Dopamine induces release of calcium from internal stores in layer II lateral entorhinal cortex fan cells. (June 2019)

• Record Type: Journal Article
• Authors: Glovaci, Iulia; Chapman, C. Andrew
• Is Part Of: Cell calcium. Volume 80(2019)
• Page Start: 103
• Page End: 111
• Publication Date: 2019-06
• Subjects: Entorhinal cortex -- Dopamine -- Calcium -- Inositol triphosphate -- Ryanodine -- Learning and memory; Calcium -- Metabolism -- Periodicals; Vertebrates -- Physiology -- Periodicals; Calcium -- Physiological effect -- Periodicals; Cell physiology -- Periodicals; Calcium in the body -- Periodicals; 572.516
• DOI: 10.1016/j.ceca.2019.04.003
• Languages: English
• ISSNs: 0143-4160

Abstract

Graphical abstract: Highlights: Effects of dopamine on somatic calcium and excitatory postsynaptic currents were examined using the calcium indicator fluo-4. Dopamine and the PI-linked D1 agonist SKF83959 increased calcium and postsynaptic currents in fan, but not pyramidal, cells. The classical D1 -like receptor agonist SKF38393 did not result in significant increases in calcium fluorescence. Blocking release of calcium from internal stores abolished calcium transients, and also blocked the dopaminergic facilitation of synaptic transmission. Dopamine-induced calcium transients were not blocked by eliminating calcium from the extracellular medium. Abstract: The entorhinal cortex plays an important role in temporal lobe processes including learning and memory, object recognition, and contextual information processing. The alteration of the strength of synaptic inputs to the lateral entorhinal cortex may therefore contribute substantially to sensory and mnemonic functions. The neuromodulatory transmitter dopamine exerts powerful effects on excitatory glutamatergic synaptic transmission in the entorhinal cortex. Interestingly, inputs from midbrain dopamine neurons appear to specifically target clusters of excitatory cells located in the superficial layers of the entorhinal cortex. We have previously demonstrated that dopamine facilitates synaptic transmission through the activation of D1 -like receptors. This facilitation of synaptic transmission is dependent on both activation of classical D1 -like-receptors, and upon activation of dopamine receptors linked to increases in phospholipase C, inositol triphosphate (IP3 ), and intracellular calcium. In the present study we combined electrophysiological recordings of evoked excitatory postsynaptic currents with imaging of intracellular calcium using the fluorescent indicator fluo-4 to monitor calcium transients evoked by dopamine in electrophysiologically identified putative fan and pyramidal cells of the lateral entorhinal cortex. Bath application of dopamine (1 μM), or the phosphatidylinositol (PI)-linked D1 -like-receptor agonist SKF83959 (5 μM), induced reliable and reversible increases in fluo-4 fluorescence and excitatory postsynaptic currents in fan cells, but not in pyramidal cells. In contrast, application of the classical D1 -like-receptor agonist SKF38393 (10 μM) did not result in significant increases in fluorescence. Blocking release of calcium from internal stores by loading cells with the IP3 receptor blocker heparin (1 mM) or the ryanodine receptor blocker dantrolene (20 μM) abolished both the calcium transients and the facilitation of evoked synaptic currents induced by dopamine. Dopamine also induced calcium transients in fan cells when calcium was excluded from the extracellular medium, further indicating that the calcium transients are linked to release from internal stores. These results indicate that following D1 -like-receptor binding, dopamine selectively induces transient elevations in intracellular calcium via activation of IP3 and ryanodine receptors, and that these elevations are linked to the facilitation of synaptic responses in putative layer II entorhinal cortex fan cells.