-Original-

Effects of Progesterone and Other Gonadal Hormones on Glutamatergic Circuits in the Retina

Mahito Ohkuma¹, Takuma Maruyama^2*, Toshiyuki Ishii², Nozomi Igarashi³, Keiko Azuma³, Tatsuya Inoue⁴, Ryo Obata³, Ei-ichi Miyachi¹ and Makoto Kaneda²

¹Department of Physiology, Fujita Health University, Aichi, Japan
²Department of Physiology, Nippon Medical School, Tokyo, Japan
³Department of Ophthalmology, Faculty of Medicine, Tokyo University, Tokyo, Japan
⁴Department of Ophthalmology, School of Medicine, Yokohama City University, Kanagawa, Japan
^*Present address: Department of Physiology, Division of Neurophysiology, School of Medicine, Tokyo Women's Medical University,
Kawada-cho 8-1, Shinjuku-ku, Tokyo 162-8666, Japan

Background: Gonadal hormones function in the retina; however, their targets have not yet been identified. Therefore, the present study examined the effects of progesterone and other gonadal hormones on glutamatergic circuits in the retina.
Methods: Extracellular glutamate concentrations, which correspond to the amount of glutamate released, were examined using an enzyme-linked fluorescent assay system. The activity of glutamatergic synapses between bipolar cells and ganglion cells was investigated using a patch clamp technique. Changes in retinal thickness during pregnancy were assessed using optical coherence tomography (OCT) images.
Results: Progesterone and pregnenolone sulfate increased extracellular glutamate concentrations, whereas estrogen and testosterone did not. Progesterone increased the activity of glutamatergic synapses between bipolar cells and ganglion cells. A temporal decrease in the thickness of the peripheral retina was observed in the 1^st trimester.
Conclusions: Progesterone, but not estrogen or testosterone, activated glutamate release in the mouse retina. Increases in the concentration of progesterone during pregnancy did not induce any detectable change in retinal thickness.

J Nippon Med Sch 2023; 90: 333-345

Keywords
retina, glutamate, progesterone

Correspondence to
Makoto Kaneda, Department of Physiology, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-ku, Tokyo 113-8602, Japan
mkaneda@nms.ac.jp

Received, November 10, 2022
Accepted, April 17, 2023