# MATERNAL B6 DEFICIENCY

> **NIH NIH R01** · JOHNS HOPKINS UNIVERSITY · 1993 · $186,103

## Abstract

The vulnerability of the developing central nervous system to insults of
maternal vitamin B-6 undernutrition has received increased attention in
recent years. Our work and that of others has shown that inadequate vitamin
B-6 nutrition during brain developments leads to neurochemical modifications
in the synaptic environment of various neurotransmitter systems in the brain
of progeny. An increasing body experimental evidence indicates that
perturbations in synaptic neurochemistry are related to a variety of
behavioral and neuropsychiatric conditions.

Our work using an animal model of inadequate maternal vitamin B-6 nutrition
produces major alterations in the ontogenesis of several neurotransmitter
systems in the offspring. These studies also show that for some
neurotransmitter systems (e.g. the GABAergic system in the cerebellum), the
animal is able to compensate and correct the neurochemical deficit by
adulthood. On the other hand, for other system (e.g. the dopaminergic in the
corpus striatum), the neurochemical deficit persists into adulthood.

Our recent finding that the putative endogenous convulsant and neurotoxin 3-
hydroxykynurenine (3HK) is increased in vitamin B-6 restricted neonatal rat
brain has important implications to the developing central nervous system.
The exposure of vulnerable neurons to such an insult can produce cell
degeneration whose symptoms may manifest themselves immediately after the
exposure or later in life according to the level of exposure that occurred.
Proposed studies are designed to assess the convulsant and neurotoxic
properties of 3HK in vivo.

Our proposed work is designed to continue the characterization of
neurochemical changes present in vitamin B-6 restricted neonatal rat brain
as well as the elucidation of underlying mechanisms which may help explain
the observed neurochemical changes.  Furthermore, the observation that
vitamin B-6 restricted animals have deficits in motor function (e.g. ataxia,
tremor, poor balance) calls for the characterization of the spontaneous
motor activity of these animals.  Therefore, we are proposing to
quantitatively assess the motor development of vitamin B-6 restricted
animals and try to correlate it with the neurochemical measurements.

These studies will continue to provide new and valuable information on the
role that vitamin B-6 plays in brain function and development.

## Key facts

- **NIH application ID:** 2198120
- **Project number:** 5R01HD020939-08
- **Recipient organization:** JOHNS HOPKINS UNIVERSITY
- **SAM.gov UEI:** FTMTDMBR29C7
- **Principal Investigator:** Tomas R Guilarte
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1993
- **Award amount:** $186,103
- **Award type:** 5
- **Project period:** 1986-07-01 → 1995-03-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/2198120

## Citation

> US National Institutes of Health, RePORTER application 2198120, MATERNAL B6 DEFICIENCY (5R01HD020939-08). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/2198120. Licensed CC0.

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