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Adult, well-nourished (W) and early-malnourished (M) male Wistar rats were injected intraperitoneally for 7 days with 20 mg/kg CIT and cortical spreading depression (CSD) was recorded for 4 h on the day following the treatment. M-animals presented lower body weights, as well as higher CSD velocities of propagation, than the W ones, as previously reported. Compared to saline-injected controls, rats treated with CIT for 7 days presented comparable body weights and lower mean CSD velocities, per hour of recording, the differences being significant at the second hour (3.29+/-0.31 versus 3.56+/-0.40 mm/min; P < 0.05). Topical, cortical application of CIT (1- and 5 mg/ml solutions over the intact dura-mater) reduced dose-dependently the CSD velocity (maximal reductions of 16.3 and 55.8% for the 1 and 5 mg/ml solutions, respectively; P < 0.05), as well as the amplitude of the CSD-slow potential change (58.2 and 88.3%). In three out of seven W-rats and in one out of seven M-rats, topical CIT (5 mg/ml) blocked CSD propagation. The effects were reverted by flushing the treated region with saline. In the M-groups, CIT affected CSD in the same manner as in the W ones. The results reinforce previous evidence for an antagonistic influence of the serotoninergic activity on CSD.

Ketogenic diets influence brain function and have been therapeutically used for anti-epileptic purposes. We investigated the effects of maternal ketogenic diets on the development of somatic and reflex responses in rat pups. These were born from mothers receiving: (i) normal fat (7%) + normal protein (17%); (ii) high-fat (55.4%) + normal protein; (iii) normal fat + low protein (8%); and (iv) high-fat + low protein (respectively, called N-17, K-17, N-8 and K-8). Ketogenic diets, but not the normal-fat diets, delayed the development of reflex and somatic responses. The effects were more evident when the ketogenic diet was associated with low protein content. The results suggest that fat excess can alter brain maturation, and this action is intensified by early protein-deficiency. Data raise concerns about the therapeutic use of ketogenic diets in newborn children.

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