Effects of maternal vitamin deficiency on the microstructure of the maternal hippocampus and behavior in offspring

Nutrition plays a critical role in the brain's function and development. Vitamin B6 in the form of pyridoxal phosphate (PLP) is required for the biosynthesis of several neurotransmitters. As vitamin B6 is not endogenously synthesized, the availability of dietary sources becomes imperative. Due to its contribution to neurological functions, severe vitamin B6 deficiency leads to an increased risk of psychiatric disorders, dementia, and neurodevelopmental disorders. This study aimed to establish a vitamin B6-deficient model in experimental animals and assess the neurodevelopmental effects in their offspring.

Two- to three-month-old female C57BL/6J mice were used in the study. They were randomly divided into control and vitamin B6-deficient groups. The control group was fed a regular diet containing 6 mg vitamin B6/kg and the vitamin B6-deficient group was fed a customized diet containing 0 mg vitamin B6/kg, for 5 weeks (n = 6). After 5 weeks, plasma PLP was assessed. The animals were bred to generate offspring. The dams were killed following weaning, and the hippocampal neurons were quantified using cresyl violet staining. The offspring were assigned the respective diet post-weaning up to 2 months of age. Learning and memory were assessed using the Morris water maze test.

The plasma PLP levels confirmed the deficiency in the deficient group compared to the control group. The viable pyramidal neurons in the cornu ammonis 3 (CA3) region of the hippocampus showed a significant difference between the control and deficient groups. Offspring born to deficient dams showed a substantial increase in latency to reach the target quadrant during the probe trial compared to the controls.

Vitamin B6 deficiency reduces memory in dams and their offspring, suggesting the importance of vitamin B6 for both brain function and development.