ZINC FACILITATES HYPEREXCITABILITY IN THE HIPPOCAMPUS OF EPILEPTIC RATS

초록

RATIONALE: At the end of this activity you should be able to describe the potential role of zinc in dentate gyrus disinhibition during epilepsy. Feed-forward inhibition in the dentate gyrus (DG) is normally able to subdue synchronous activity entering the hippocampus via the perforant path. In temporal lobe epilepsy zinc co-released from recurrent mossy fibers is hypothesized to disrupt this inhibition, reducing the DG's ability to protect downstream targets: particularly CA3. This hypothesis hinges on two points: in epilepsy recurrent mossy fiber connections onto granule cells are prevalent and synaptic GABAA receptors become zinc sensitive. It is not known if zinc can affect DG function or whether these effects are specific to changes in the DG associated with epilepsy. We therefore tested zinc’s ability to disrupt DG gatekeeper function in control and epileptic animals and compared these results to partial disinhibition with the GABAA antagonists picrotoxin or bicuculline.