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.
Early treatment with OH facilitates recognition memory and CSD, and in association with unfavorable lactation (L) impaired recognition memory, but not anxiety behavior, in the adult brain. OH treatment and L lactation condition seem to interact regarding OH action on memory, but not on CSD. Data suggest a long-lasting differential effect that might be related to the lasting hormonal action on brain excitability. We postulate and discuss the possibility that these findings may be implicated in human neurological diseases.
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