Abstract
The parathyroid hormone-related peptide (PTHrP) and PTH/PTHrP receptor genes are widely expressed in the CNS and both are highly expressed in the cerebellar granule cell. We have shown previously that PTHrP gene expression in granule cells is depolarization-dependent in vitro and is regulated specifically by Ca 2+ influx via L-type voltage-sensitive calcium channels (L-VSCCs). Kainic acid induces long-latency excitotoxicity in granule cells via L-VSCC-mediated Ca 2+ influx. Here, we show that PTHrP is just as effective as the L-VSCC blocker, nitrendipine (NTR), in preventing kainate excitotoxicity. A competitive inhibitor of PTHrP binding abrogates its neuroprotective effect. Both NTR and PTHrP decrease 45Ca 2+ influx to the same degree. These findings suggest that PTHrP functions in an autocrine/paracrine neuroprotective feedback loop that can combat L-VSCC-mediated excitotoxcity.
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