Abstract

AbstractBackgroundDevelopment of neurobehavioural disorders can occur in the postnatal life of foetuses prenatally exposed to alcohol, regardless of the alcohol type consumed during pregnancy. Hence, the need to investigate the efficacy of proposed pharmaco‐nutritional therapy in mediating potential behavioural and cholinergic impairments in prenatal alcohol exposed (PAE) fetuses.MethodWe investigated whether PAE exacerbates anxiety, motor coordination, cognitive function, cerebral cortex acetylcholinesterase (ACh) activity, DNA fragmentation and assessed associations among parental and PAE rats’ cerebral cortex ACh activity. Thirty female Wistar rats were mated in the following groups (n = 6): 1: Negative control (distilled water only), 2: Positive control (40% EtOH), 3: local gin (LG), 4: local gin+egg yolk solution(LGEY) 5: local gin +egg yolk solution+folic acid(LGEYFA). Statistical significance of obtained data was measured at p<0.05 using regression model, ANOVA and Tukey’s PostHoc tests (GraphPad 5).ResultWhen compared to the negative control, all alcohol groups (supplemented or not) had significantly lower latency of fall, working memory, percentage alternation etc. Although the brain weight of PAE rats in group 2 (positive control) did not change significantly (p = 0.159), critically reduced brain weights seen in group 3 (LG, p<0.001) were normalized in the supplemented groups (4‐LGEY and 5‐LGE). Cortex protein levels was unchanged in all maternal rats regardless of alcohol intubation. However, ACh cerebral cortex activity was significantly reduced in PAE rats from non‐supplemented groups (2 and 3). Necrosis and fragmentation were also seen in agarose gel electrophoregram (AGE) of gDNA isolated from PAE rats’ brain.ConclusionPrenatal alcohol exposure predisposes to severe neurobehavioural and cognitive deficits while gestational folic acid+egg yolk solution may be a therapeutic target for high risk PAE pregnancies.

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