Optical Coherence Tomography of Animal Models of Retinitis Pigmentosa: From Animal Studies to Clinical Applications

Table 2

Summary of comparison of SD-OCT and structural findings in animal models of retinitis pigmentosa.

Animal models	Gene	Function	SD-OCT findings	EM and LM findings	References
RCS^–/–	mertk	Phagocytosis of RPE	Hyperreflective zone in IS-OS layer	Deposition of lamellar materials	[34, 36]
			Thinning of ONL	Degeneration of IS-OS
RHO P23H	RHO (P23H)	Phototransduction	Hyperreflective zone in IS-OS layer	Disarrangement of OS discs	[43, 44]
			Thinning of ONL	Degeneration of IS-OS
RHO S334ter	RHO (S334ter)	Phototransduction	Hyperreflective zone in IS-OS layer	Degeneration of IS-OS	[47]
			Thinning of ONL	Deposition of granular materials
RHO^–/–	RHO	Phototransduction	Absence of EZ and IZ	Absence of OS	[33, 50–52]
			Hyporeflective zone under ELM	Short IS
Rpe65^–/–	Rpe65	Visual cycle	Hyperreflective zone in IS-OS layer	Degeneration of IS-OS	[35, 50]
			Thinning of ONL	Shortage of OS length
				Lipid deposition in RPE
rd12	Rpe65 (R44ter)	Visual cycle	Hyperreflective zone in IS-OS layer	Disorganized OS	[64]
			Thinning of ONL	Intracellular vacuoles in ONL
				Lipid deposits in RPE
rd 1	Pde6β (R560C)	Phototransduction	Extremely thin ONL		[33, 52, 70]
rd10	Pde6β (Y347ter)	Phototransduction	Transiently hyperreflective ONL	Intracellular vacuoles in ONL	[60, 66, 70, 71]
Arr1^–/–	Arrestin 1	Quenching of rhodopsin		IS vesiculation	[75]
			Diffuse hyperreflective ONL by light exposure	Disruption of IS-OS junction
				Condensation of nuclei in ONL

IS-OS, inner and outer segments; ONL, outer nuclear layer; EZ, ellipsoid zone; IZ, interdigitation zone; RPE, retinal pigment epithelium.