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Calcium (Ca 2+ ) is a critical secondary messenger in all neurons that coordinates important mechanisms of cell physiology. In vasopressin (VP) neurons of supraoptic nucleus (SON) it’s required for somatodendritic release of VP and the slow afterhyperpolarization (sAHP), both of which coordinate neuronal output and thus control stimulus-secretion coupling. Recently, our lab demonstrated that VP sAHPs require endoplasmic reticulum (ER) Ca 2+ for activation and that mitochondrial Ca 2+ buffering shapes the spatiotemporal trajectory. We also have recent data demonstrating electrotonic segregation between cell compartments. Given the Ca 2+ dependence of somatodendritic release and sAHPs, delineation of somatodendritic release from axonal release, and the decoupling of somatic and dendritic electrontonic properties, we hypothesized that calcium dynamics also may be compartmentally segregated as well. Utilizing patch clamp electrophysiology, live calcium imaging, and focal UV uncaging, we probed the spatiotemporal trajectory of rapidly evoked Ca 2+ responses in VP neuron somas and dendrites with corresponding membrane potential. UV Ca 2+ uncaging at the soma evokes a membrane sAHP and robust increase in cytosolic Ca 2+ that propagates into the dendrites. Conversely, Ca 2+ uncaged in dendrites propagates bidirectionally from the UV flash but does not penetrate the soma; no membrane hyperpolarization was observed under these conditions. Disabling mitochondrial Ca 2+ buffering with Ru360 in the pipette amplifies Ca 2+ signasl and sAHPs in somas and dendrites; Ca 2+ uncaging in dendrites penetrates soma and can evoke sAHPs under these circumstances. Together, these results suggest that under normal conditions, Ca 2+ movement between compartments in VP neurons is unidirectional (soma to dendrite), and that sAHP channels require somatic Ca 2+ increases. Moreover, Ca 2+ uptake by mitochondria is a critical mechanism that tightly controls the magnitude and progagation of dendritic Ca 2+ signals between dendritic and somatic compartments, thus playing an important role in regulating intrinsic mechanisms and ultimately, their neuronal output. NIH K99HL168434 (M.K.K.); R01 HL162575-01 (J.E.S.). This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.
Kirchner et al. (Wed,) studied this question.