Mason Eye Institute

Bo Lei, PhD

Assistant Professor

Department of Veterinary Medicine & Surgery
Department of Ophthalmology
A253 Clydesdale Hall
379 E. Campus Dr.
Columbia, MO 65211
(573) 884-1759

CURRENT RESEARCH

Neurophysiology in Retinal Degenerative Diseases

Figure 1: Dark- and light-adapted ERG of a normal wild type (C57BL/6, left column), a coneless (cpfl1/cpfl1, middle column) and a rodless (rho-/-, right column) mouse. In coneless mouse, the light-adapted ERG were extinguished, the dark-adapted ERG existed. In rodless rho-/- mouse, the light-adapted responses were normal, the dark-adapted ERG was reduced. The residual b-wave was similar to the light-adapted ERG.

In vision science research laboratory and ophthalmology electrodiagnostic laboratory, we study neurophysiology in retinal disease in animal models and human patients. The clinical terms for these diseases are retinal degeneration, macular dystrophy and retinitis pigmentosa. Our research goals are to investigate phototransduction and signal transmission in healthy and diseased retinas and to develop non-invasive function tests for retinal disease diagnosis and therapeutic interventions.

We have several mouse models of retinal degeneration caused by genetic defects specific to the retina. These mutations disturb signal generation and transmission between retinal neurons. Retinal neural function and dysfunction are studied by visual electrophysiology (electroretinogram, ERG) and pupillary light reflex (PLR). Recently we have developed a protocol to detect rod- and cone-driven responses and an infrared PLR recording system. We manipulate synaptic transmission between photoreceptors and bipolar or amacrine cell with glutamate analogs to probe the origins of retinal ERG responses and mechanisms involved. Particular focus is on probing synaptic properties of the retinal neurocircuitry, to understand the consequence of noise on the visual signals. Comparing the ERG between species allows us to probe the effects of retinal degeneration on human vision.

Figure 2: Mouse pupillary light reflex (PLR) recorded with an infrared video camera.

Figure 3: PLR and ERG recorded in a normal (C57BL/6J) and a retinal degeneration (rd 12) mouse. The PLR and ERG responses greatly reduced in diseased retina.

Publications

Lei B, Tullis GE, Kirk MD, Zhang K and Katz ML. Ocular phenotype in a mouse gene knockout model for infantile neuronal ceroid-lipofuscinosis (CLN1). J Neurosci Res. 2006;84:1139-1149.

Lei B, Yao G, Zhang K, Hofeldt KJ. Chang B. Study of rod- and cone-driven oscillatory potentials (OPs) in mouse. Invest Ophthalmol Vis Sci. 2006;47(6):2732-2738 .

Yao G, Zhang K, Bellassai M, Chang B, Lei B. Ultraviolet light–induced and green light-induced transient pupillary light reflex in mice. Curr Eye Res. 2006;31(11):925-33.

Lei B, Yao G. Spectral attenuation of crystalline lens of mouse, rat, pig and human at wavelengths from 360nm to 1020nm. Exp Eye Res. 2006 ;83:610–614.

Gehlbach P, Hose S, Lei B, et al. Developmental abnormalities in the Nuc1 rat retina: A spontaneous mutation that affects neuronal and vascular remodeling and retinal function. Neuroscience. 2006;137(2):447-61.

Hyman JA, Vaegan, Lei B, Narfström KL. Electrophysiologic differentiation of homozygous and heterozygous Abyssinian-crossbred cats with late-onset hereditary retinal degeneration. Am J Vet Res. 2005;66(11):1914-1921.

Dierks D, Lei B, Zhang K, Hainsworth DP. Intravitreal triamcinolone acetonide augments the rod electroretinogram (ERG) b-wave in rabbit. Arch Ophthalmol. 205; 123(11):1563-9.

Wendt KD, Lei B, Schachtman TR, Tullis GE, Ibe ME, and Katz ML. Behavioral assessment in mouse models of neuronal ceroid lipofuscinosis using a light-cued T-maze. Behav Brain Res. 2005; 161(2):175-82.

Bush RA, Lei B, Tao W, et al. Encapsulated cell-based intraocular delivery of ciliary neurotrophic factor in normal rabbit: dose-dependent effects on ERG and retinal histology. Invest Ophthalmol Vis Sci. 2004;45(7):2420-30.

Zhang C, Lei B, Lam TT, Yang F, Sinha D, Tso MO. Neuroprotection of photoreceptors by minocycline in light-induced retinal degeneration. Invest Ophthalmol Vis Sci. 2004;45(8):2753-59.

Lei B. Scotopic and photopic electroretinogram of weak I-type guinea pig (Cavis porcellus): comparison with monkey and rat. Documenta Ophthalmologica. 2003;106(3):243-9.

Zemel E, Lei B, Perlman I. NADPH diaphorase activity in the rabbit retina is modulated by glutamatergic pathways. J Comp Neurol. 2001;431(1):28-38.

Jamison JA, Bush RA, Lei B, Sieving PA. Characterization of the rod photoresponse isolated from the dark-adapted primate ERG. Vis Neurosci. 2001;18(3):445-455.

Perlman I, Segev E, Mazawi N, Merhav-Armon T, Lei B, Leibu R.Visual evoked cortical potential can be used to differentiate between uncorrected refractive error and macular disorders. Documenta Ophthalmologica. 2001;102(1):41-62.

Lei B, Bush RA, Milam AH, Sieving PA. Human melanoma-associated retinopathy (MAR) antibodies alter the retinal ON-response of the monkey ERG in vivo. Invest Ophthalmol and Vis Sci. 2000;41: 262-266.

Hrach CJ, Johnson MW, Hassan AS, Lei B, Sieving PA, Elner VM. Retinal toxicity of commercial intravitreal tissue plasminogen activator solution in cat eyes. Arch Ophthalmol. 2000;118:659-663.

Lei B, Perlman I. The contributions of voltage- and time-dependent potassium conductance to the electroretinogram in rabbits. Vis Neurosci.1999;16:743-754.

Zemel E, Eyal O, Lei B, Perlman I. NADPH diaphorase reactivity in the mammalian retina is modulated by the state of visual adaptation. Vis Neurosci. 1996;13:863-871.

Ding FD, Zhang X, Yang JC, Lei B, et al. A research of clinical genetics of family retinitis pigmentosa. Chinese Ophthalmic Res. 1996;14:203-206.

Zemel E, Loewenstein A, Lei B, Lazar M, Perlman I. Ocular pigmentation protects the rabbit retina from gentamicin-induced toxicity. Invest Ophthalmol Vis Sci. 1995;36:1875-1884.