Synaptotagmin IV is a product of immediate early-response gene. It is involved in the regulated neurosecretion in the brain. Its putative role, however, in vesicular transport and localization in secretor y vesicles is still a matter of debate. Here we followed the spatiotemporal pattern of synaptotagmin IV protein upregulation in the hippocampus, caudate putamen, nucleus accumbens, nucleus amygdalae, piriform and entorhinal cortices of rats with kainate-induced seizures. We found that upregulation pattern paralleled the direction of depolarization through the hippocampus and also reflecting seizure activity spreading to other brain regions. We speculate that synaptotagmin IV may have a role in the vesicular transport of the upregulated peptides and proteins involved in the plasticity and/or neurodegeneration provoked by the kainate.

Periodontitis is characterized by periodontal tissue destruction, including the alveolar bone. One of its critical components is the release of pro-inflammatory neuropeptides from sensory nerve endings innervating the periodontium. Since nerve growth factor (NGF) has been reported to up-regulate neuropeptides in sensory neurons, we hypothesized that it would be increased in ligature-induced periodontitis in rats, and that systemic NGF neutralization would reduce the periodontitis-associated alveolar bone resorption. Real-time PCR analysis disclosed a statistically significant time-dependent up-regulation of NGF mRNA in gingiva during 2 weeks of periodontitis. Interestingly, NGF up-regulation was also detected in the contralateral gingiva. In addition, immunohistochemistry of trigeminal ganglion neurons innervating the gingivomucosa demonstrated increased expression of TrkA receptor for NGF. Systemic anti-NGF treatment during periodontitis significantly reduced interleukin-1beta expression in gingiva and bilateral alveolar bone resorption. This suggests that NGF promotes periodontal inflammation and implicates a possible use of anti-NGF treatment in periodontitis.

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