Abstract
Maternal hyperhomocysteinemia is one of the common complications of pregnancy that causes offspring cognitive deficits during postnatal development. In this study, we investigated the effect of prenatal hyperhomocysteinemia (PHHC) on inflammatory, glial activation, and neuronal cell death markers in the hippocampus of infant rats. Female Wistar rats received L-methionine (0.6 g/kg b.w.) by oral administration during pregnancy. On postnatal days 5 and 20, the offspring’s hippocampus was removed to perform histological and biochemical studies. After PHHC, the offspring exhibited increased brain interleukin-1β and interleukin-6 levels and glial activation, as well as reduced anti-inflammatory interleukin-10 level in the hippocampus. Additionally, the activity of acetylcholinesterase was increased in the hippocampus of the pups. Exposure to PHHC also resulted in the reduced number of neurons and disrupted neuronal ultrastructure. At the same time, no changes in the content and activity of caspase-3 were found in the hippocampus of the pups. In conclusion, our findings support the hypothesis that neuroinflammation and glial activation could be involved in altering the hippocampus cellular composition following PHHC, and these alterations could be associated with cognitive disorders later in life.
Highlights
Maternal hyperhomocysteinemia (HHC) is one of the common complications of pregnancy that causes various functional impairments of the offspring brain
A comparative study of the structural organization of the CA1 area of the dorsal hippocampus of pups subjected to prenatal hyperhomocysteinemia (PHHC) was carried out using the Nissl method
Our results show that PHHC enhances AChE activity in the hippocampus of rats on P5, suggesting a reduction in acetylcholine levels leading to a proinflammatory state
Summary
Maternal hyperhomocysteinemia (HHC) is one of the common complications of pregnancy that causes various functional impairments of the offspring brain. Studies of the prenatal HHC (PHHC) effect in male rats and mice revealed a decrease in locomotor activity and significant disorders of various types of memory, in particular, in the Morris test [1,2,3,4]. Violation of the reflexes formation [5] and the presence of anxiety was reported in the offspring of rats with PHHC [6], which may cause memory impairment. Our previous data indicate that mature female rats whose mothers had elevated homocysteine (Hcy) level during pregnancy demonstrated disorders of short-term and long-term memory, as well as spatial orientation [7]. Population-based studies have shown that folate deficiency, high total Hcy and/or low vitamin B12 levels in early pregnancy had long-term effects on fetal and child brain development. The elucidation of the mechanisms of the consequences of PHHC remains actual and requires further research
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