Int J Physiol Pathophysiol Pharmacol 2010;2(1):69-72.
Original Article Histologic examination of the eye of acid-sensing ion channel 1a knockout mice
James A. Render, Katherine R. Howe, Amanda M. Wunsch, Silvia Guionaud, Peter J. Cox, John A. Wemmie
Drug Safety Research and Development, Pfizer, Groton, USA; Drug Safety Research and Development, Pfizer, Sandwich, UK ; Departments of Psychiatry and Neurosurgery, Neuroscience Program, The University of Iowa, and Department of Veterans Affairs Medical Center, Iowa City, IA 52242; Pain Therapeutics, Pfizer, Sandwich, UK
Received March 4, 2010, accepted March 18, 2010, available online March 22, 2010
Abstract: Various subtypes of the acid sensing ion channel have been detected in the retina of rodents and other mammalian species, but the functional importance of this finding is not clearly understood. The purpose of the study was to determine if retinal degeneration was present in ASIC1a–/– mice. The eyes of ASIC1a–/– mice, heterozygote ASIC1a+/– mice, and wild type ASIC1a+/+ mice that were 5 or 22-27 weeks old were processed by routine histotechnological methods and examined for histologic changes in the retina and other portions of the eye. Additional sections of eyes from ASIC1a–/– and ASIC1a+/+ mice were labeled with peanut agglutinin (PNA) to evaluate cone photoreceptors. The retinas of ASIC1a–/–, ASIC1a+/–, and ASIC1a+/+ mice at 5 or 22-27 weeks of age were unremarkable and no morphologic changes in cone photoreceptors were detected. Additional findings detected in the eye of ASIC1a+/+ mice included swelling of lens fibers or cataract that were also detected in some of the ASIC1a–/– or ASIC1a+/– mice. Lenticular findings were not considered to be associated with an absence of ASIC1a. (IJPPP1003002).
Key words: ASIC1a, knockout mice, retina, acid-sensing ion channel
Address all correspondence to: John Wemmie MD, PhD Departments of Psychiatry and Neurosurgery Neuroscience Program The University of Iowa, and Department of Veterans Affairs Medical Center Iowa City, IA 52242 Tel. (319) 384-3173 Fax. (319) 384-3176 E-mail: firstname.lastname@example.org