2021Acta Neurobiologiae ExperimentalisOpen access

Effects of scopolamine treatment and consequent convulsion development in c‑fos expression in fed, fasted, and refed mice

Aslı Zengin Türkmen, Asiye Nurten, Mıne Ergüven, Emine Bilge

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Abstract

Fasting, anticholinergics, and seizures affect c‑fos activation in the brain. Additionally, antimuscarinic treated fasted animals develop convulsion soon after re‑feeding. Therefore, we assessed whether c‑fos expression changes in fed, fasting, and refed animals and how scopolamine treatment affects these changes. We further assessed whether there is a change in c‑fos expression after convulsions. For this purpose, BALB/c mice fasted for 1, 3, 6, 12, 24 and 48 h periods were used. The animals were treated with saline or scopolamine. Half\r\nof the animals treated with saline or scopolamine were given food 20 min after injection. All animals were observed for development of convulsions for 30 min. At the end of this period, the brains of all animals were removed, and the percentage of c‑fos active cells in the hypothalamus was determined immunohistochemically. Convulsions occurred within 1‑48 h of fasting, after scopolamine treatment and re‑feeding. Compared to fed animals, c‑fos expression was not significantly changed in those undergoing different fasting periods, but significantly decreased after 12 h fasting. After animals were allowed to eat, c‑fos activation significantly increased in the 1, 3, 6 and 12 refed‑saline groups and decreased in the 48 refed‑saline group. Scopolamine treatment in 1‑24 h fasted animals increased c‑fos expression, but decreased in 48 h fasted animals. Whereas convulsion development in scopolamine‑treated 3, 6, 12 and 24 h refed animals suppressed c‑fos expression. These results demonstrate that re‑feeding and scopolamine treatment induces neuronal activity in the hypothalamus, while scopolamine induced convulsions after food intake suppressed the c‑fos activity.

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Fasting, anticholinergics, and seizures affect c‑fos activation in the brain. Additionally, antimuscarinic treated fasted animals develop convulsion soon after re‑feeding. Therefore, we assessed whether c‑fos expression changes in fed, fasting, and refed animals and how scopolamine treatment affects these changes. We further assessed whether there is a change in c‑fos expression after convulsions. For this purpose, BALB/c mice fasted for 1, 3, 6, 12, 24 and 48 h periods were used. The animals were treated with saline or scopolamine. Half\r\nof the animals treated with saline or scopolamine were given food 20 min after injection. All animals were observed for development of convulsions for 30 min. At the end of this period, the brains of all animals were removed, and the percentage of c‑fos active cells in the hypothalamus was determined immunohistochemically. Convulsions occurred within 1‑48 h of fasting, after scopolamine treatment and re‑feeding. Compared to fed animals, c‑fos expression was not significantly changed in those undergoing different fasting periods, but significantly decreased after 12 h fasting. After animals were allowed to eat, c‑fos activation significantly increased in the 1, 3, 6 and 12 refed‑saline groups and decreased in the 48 refed‑saline group. Scopolamine treatment in 1‑24 h fasted animals increased c‑fos expression, but decreased in 48 h fasted animals. Whereas convulsion development in scopolamine‑treated 3, 6, 12 and 24 h refed animals suppressed c‑fos expression. These results demonstrate that re‑feeding and scopolamine treatment induces neuronal activity in the hypothalamus, while scopolamine induced convulsions after food intake suppressed the c‑fos activity.

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Available abstract

Fasting, anticholinergics, and seizures affect c‑fos activation in the brain. Additionally, antimuscarinic treated fasted animals develop convulsion soon after re‑feeding. Therefore, we assessed whether c‑fos expression changes in fed, fasting, and refed animals and how scopolamine treatment affects these changes. We further assessed whether there is a change in c‑fos expression after convulsions. For this purpose, BALB/c mice fasted for 1, 3, 6, 12, 24 and 48 h periods were used. The animals were treated with saline or scopolamine. Half\r\nof the animals treated with saline or scopolamine were given food 20 min after injection. All animals were observed for development of convulsions for 30 min. At the end of this period, the brains of all animals were removed, and the percentage of c‑fos active cells in the hypothalamus was determined immunohistochemically. Convulsions occurred within 1‑48 h of fasting, after scopolamine treatment and re‑feeding. Compared to fed animals, c‑fos expression was not significantly changed in those undergoing different fasting periods, but significantly decreased after 12 h fasting. After animals were allowed to eat, c‑fos activation significantly increased in the 1, 3, 6 and 12 refed‑saline groups and decreased in the 48 refed‑saline group. Scopolamine treatment in 1‑24 h fasted animals increased c‑fos expression, but decreased in 48 h fasted animals. Whereas convulsion development in scopolamine‑treated 3, 6, 12 and 24 h refed animals suppressed c‑fos expression. These results demonstrate that re‑feeding and scopolamine treatment induces neuronal activity in the hypothalamus, while scopolamine induced convulsions after food intake suppressed the c‑fos activity.

Key concepts: Convulsion, c-Fos, Scopolamine, Saline, Endocrinology, Internal medicine, Hypothalamus, Medicine

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