MC 6486
Speaker
Neil Magoski
School of Medicine, Department of Biomedical and Molecular Sciences, Queen's University
Title
Control of synchronous bursting in neuroendocrine cells by a cationic conductance and electrical synapses
Abstract
Many key behaviours, including drinking, ovulation, lactation, and birth, are initiated or influenced by neuroendocrine cells releasing hormones into the blood stream. To secrete a bolus of hormone in a well-timed manner, many neuroendocrine cells fire synchronous bursts of action potentials en masse. An example of this can be found in the bag cell neurons of Aplysia californica, a marine snail used extensively in neurobiological research. Bag cell neurons are a group of neuroendocrine cells that trigger reproduction by undergoing a prolonged afterdischarge of synchronous action potentials. The neurons are normally quiet, but following synaptic input they fire tonically (for up to 30 min) and secrete egg-laying hormone into the circulation, where it acts on multiple targets to induce ovulatory behaviours. The transition from quiescence to bursting is due in part to opening of a non-selective cation channel that drives the cells to fire. Synchronization of firing arises from electrical synapses, which are intercellular channels (gap junctions) that permit current to flow between neurons. This presentation will show how multiple intracellular chemical messengers, including calcium and products from an enzyme called phospholipase C, activate the cation channel in a temporally distinct manner. With respect to electrical synapses, rather than a scenario where a bursting neuron is linked to other non-burster cells, results indicate that the biophysical properties of the gap junctions are more suited to synchronizing independently bursting neurons. Mechanisms such as these demonstrate how neuroendocrine cells can achieve collective activity to ensure appropriate hormone secretion and evoke fundamental behaviours.