Objective: To investigate the distribution and biological roles of voltage-dependent calcium channel (VDCC) α1F subunit in murine retina.

Methods: Experimental study.α1F(-/-) (homozygous mutant) mice (n = 35) and α1F(+/+) (wild type) mice (n = 35) were used in this study. Immunohistochemistry was performed to determine the expression of VDCC α1F subunit in the mouse retina. Retinae in α1F(-/-) mice and age-matched control mice at 3, 6, 9, 14-day and 3-month after birth were paraffin embedded, sectioned and HE stained, and full-field electroretinogram (ERG) were also recorded at these time points.Statistics were based on independent samples t-test.

Results: (1) α1F subunit was absent in α1F(-/-) mice retina. But in α1F(+/+) mice retina, α1F subunit was expressed most strongly in the outer plexiform layer (OPL), less in the inner plexiform layer (IPL) and ganglion cell layer (GCL). (2) OPL thickness in the subunit deficient mice gradually reduced after birth and lost at adult age. (3) In dark-adapted ERGs,standard response showed that the b-wave amplitude of α1F(-/-) mice [(163.8 ± 26.7) µV] significantly decreased compared with that of α1F(+/+) mice [(408.4 ± 54.5) µV] (t = -9.017, P = 0.000), whereas the a-wave amplitude of α1F(-/-) group [(208.2 ± 27.3) µV] was similar to that of control group [(196.0 ± 24.2) µV] (t = 0.748, P = 0.476).

Conclusion: This study demonstrates that the lack of VDCC α1F subunit affect the structure and function in the OPL of the murine retina.

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