E.M. Rzavina – Post-graduate Student, Department of Physiology and General Pathology, 

Faculty of Fundamental Medicine, Lomonosov Moscow State University

E-mail: klochikhinaem@gmail.com

A.K. Erdiakov – Ph.D. (Biol.), Department of Physiology and General Pathology, Faculty of Fundamental 

Medicine, Lomonosov Moscow State University

V.A. Kovaleva – Student, Department of Physiology and General Pathology, 

Faculty of Fundamental Medicine, Lomonosov Moscow State University

E.V. Ivanov – Post-graduate Student, Department of Physiology and General Pathology, 

Faculty of Fundamental Medicine, Lomonosov Moscow State University 

Email ivanovev101@gmail.com

S.A. Gavrilova – Ph.D. (Biol.), Associate Professor, Department of Physiology and General Pathology, 

Faculty of Fundamental Medicine, Lomonosov Moscow State University

E-mail: sgavrilova@mail.ru

V.B. Koshelev – Dr. Sc. (Biol.), Professor, Head of Department of Physiology and General Pathology, 

Faculty of Fundamental Medicine, Lomonosov Moscow State University 

E-mail: KoshelevVladimir1953@yandex.ru

G.R. Galstyan – Dr. Sc. (Med.), Professor, National Medical Center of Endocrinology 

Russian Ministry of Health (Moscow)

E-mail: galstyangagik964@gmail.com

Diabetic retinopathy is one of the most serious complications of diabetes, as well as the most common cause of blindness in people aged 20-74. In clinical practice, the earliest diagnosis of diabetic retinopathy is carried out using electroretinography (ERG). The use of ERG to determine the functional activity of the retina in rats in experimental model of diabetes will allow us to identify retinal neuropathy earlier than other symptoms and to investigate the initial stages of the development of diabetic retinopathy.

Experimental diabetes mellitus was caused by intraperitoneal injection of streptozotocin at a dose of 65 mg/kg, dissolved in

0.1 M sodium citrate buffer (pH = 4.5) (DM group). The control group of animals (CB group) was injected intraperitoneally with a similar dose of sodium citrate buffer. Three days later, the level of glucose in the venous blood from the tail vein was determined to verify the development of hyperglycemia. Rats with a glucose level of less than 15 mM were excluded from the DM group. Insulin Detemir (1.5 U/kg) was injected subcutaneously daily throughout the entire study. ERG was performed to animals narcotized by chloral hydrate (intraperitoneally at a dose of 0.3 g/kg) before DM modeling and, depending on the group, at 70, 78, 86 or 94 days from the time of the control measure of blood glucose levels.

Even by 94 days of DM, the response of the rod system remains virtually unchanged, as well as the mixed response of rods and cones. The earliest signal of deterioration of visual function during the development of diabetes was a decrease in the amplitudes of the waves of oscillatory potentials, but not an increase in their latencies. The b-wave of the cone-type response to various color stimuli turned out to be more sensitive to prolonged hyperglycemia: by 70 days of diabetes development, a significant increase in b-wave latency is observed in response to blue and green light stimuli compared with the CB group on average by 27.6% and 19.4% respectively (p<0.05). By day 78, significant differences in b-wave latencies between DM and CB groups were recorded in response to any color stimuli. The b-wave latencies gradually increase during the diabetes progresses as the observation period increases. The latency of the a-wave cone response does not change significantly. As diabetes mellitus develops, the amplitudes of the rhythmic response do not change significantly when stimulated with a frequency of 8 and 12 Hz in rats of the DM group compared with the CB group. The response of the rod system, as well as the rhythmic response, remained virtually unchanged from the 70th to the 94th day after the development of hyperglycemia. Our results suggest that hyperglycemia may be a major factor in the dysfunction of the cells of the inner layers of the retina in diabetes mellitus.

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