The exercise-dependent attenuation of the effects of MSG confirms our previous results in rats treated subcutaneously with MSG. CSD results suggest two distinct mechanisms for gavage and topical MSG administration. Additionally, data suggest that exercise can help protect the developing and adult brain against the deleterious actions of MSG.

The brain of mammals is one important target organ for the action of gonadal steroids and, when occurring during development, this hormonal influence may result in important repercussion on the brain electrophysiological properties at adulthood, some of which depending on the brain excitability. Here we have characterized in early-ovariectomized adult rats the brain ability to propagate the excitability-related phenomenon known as cortical spreading depression (CSD), as an index of the cerebral electrophysiological effects of the early-induced absence of the ovarian hormones. Wistar female rat pups (7-day old) underwent bilateral ovariectomy (Ovx group; n=21) or Sham surgery (Sham group; n=22), or no surgery (Naive group; n=22). When the pups became adult (90-130 days), they were submitted to the recording of CSD (electrocorticogram and slow DC-voltage variation) in two points of the cortical surface during 4h. Compared with both Naïve and Sham controls, bilateral ovariectomy early in life resulted in significantly higher body weights (from days 50-65 onwards) and severely reduced uterus weights at adulthood. Furthermore, in the Ovx animals the amplitudes and durations of the DC-potential changes of CSD were higher, and the CSD propagation velocities were reduced. Another group of rats ovariectomized in adulthood did not present such CSD alterations. It is concluded that ovariectomy during brain development is causally associated with the CSD changes in the adult brain, indicating a long-lasting effect, which we suggest as being related to the long-term suppression of the action of the ovarian hormones on brain excitability.

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Our results documented a novel effect of DGW on memory and CSD. SA dose-dependently facilitated CSD, suggesting its involvement on the DGW action. DGW is considered a potential supplement to improve brain development and function in malnourished children, and this shall be further translationally investigated.

Background: Postnatal overnutrition has been associated with lasting impairment of cognitive function. On the other hand, virgin coconut oil (CO) and environmental enrichment (EE) have been associated with the improvement of memory function. Objectives: To evaluate whether CO and EE could counteract any possible memory impairment caused by overnutrition during rats’ postnatal period. Methods: Rats were suckled in litters of either 9 (N, nourished) or 3 (ON, overnourished) pups. At 7 to 30 days of life, N and ON animals were treated with CO (10 ml/kg/d) or vehicle (V). At 36 days old, rats were exposed to EE during a 4-week period. Recognition memory was investigated in young and adult groups to evaluate rats’ memory after CO supplementation period and after exposure to an EE, respectively. Lastly, murinometric evaluation and blood collection were performed. Results: ON young rats displayed a treatment-dependent impairment of memory (p < 0.001). Additionally, CO coupled with overnutrition had age-dependent effects on memory. At adulthood, CO&ON rats were not able to recognize novel object placement (novel versus familiar, p > 0.05); however, CO&ON rats that were exposed to EE performed this task successfully (p < 0.0001). Conclusions: The etiology of diseases characterized by memory impairment can date back to lactation. Nutrition during this critical period can influence cognitive function. Early-life overnutrition, coupled with CO, has age-dependent effects on recognition memory. Our data suggests EE can rescue the memory impairment found in CO&ON adult rats.