DOI 10.1016/j.neulet.2026.138519
The distribution map of α4 and α7 subunits of nAch receptors in the olfactory bulb of male rat neonates born to STZ-induced hyperglycemia model mothers.
Аннотация
BACKGROUND
Alpha4 and alpha7 nicotinic acetylcholine receptors (nAChRs) are critical for neuronal survival and are highly expressed in the rat olfactory bulb (OB). Gestational diabetes mellitus (GDM) affects the central nervous system, including the OB. This study investigates the effects of maternal diabetes on the distribution of alpha4 and alpha7 nAChR subunits in the OB of male rat neonates.
METHODS
Timed-pregnant female Wistar rats were randomly assigned to three groups: Control (no intervention), Stz (streptozotocin, 45 mg/kg, i.p.), and Stz + Ins (streptozotocin, 45 mg/kg, i.p., plus 4-6 units of Neutral Protamine Hagedorn insulin, subcutaneous daily). One week after STZ-induced hyperglycemia confirmation, females were mated with non-diabetic males, with vaginal plaque observation marking gestation day 1. After natural childbirth, Male pups were divided into two age subgroups: postnatal day 7 (P7, n = 4) and postnatal day 14 (P14, n = 4). Brains were extracted for immunohistochemical analysis of alpha4 and alpha7 nAChR expression and dark neuron counts.
RESULTS
The optical density (OD) of alpha4 and alpha7 nAChRs in the Stz group was significantly lower than in the Control group across all OB layers at P7 and P14. Conversely, the Stz + Ins group exhibited significantly higher OD compared to the Stz group. Dark neuron counts were significantly elevated in the Stz group compared to the Control and Stz + Ins groups, particularly in the mitral cell layer.
CONCLUSION
Maternal hyperglycemia reduces nAChR expression and increases dark neuron populations in the OB of neonatal rats, potentially contributing to olfactory dysfunction. Insulin treatment mitigates these adverse effects.
Предметные рубрики MeSH
Подготовка и перевод публикации
Обработка статьи · этапы, ошибки и управление
Ошибки и ограничения
История · было → стало
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