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The Journal of Neuroscience, 0000, 20:RC103:1-5

RAPID COMMUNICATION
Inositol 1,4,5-Triphosphate-Evoked Responses in Midbrain Dopamine Neurons

Hitoshi Morikawa¹, Farzin Imani², Kamran Khodakhah², and John T. Williams¹

¹ Vollum Institute, Oregon Health Sciences University, Portland, Oregon 97201, and ² Department of Physiology and Biophysics, University of Colorado Health Sciences Center, Denver, Colorado 80262

Synaptically released glutamate evokes slow IPSPs mediated by metabotropic glutamate receptors (mGluRs) in midbrain dopamine neurons. These mGluR IPSPs are caused by release of Ca²⁺ from intracellular stores and subsequent activation of small-conductance Ca²⁺-activated K⁺ channels (SK channels). To further investigate the intracellular mechanisms involved, the effect of photolyzing intracellular caged inositol 1,4,5-triphosphate (InsP₃) on membrane conductance and intracellular Ca²⁺ concentration ([Ca²⁺]_i) was examined in rat midbrain slices. Photolytic release of InsP₃ elicited a transient outward current and a sharp rise in [Ca²⁺]_i that lasted for ~5 sec. Apamin, a blocker of SK channels, abolished the InsP₃-induced outward current without affecting the rise in [Ca²⁺]_i. Depleting intracellular Ca²⁺ stores with cyclopiazonic acid completely blocked both the outward current and the Ca²⁺ transient elicited by InsP₃. InsP₃-evoked Ca²⁺ mobilization was not affected by blockade of ryanodine receptors with ruthenium red, whereas depleting ryanodine-sensitive Ca²⁺ stores with ryanodine almost eliminated InsP₃-induced Ca²⁺ release. Increasing the size of intracellular Ca²⁺ stores by means of prolonged depolarization added a late component to the outward current and a slow component to the rising phase of [Ca²⁺]_i. These effects of depolarization were blocked by ruthenium red. These results show that InsP₃ activates SK channels by releasing Ca²⁺ from InsP₃-sensitive stores that also contain ryanodine receptors. Increasing intracellular Ca²⁺ stores boosts InsP₃-evoked responses by invoking Ca²⁺-induced Ca²⁺ release through ryanodine receptors. This intracellular signaling pathway may play a significant role in regulating the excitability of midbrain dopamine neurons.

Key words: intracellular Ca²⁺; inositol 1,4,5-triphosphate; inositol 1,4,5-triphosphate receptors; ryanodine receptors; SK channels; midbrain dopamine neurons; flash photolysis

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Copyright © 0000 Society for Neuroscience  0270-6474/00/$05.00/0

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