Gene expression profile in retinal excitotoxicity induced by L-glutamate in neonatal rats

Author:

Mitori Hikaru12,Izawa Takeshi2,Kuwamura Mitsuru2,Matsumoto Masahiro1,Yamate Jyoji2

Affiliation:

1. Drug Safety Research Labs., Astellas Pharma Inc., 21 Miyukigaoka, Tsukuba-shi, Ibaraki, 305-8585, Japan

2. Laboratory of Veterinary Pathology, Graduate School of Life and Environmental Sciences, Osaka Prefecture University, Rinku Ourai Kita 1-58 Izumisano-shi, Osaka 598-8531, Japan

Publisher

Japanese Society of Toxicologic Pathology

Subject

Toxicology,Pathology and Forensic Medicine

Reference24 articles.

1. 1. Lipton SA, and Rosenberg PA. Excitatory amino acids as a final common pathway for neurologic disorders. N Engl J Med. 330: 613–622. 1994.

2. 2. Rothstein JD. Excitotoxicity hypothesis. Neurology. 47(Suppl 2): S19–S25, discussion S26. 1996.

3. 3. Donello JE, Padillo EU, Webster ML, Wheeler LA, and Gil DW. alpha(2)-Adrenoceptor agonists inhibit vitreal glutamate and aspartate accumulation and preserve retinal function after transient ischemia. J Pharmacol Exp Ther. 296: 216–223. 2001.

4. 4. Martin KR, Levkovitch-Verbin H, Valenta D, Baumrind L, Pease ME, and Quigley HA. Retinal glutamate transporter changes in experimental glaucoma and after optic nerve transection in the rat. Invest Ophthalmol Vis Sci. 43: 2236–2243. 2002.

5. 5. Sullivan RK, Woldemussie E, Macnab L, Ruiz G, and Pow DV. Evoked expression of the glutamate transporter GLT-1c in retinal ganglion cells in human glaucoma and in a rat model. Invest Ophthalmol Vis Sci. 47: 3853–3859. 2006.

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