Aims: Glutamine (Gln) participates in the so-called "brain glutamine-glutamate cycle" and therefore it is likely to influence brain excitability. Here we investigated, in weaned well-nourished and early-malnourished rats, the effects of previous Gln oral supplementation, during the brain development period, on cortical spreading depression (CSD), an excitability-related brain phenomenon.
Main methods: Male Wistar (W) suckling rat pups, well-nourished (litters with 6 pups) and malnourished (M) during lactation (by increasing the litters to 12 pups), received Gln (500 mg/kg/day) by gavage during postnatal days 7 to 27. At 30-40 days of life, they were submitted to a cortical spreading depression (CSD) recording session during 4 h, on 2 cortical parietal points of the right hemisphere. CSD velocity propagation was calculated from the time required for a CSD wave to cross the inter-electrode distance.
Key findings: In both nutritional condition, Gln rats presented higher (p<0.05) CSD propagation velocities (W-Gln, 4.22+/-0.23; M-Gln, 4.51+/-0.27 mm/min), as compared to water-treated controls (W-Wa, 3.77+/-0.21; M-Wa, 4.15+/-0.18 mm/min). This water control group did not differ from a naive control group that was not submitted to the gavage procedure. A fourth group, treated with a "placebo amino acid" (glycine), also displayed CSD velocities in the control range.
Significance: The results indicate that Gln supplementation during brain development facilitates cortical spreading depression propagation, as judged by the higher CSD velocities, and this effect is not abolished by malnutrition. Data support the idea of Gln-related changes in brain excitability, during neural development.