Research Faculty

Maureen McCall, Ph.D.

Maureen McCall, Ph.D.

Professor, Department of
Ophthalmology and
Visual Sciences


301 E. Muhammad Ali Boulevard, Louisville KY 40202
Telephone: 502-852-3386 (office) 502-852-0162 (lab) Fax: 502-852-3588

B.S. & MS.:

University of Maryland, College Park M.D. – 1974 - 1977


Neurobiology – The University at Albany, Albany, NY – 1983

Postdoctoral Research:

(1) Visual System Plasticity & Processing (P.D. Spear) Departments of Psychology & Ophthalmology, University of Wisconsin, Madison, WI – 1983-1987
(2) Circuitry Underlying Basic Retinal Signaling (L.R. Stanford) Waisman Center, University of Wisconsin, Madison, WI – 1987-1992
(3) Genetic Manipulation of the Nervous System (A. Messing) School of Veterinary Medicine, University of Wisconsin, Madison, WI – 1992-1993

Faculty positions:

(1) Assistant/Associate Scientist, Waisman Center on Mental Retardation & Human Development, University of Wisconsin, Madison, WI – 1993-1996
(2) Assistant/Associate/Professor, Department of Psychological & Brain Sciences, University of Louisville, Louisville, KY, 1997 – 2007
(3) Professor, Department of Ophthalmology & Visual Sciences, University of Louisville, Louisville, KY, 2007 – present.
(4) Joint appointments - Departments of : Anatomical Sciences & Neurobiology and Psychological & Brain Sciences.


My research uses electrophysiological techniques to evaluate normal retinal function, dysfunction caused by blinding retinal diseases and the restoration of function using a variety of therapeutic strategies. We can use our understanding or normal retinal function and disease-related changes to construct optimal therapeutic strategies and evaluate how they ameliorate the effects of disease.

Retinitis pigmentosa (RP) is a family of blinding eye diseases caused by photoreceptor degeneration. The absence of the cells that for this primary signal leads to blindness. My interest in RP involves the evaluation of therapies to restore vision: replacing degenerated photoreceptors either with: (1) new stem or other embryonic cells, manipulated to become photoreceptors or (2) prosthetics devices that replace the photoreceptor signal with an electronic signal to light.

Glaucoma is caused by increased intraocular pressure and leads to ganglion cell death, which eliminates the link between the retinal output and central visual processing. We are parsing out of the effects of increased intraocular pressure and aging on ganglion cells.

Congenital Stationary Night Blindness (CSNB) is a family of diseases in which signaling is eliminated between rod photoreceptors and their postsynaptic targets, rod bipolar cells. This deafferents the retinal circuit that is responsible for vision under dim lighting. My interest in CSNB involves understanding the basic interplay between excitation and inhibition in the retinal circuit and its normal development. Because of the targeted nature of this disease, we are hopeful that a gene therapy approach can be developed to restore night vision.

My work utilizes rodent disease models whose mutations mimic those found in human patients. While molecular manipulation of rodents is a fairly common approach, we have recently developed a mutant NIH miniature swine model of a common form of autosomal dominant RP (Pro23His rhodopsin mutation) in collaboration with the National Swine Resource Research Center at University of Missouri. More genetically modified mini-swine models are in the pipeline to examine other retinal diseases.


(15 selected publications from 52)

  1. van Genderen MM, Bijveld MM, Claassen YB, Florijn RJ, Pearring JN, Meire FM, McCall MA, Riemslag FC, Gregg RG, Bergen AA, Kamermans M. Mutations in TRPM1 are a common cause of complete congenital stationary night blindness. Am J Hum Genet. 2009 Nov;85(5):730-6. Epub 2009 Nov 5. PMID: 19896109
  2. McCall MA, Gregg RG. Comparisons of structural and functional abnormalities in mouse b-wave mutants. J Physiol. 2008 Sep 15;586(Pt 18):4385-92. Epub 2008 Jul 24. PMID: 18653656
  3. Maddox DM, Vessey KA, Yarbrough GL, Invergo BM, Cantrell DR, Inayat S, Balannik V, Hicks WL, Hawes NL, Byers S, Smith RS, Hurd R, Howell D, Gregg RG, Chang B, Naggert JK, Troy JB, Pinto LH, Nishina PM, McCall MA.Allelic variance between GRM6 mutants, Grm6nob3 and Grm6nob4 results in differences in retinal ganglion cell visual responses. J Physiol. 2008; 586(18):4409-24. PMID: 18687716
  4. Gregg RG, Kamermans M, Klooster J, Lukasiewicz PD, Peachey NS, Vessey KA, McCall MA. Nyctalopin expression in retinal bipolar cells restores visual function in a mouse model of complete X-linked congenital stationary night blindness. J Neurophysiol. 2007 Nov;98(5):3023-33. Epub 2007 Sep 19. PMID: 17881478
  5. Eggers ED, McCall MA, Lukasiewicz PD.Presynaptic inhibition differentially shapes transmission in distinct circuits in the mouse retina. J Physiol. 2007 Jul 15;582(Pt 2):569-82. Epub 2007 Apr 26. PMID: 17463042
  6. Pinto LH, Vitaterna MH, Shimomura K, Siepka SM, Balannik V, McDearmon EL, Omura C, Lumayag S, Invergo BM, Glawe B, Cantrell DR, Inayat S, Olvera MA, Vessey KA, McCall MA, Maddox D, Morgans CW, Young B, Pletcher MT, Mullins RF, Troy JB, Takahashi JS. Generation, Identification and Functional Characterization of the nob4 Mutation of Grm6 in the Mouse Vis Neurosci. 2007 Jan-Feb;24(1):111-23. PMID: 17430614
  7. DeMarco PJ Jr, Yarbrough GL, Yee CW, McLean GY, Sagdullaev BT, Ball SL, McCall MA. Stimulation via a subretinally placed prosthetic elicits central activity and induces a trophic effect on visual responses. Invest Ophthalmol Vis Sci. 2007 Feb;48(2):916-26. PMID: 17251495
  8. Sagdullaev BT, McCall MA, Lukasiewicz PD. Presynaptic inhibition modulates spillover, creating distinct dynamic response ranges of sensory output. Neuron. 2006 Jun 15;50(6):923-35. PMID: 16772173
  9. Chang B, Heckenlively JR, Bayley PR, Brecha NC, Davisson MT, Hawes NL, Hirano AA, Hurd RE, Ikeda A, Johnson BA, McCall MA, Morgans CW, Nusinowitz S, Peachey NS, Rice DS, Vessey KA, Gregg RG. The nob2 mouse, a null mutation in Cacna1f: Anatomical and functional abnormalities in the outer retina and their consequences on ganglion cell visual responses. Vis Neurosci. 2006 Jan-Feb;23(1):11-24. PMID: 16597347
  10. Demas J, Sagdullaev BT, Green E, Jaubert-Miazza L, McCall MA, Gregg RG, Wong RO, Guido W. Failure to Maintain Eye-Specific Segregation in nob, a Mutant with Abnormally Patterned Retinal Activity. Neuron. 2006 Apr 20;50(2):247-59. PMID: 16630836
  11. Sagdullaev BT, McCall MA. Stimulus size and intensity alter fundamental receptive-field properties of mouse retinal ganglion cells in vivo. Vis Neurosci. 2005 Sep-Oct;22(5):649-59. PMID: 16332276
  12. Sagdullaev BT, Aramant RB, Seiler MJ, Woch G, McCall MA.Retinal transplantation-induced recovery of retinotectal visual function in a rodent model of retinitis pigmentosa. Invest Ophthalmol Vis Sci. 2003 Apr;44(4):1686-95. PMID: 12657610
  13. Gregg RG, Mukhopadhyay S, Candille SI, Ball SL, Pardue MT, McCall MA, Peachey NS. Identification of gene responsible for the mouse nob (no b-wave) mutant. Invest Ophthalmol Vis Sci. 2003 Jan;44(1):378-84. PMID: 12506099
  14. McCall MA, Lukasiewicz PD, Gregg RG, Peachey NS. Elimination of the ᵨ1 subunit abolishes Elimination of the rho1 subunit abolishes GABA(C) receptor expression and alters visual processing in the mouse retina. J Neurosci. 2002 May 15;22(10):4163-74. PMID: 12019334
  15. Woch G, Aramant RB, Seiler MJ, Sagdullaev BT, McCall MA. Retinal transplants restore visually evoked responses in rats with photoreceptor degeneration. Invest Ophthalmol Vis Sci. 2001 Jun;42(7):1669-76. PMID: 11381076