Vitamin E attenuates alterations in learning, memory and BDNF levels caused by perinatal ethanol exposure

ABSTRACT

Objective: Alcohol exposure during pregnancy affects the developing fetus and causes a variety of physical and neurological abnormalities. Here we aim to study the effects of vitamin E on spatial learning and memory deficits and on changes in hippocampal brain-derived neurotrophic factor (BDNF) levels following perinatal ethanol exposure in rats.

Method: Pregnant Wistar rats received ethanol (4 g/kg) and vitamin E (doses of 100, 200, and 400 mg/kg) on day 0 of gestation (GD) until weaning (28 days). On postnatal days (PND) 29, the performance of spatial learning and memory of rats were measured using the Morris water maze (MWM). The expression of BDNF protein levels in the hippocampus was assayed using BDNF ELISA kits.

Results: Ethanol exposed group showed higher escape latency during training, reduced time spent in the target quadrant, higher escape location latency and average proximity in probe test. Vitamin E with doses of 100, 200 and 400 mg/kg significantly reduced escape latency during training. Also, vitamin E (400 mg/kg) significantly increased time spent in target quadrant, decreased escape location latency and average proximity in probe test. Maternal ethanol treatment significantly reduced the expression of BDNF protein in the hippocampus of offspring, whereas administration of vitamin E (400 mg/kg) significantly increased hippocampal BDNF in ethanol-treated rats.

Discussion: Vitamin E administration dose-dependently ameliorate learning and memory deficits induced by perinatal ethanol exposure and increased hippocampal BDNF levels. BDNF may be implicated in the beneficial effects of vitamin E on learning and memory in the perinatal ethanol-exposed rat.

KEYWORDS:

• Ethanol
• vitamin E
• spatial memory
• brain-derived neurotrophic factor
• rat offspring

Acknowledgments

This work was supported by the [Cognitive Sciences and Technologies Council in IRAN] under Grant [number; 4564]. We acknowledge Damghan University for supporting this work as part of a Ph.D. degree thesis project in Animal Physiology.

Disclosure statement

The authors declare that they have no conflict of interest.

Additional information

Funding

This work was supported by the Cognitive Sciences and Technologies Council in IRAN under grant [number 4564].

Notes on contributors

Rahebeh Mahdinia

Rahebeh Mahdinia obtained her M.Sc. degree in Physiology from the Ferdowsi University, Mashhad, Iran. She is Ph.D. student of Animal Physiology in Damghan University, Damghan, Iran.

Iran Goudarzi

Iran Goudarzi is an associate professor of Physiology at Damghan University, Damghan, Iran. She received her M.Sc. and doctorate of Physiology from the University of Tarbiat Modares, Tehran, Iran. Her research interests include Neurodegeneration, Neuroprotection, stress, and Fetal Alcohol Syndrome.

Taghi Lashkarbolouki

Taghi Lashkarbolouki is an assistant professor of Biochemistry at Damghan University, Damghan, Iran. He received his doctorate of Institute of Biochemistry and Biophysic of Tehran University, Tehran, Iran.

Mahmoud Elahdadi Salmani

Mahmoud Elahdadi Salmani is an associate professor of Physiology at Damghan University, Damghan, Iran. He received his M.Sc. and doctorate of Physiology from the University of Tarbiat Modares, Tehran, Iran. His research interests include Orexin, Stress, and Epilepsy.