Iron deficiency (ID) is a common nutrient deficiency worldwide. This condition is linked to changes in myelin formation, dopaminergic function, and energy metabolism. Early ID results in persistent long-term cognitive and behavioral disturbances in children, despite a return to normal iron status. The present study assesses formerly ID adult rats on maze learning tasks that depend on specific brain regions related to learning, specifically the hippocampus, striatum, and amygdala. Rat dams were fed ID chow starting on gestational Day 2 through postnatal Day 7, and behavioral testing began at postnatal Day 65--following a return to normal iron status. Formerly ID rats exhibited delayed acquisition of the hippocampus-dependant task and no differences from controls on the striatum- and amygdala-dependent tasks. These findings likely reflect long-term reduction in but not abolition of hippocampus-dependent learning and preserved function in other brain structures (e.g., striatum and amygdala).

Prior research suggests that a coulometric relation (Intensity x Duration) determines whether an opioid or nonopioid hypoalgesic system is activated by afferent nociceptive information. Using a paradigm that generates a brainstem-mediated hypoalgesia on the tail-flick test, we found that a coulometric relation does not predict either the emergence or the form of shock-induced hypoalgesia in decerebrate rats. In fact, no evidence was obtained that the brainstem's opioid hypoalgesic system can be activated by ascending neurons. More severe shocks elicited hypoalgesia in spinalized rats. Although a coulometric relation did not predict the emergence of hypoalgesia in spinalized rats, shock severity did predict the form of the hypoalgesia; the least severe shocks elicited an opioid hypoalgesia, and the more severe shocks generated a nonopioid hypoalgesia. A similar pattern of data was observed in intact rats exposed to the least severe shock parameters.

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