both alleles (RGS9-1 -/-) were tested between the ages 8-10 weeks with electroretinographic (ERG) protocols that isolate cone-driven responses. Immunohistochemistry was performed with a primary antibody against RGS9-1 (anti-RGS9-1c), with the secondary conjugated to fluorescein isothiocyanate, and with rhodamine-conjugated peanut agglutinin. Results: (1) Immunohistochemistry showed RGS9-1 to be strongly expressed in the cones of wildtype (WT is C57BL/6) mice, but absent from the cones of RGS9-1 mice. (2) Cone-driven b-wave responses of dark-adapted RGS9-1 -/- mice had saturating amplitudes and sensitivities in the midwave and UV regions of the spectrum equal to or slightly greater than those of WT (C57BL/6) mice. (3) Cone-driven b-wave and a-wave responses of RGS9-1 -/- mice recovered much more slowly than those of WT after a strong conditioning flash: for a flash estimated to isomerize 1.2% of the M-cone pigment and 0.9% of the UV-cone pigment, recovery of 50% saturating amplitude was approximately 60-fold slower than in WT. Conclusions: (1) The amplitudes and sensitivities of the cone-driven responses indicate that cones and cone-driven neurons in RGS9-1 -/- mice have normal generator currents. (2) The greatly retarded recovery of cone-driven responses of RGS9-1 -/- mice relative to those of WT mice establishes that RGS9-1 is required for normal inactivation of the cone phototransduction cascades of both UV- and M-cones.

AB - Purpose: To test the hypothesis that Regulator of G-protein Signaling 9 (RGS9-1) is necessary for the normal inactivation of retinal cones. Methods: Mice having the gene RGS9-1 inactivated in both alleles (RGS9-1 -/-) were tested between the ages 8-10 weeks with electroretinographic (ERG) protocols that isolate cone-driven responses. Immunohistochemistry was performed with a primary antibody against RGS9-1 (anti-RGS9-1c), with the secondary conjugated to fluorescein isothiocyanate, and with rhodamine-conjugated peanut agglutinin. Results: (1) Immunohistochemistry showed RGS9-1 to be strongly expressed in the cones of wildtype (WT is C57BL/6) mice, but absent from the cones of RGS9-1 mice. (2) Cone-driven b-wave responses of dark-adapted RGS9-1 -/- mice had saturating amplitudes and sensitivities in the midwave and UV regions of the spectrum equal to or slightly greater than those of WT (C57BL/6) mice. (3) Cone-driven b-wave and a-wave responses of RGS9-1 -/- mice recovered much more slowly than those of WT after a strong conditioning flash: for a flash estimated to isomerize 1.2% of the M-cone pigment and 0.9% of the UV-cone pigment, recovery of 50% saturating amplitude was approximately 60-fold slower than in WT. Conclusions: (1) The amplitudes and sensitivities of the cone-driven responses indicate that cones and cone-driven neurons in RGS9-1 -/- mice have normal generator currents. (2) The greatly retarded recovery of cone-driven responses of RGS9-1 -/- mice relative to those of WT mice establishes that RGS9-1 is required for normal inactivation of the cone phototransduction cascades of both UV- and M-cones.

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