Postnatal nutritional iron deficiency impairs dopaminergic-mediated synaptic plasticity in the CA1 area of the hippocampus

Abstract

ObjectivesDevelopmental iron deficiency (ID) has been shown to put children at risk for compromised learning and memory capacity, and it has also been shown to impair hippocampus-dependent forms of memory as well as hippocampal synaptic transmission. Catecholamines are known to play a pivotal role in memory consolidation, and studies have demonstrated that perinatal ID alters dopaminergic systems in various brain areas. It is not known, however, whether perinatal ID impairs dopaminergic synaptic plasticity in learning and memory structures such as the hippocampus. The objective of the present study was to examine dopaminergic-mediated synaptic efficacy in the hippocampus of mice subjected to an ID or control (CN) diet.MethodsThe present study used electrophysiological brain slice methods to examine dopaminergic-mediated synaptic efficacy in the hippocampus of mice subjected to an ID or CN diet from postnatal day (P) P0 through P20. Hippocampal brain slices were prepared in young (P26–30) and adult animals (P60–64). Synaptic efficacy was measured in CA1 neurons by examining population spike amplitude. Slices were treated with the dopaminergic agonist SKF-38393.ResultsSlices obtained from young and adult CN mice exhibited a long-lasting increase in synaptic efficacy as the result of SKF-38393 perfusion while the young and adult ID slices showed little or no increase.DiscussionThe present study demonstrates that postnatal ID produces long-lasting impairments in dopaminergic-dependent synaptic plasticity in the hippocampus. These impairments may play a role in the learning and memory deficits known to result from ID.