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Senior Investigator

Section on Retinal Ganglion Cell Biology

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Building 6, Room 2126 Center DriveBethesda, MD 20892-0606

301-496-8524

[email protected]

Glaucoma is the second leading cause of blindness in developed countries. It is a group of optic neuropathies characterized by the death of retinal ganglion cells (RGCs), leading to a specific deformation of the optic nerve head. Peripheral vision declines initially whilst central vision loss occurs much later. Elevated intraocular pressure (IOP) is one of the main risk factors in glaucoma and is currently the only target for treatment. It is not completely understood how elevated IOP leads to RGC dysfunction and death and better understanding may pave the way for the development of direct neuroprotective strategies. Several genes have been implicated in glaucoma pathogenesis and current research focusses on identifying other contributing genes. This section conducts basic research on glaucoma, understanding the underlying genetics as well developing new neuroprotective and axogenic strategies.

Our interests are concentrated on early changes in the glaucomatous retina and the optic nerve. Since it is hard to study such changes in human subjects, we use existing animal models and develop genetic rodent and zebrafish models of glaucoma for our investigations; subsequently we plan to confirm and apply our results to humans. Another main area of our research is the identification of new genes involved in glaucoma. This requires parallel studies on genes that are important for the function of the retina, the optic nerve and aqueous humor outflow system in the normal eye. We are particularly interested in genes encoding olfactomedin domain-containing proteins. Some of these proteins (Olfactomedin 1, 2 and 3) interact with the AMPA receptor complex and our investigative effects are focused on such interactions and the consequences to the physiological function of AMPA receptors in both brain and retina.

Treatments currently available for glaucoma exert their effects by reducing IOP, the most important risk factor for the onset and progression of the disease, but have no direct effects on RGCs or the optic nerve. They are not always optimally effective in slowing the progression of the disease and in a significant number of cases, glaucoma occurs independent of raised IOP. Thus, the development of novel, neuroprotective glaucoma therapies are of great importance. We are interested in investigating the potential neuroprotective benefits of mesenchymal stem cell (MSC) transplantation, which has produced encouraging results in different models of CNS degeneration. We examine neuroprotective effects of several factors as well as exosomes produced by MSCs, intending not only to better understand their mechanism of action but also, subsequently apply identified protective reagents as a glaucoma treatment.

Dr. Stanislav Tomarev was awarded a Ph.D. in 1977 and a Doctor of Sciences in 1987 from the N. K. Koltzov Institute of Developmental Biology, Russian Academy of Sciences; the latter is the highest academic status degree in Russia, roughly equivalent to a full professorship. In 1989, after 15 years of research in the N. K. Koltzov Institute of Developmental Biology, Dr. Tomarev joined NEI, where he leads the Section on Retinal Ganglion Cell Biology. His laboratory investigates molecular mechanisms of glaucoma with the main focus on the genes, proteins and signaling pathways that might be essential for RGC and optic nerve development, function, survival, and regeneration.

Selected Publications

Johnson TV, DeKorver NW, Levasseur VA, Osborne A, Tassoni A, Lorber B, Heller JP, Villasmil R, Bull ND, Martin KR, Tomarev SI. . 2014;137(Pt 2):503-19.

Figure 10.

Spectrograms of adult and embryonic RPCH-activated motor patterns. , Adult PD, LP and DG spectrograms, total recording time in 10 m RPCH from Figure 9 . , Embryonic pdm, lpm, and dgm spectrograms, total recording time in 10 m RPCH, preparation shown in Figure 9 .

When we calculated the mean fundamental frequencies of activity in adults, we found that LP neurons were silent in control saline (data not shown), but were active in RPCH at 0.17 ± 0.09 Hz ( n = 7) ( MADRID Mules purple Excellent For Sale FcdqoR
A ). RPCH did not significantly change the mean fundamental frequency of activity in adult PD neurons compared with control saline (mean fundamental frequencies: in control saline, 0.13 ± 0.05 Hz, n = 7; in RPCH, 0.19 ± 0.11 Hz, n = 7; paired t test, p = 0.17, n = 7) ( Buy Cheap Websites Geniue Stockist Cheap Online Bally Patent Leather SquareToe Pumps Buy Cheap Marketable Choice For Sale jNDjMdmkW
A , control saline data not shown). In RPCH, DG neurons produced bursts at a mean fundamental frequency (0.04 ± 0.01 Hz, n = 7) that was significantly slower than that of DG neurons in control saline (0.83 ± 0.53 Hz, n = 7; paired t test, p = 0.01, n = 7) ( Fig. 11 A , control data not shown). In RPCH, the mean fundamental frequencies of activity in LP and PD were not significantly different (one-way ANOVA, p = 0.64, n = 7), but the mean frequencies of activity in both LP and PD neurons were faster than DG neurons (one-way ANOVA, p = 0.004, n = 7) ( Fig. 11 A ).

Figure 11.

Summary of frequency and phase relationships of adult and embryonic RPCH-activated motor patterns. , Output from adult ( , ) and embryonic ( , ) neurons during 10 m RPCH application. , The mean fundamental frequencies of activity in adult PD and LP neurons were not significantly different (one-way ANOVA, = 0.64, = 7), but both were faster than the mean fundamental frequency of activity in adult DG neurons (one-way ANOVA, = 0.004, = 7). Significant difference, ** < 0.01. , The mean fundamental frequencies of activity in embryonic lpm and pdm were not statistically different (one-way ANOVA, = 0.80, = 7), but both were both faster than the mean fundamental frequency of activity in embryonic dgm (one-way ANOVA, = 0.001, = 7). , Phase relationships of activity in adult LP ( = 7) and DG ( = 7) neurons in the PD phase. , Phase relationships of activity in embryonic lpm ( = 7) and dgm ( = 7) neurons in the pdm phase.

In control saline, all embryonic neurons were silent after neuromodulatory inputs were removed. In RPCH, the mean fundamental frequencies of the activity in lpm (0.10 ± 0.03 Hz, n = 7) and pdm (0.11 ± 0.04 Hz, n = 7) were not statistically different (one-way ANOVA, p = 0.80, n = 7), and the mean fundamental frequencies of activity in both lpm and pdm were faster than dgm (0.04 ± 0.14 Hz, n = 7) (one-way ANOVA, p = 0.001, n = 7) ( Fig. 11 B ). RPCH-induced events were typical of EJPs.

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