Sprague-Dawley male rats, fed with a tryptophan-deficient and 8% protein corn-based diet were compared with a group of animals fed with 8% protein alone, and with a group fed with Chow Purina containing 23% protein. Retardation of Bergmann glial cell maturation and a concomitant retardation in granule cell migration were observed in the corn-fed group at 21 days. At 30 days of age, the dendrites of granule cells of both hypoproteic and corn-fed groups were larger than those of the Chow-fed animals. At 60 days of age, dendritic arborization of Purkinje cells was more profuse in both the hypoproteic and corn-fed rats compared with the Chow-fed group. This retardation in granule cell migration could be partially due to Bergmann glial cell immaturity. Consequently, several plastic and maybe compensatory events in both granule and Purkinje cells could have occurred, due to tryptophan deficiency resulting from the corn-based diet.

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To evaluate the effects on the GABAergic system, Wistar rats were raised on a chronically protein- and tryptophan-restricted diet with 8% protein, based on either Purina chow or corn. There was a significant decrease in both body and cerebral weight in the restricted animals compared with the control group fed with a 23% protein diet. In animals fed mainly corn, glutamic acid decarboxylase (GAD) activity increased significantly at the ages studied (14, 30, and 60 days) in the cerebral cortex and hippocampus. In the same way, gamma-aminobutyric acid (GABA) release decreased significantly in early life in both brain regions, then increased in 30-60-day-old animals corn-fed predominantly in the cerebral cortex. The reduction in GABA release may be attributable to a decrease in GABAergic cell density, which could induce an over-activation of 5-hydroxytryptamine (5-HTergic) receptors, leading in turn to the observed enhancement of GAD activity. Taken together, these results may represent a plastic response by GABAergic neurons to (5-HTergic under-stimulation in mainly corn-fed animals.

A Golgi study of third-layer pyramidal neurons from the corticofrontal cortex of tryptophan-restricted rats was carried out. At 40 days of age, dendritic arborization from treated rats was less profuse than that seen in control rats, and enlargement of dendritic processes, as well as an increase of the number of dendritic spines, were observed in 60-day-old rats. These plastic responses could be mediated either by a decrease in serotonin, which acts on the serotoninergic receptors of pyramidal neurons, or through an indirect mechanism mediated by cortical interneurons, or by serotoninergic modulation of the activity of other cortical neurotransmitters such as acetylcholine. Also, it could represent compensatory mechanisms underlying behavioral performance in some paradigms related to several cognitive processes.

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