| First Author | Rebellato P | Year | 2019 |
| Journal | Neuroscience | Volume | 402 |
| Pages | 78-89 | PubMed ID | 30677486 |
| Mgi Jnum | J:276190 | Mgi Id | MGI:6314120 |
| Doi | 10.1016/j.neuroscience.2019.01.015 | Citation | Rebellato P, et al. (2019) The T-type Ca(2+) Channel Cav3.2 Regulates Differentiation of Neural Progenitor Cells during Cortical Development via Caspase-3. Neuroscience 402:78-89 |
| abstractText | Here we report that the low-voltage-dependent T-type calcium (Ca(2+)) channel Cav3.2, encoded by the CACNA1H gene, regulates neuronal differentiation during early embryonic brain development through activating caspase-3. At the onset of neuronal differentiation, neural progenitor cells exhibited spontaneous Ca(2+) activity. This activity strongly correlated with the upregulation of CACNA1H mRNA. Cells exhibiting robust spontaneous Ca(2+) signaling had increased caspase-3 activity unrelated to apoptosis. Inhibition of Cav3.2 by drugs or viral CACNA1H knock down resulted in decreased caspase-3 activity followed by suppressed neurogenesis. In contrast, when CACNA1H was overexpressed, increased neurogenesis was detected. Cortical slices from Cacna1h knockout mice showed decreased spontaneous Ca(2+) activity, a significantly lower protein level of cleaved caspase-3, and microanatomical abnormalities in the subventricular/ventricular and cortical plate zones when compared to their respective embryonic controls. In summary, we demonstrate a novel relationship between Cav3.2 and caspase-3 signaling that affects neurogenesis in the developing brain. |
