Neonatal l-glutamine modulates anxiety-like behavior, cortical spreading depression, and microglial immunoreactivity: analysis in developing rats suckled on normal size- and large size litters

• Published in: Amino acids 2017-02, Vol.49 (2), p.337-346
• Main Authors: de Lima, Denise Sandrelly Cavalcanti, Francisco, Elian da Silva, Lima, Cássia Borges, Guedes, Rubem Carlos Araújo
• Format: Article
• Language: English
• Subjects: Analytical Chemistry; Animals; Animals, Newborn; Anxiety; Anxiety - drug therapy; Biochemical Engineering; Biochemistry; Biomedical and Life Sciences; Body Weight - drug effects; Cortical Spreading Depression - drug effects; Dose-Response Relationship, Drug; Glutamine - administration & dosage; Glutamine - pharmacology; Life Sciences; Litter Size; Male; Microglia - drug effects; Microglia - immunology; Neurobiology; Original Article; Proteomics; Rats, Wistar
• ISSN: 0939-4451; 1438-2199
• DOI: 10.1007/s00726-016-2365-2

In mammals, l -glutamine (Gln) can alter the glutamate-Gln cycle and consequently brain excitability. Here, we investigated in developing rats the effect of treatment with different doses of Gln on anxiety-like behavior, cortical spreading depression (CSD), and microglial activation expressed as Iba1-immunoreactivity. Wistar rats were suckled in litters with 9 and 15 pups (groups L 9 and L 15 ; respectively, normal size- and large size litters). From postnatal days (P) 7–27, the animals received Gln per gavage (250, 500 or 750 mg/kg/day), or vehicle (water), or no treatment (naive). At P28 and P30, we tested the animals, respectively, in the elevated plus maze and open field. At P30–35, we measured CSD parameters (velocity of propagation, amplitude, and duration). Fixative-perfused brains were processed for microglial immunolabeling with anti-IBA-1 antibodies to analyze cortical microglia. Rats treated with Gln presented an anxiolytic behavior and accelerated CSD propagation when compared to the water- and naive control groups. Furthermore, CSD velocity was higher ( p