Golgi-specific DHHC type zinc finger protein is decreased in neurons of intractable epilepsy patients and pentylenetetrazole-kindled rats.

Golgi-specific DHHC type zinc finger protein (GODZ) is a member of the DHHC protein family, and its enzymatic activity is regulated by fibroblast growth factor or Src kinase-mediated tyrosine phosphorylation. In cultured neurons, GODZ affects the numbers of calcium ions channels, α-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid receptors, N-methy-D-aspartate receptors, and γ-aminobutyric acid A receptors on postsynaptic membrane by palmitoylation, thus modulating synaptic plasticity. As the change in synaptic plasticity plays a role in epilepsy, GODZ may play roles in epilepsy. However, the expression of GODZ has never been investigated in brain tissues in vivo, and its change during epilepsy is still unclear. In this study, the cellular distribution of GODZ in brain tissues of both patients and rats was determined using double-labeled immunofluorescence and the levels of GODZ protein and mRNA among intractable epilepsy patients, pentylenetetrazole (PTZ)-kindled rats, and controls were measured using immunohistochemistry, Western blot, and real-time quantitative polymerase chain reaction. GODZ expression was identified on cytomembranes and in the cytoplasm of neurons in the temporal neocortex of intractable epilepsy patients and in the hippocampus and the adjacent temporal cortex of PTZ-kindled rats, but not in astrocytes. Decreased GODZ protein and mRNA were identified in brain tissues of intractable epilepsy patients and PTZ-kindled rats compared with the controls. In conclusion, GODZ is expressed in neurons, but not astrocytes, and epilepsy may reduce the protein and mRNA levels of GODZ, indicating a possible role of GODZ in the pathogenesis or the pathophysiology of epilepsy.