QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

HOME  |   SEARCH  |   ARCHIVE  |   SUBSCRIBE  |   CONTACT  |   HELP

This Article Full Text Full Text (PDF) Submit an eLetter Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (34) Citing Articles via Google Scholar Google Scholar Articles by Morikawa, H. Articles by Williams, J. T. Search for Related Content PubMed PubMed Citation Articles by Morikawa, H. Articles by Williams, J. T.

 Previous Article  |  Next Article 

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

---

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

This article has been cited by other articles:

				S. Manita and W. N. Ross Synaptic Activation and Membrane Potential Changes Modulate the Frequency of Spontaneous Elementary Ca2+ Release Events in the Dendrites of Pyramidal Neurons J. Neurosci., June 17, 2009; 29(24): 7833 - 7845. [Abstract] [Full Text] [PDF]

				J. W. Theile, H. Morikawa, R. A. Gonzales, and R. A. Morrisett Role of 5-Hydroxytryptamine2C Receptors in Ca2+-Dependent Ethanol Potentiation of GABA Release onto Ventral Tegmental Area Dopamine Neurons J. Pharmacol. Exp. Ther., May 1, 2009; 329(2): 625 - 633. [Abstract] [Full Text] [PDF]

				A. M. Hagenston, J. S. Fitzpatrick, and M. F. Yeckel MGluR-Mediated Calcium Waves that Invade the Soma Regulate Firing in Layer V Medial Prefrontal Cortical Pyramidal Neurons Cereb Cortex, February 1, 2008; 18(2): 407 - 423. [Abstract] [Full Text] [PDF]

				G. Cui, B. E. Bernier, M. T. Harnett, and H. Morikawa Differential Regulation of Action Potential- and Metabotropic Glutamate Receptor-Induced Ca2+ Signals by Inositol 1,4,5-Trisphosphate in Dopaminergic Neurons J. Neurosci., April 25, 2007; 27(17): 4776 - 4785. [Abstract] [Full Text] [PDF]

				A. Verkhratsky Physiology and Pathophysiology of the Calcium Store in the Endoplasmic Reticulum of Neurons Physiol Rev, January 1, 2005; 85(1): 201 - 279. [Abstract] [Full Text] [PDF]

				R. E. Hoesch, D. Weinreich, and J. P. Y. Kao Localized IP3-Evoked Ca2+ Release Activates a K+ Current in Primary Vagal Sensory Neurons J Neurophysiol, May 1, 2004; 91(5): 2344 - 2352. [Abstract] [Full Text] [PDF]

				M. E Larkum, S. Watanabe, T. Nakamura, N. Lasser-Ross, and W. N Ross Synaptically activated Ca2+ waves in layer 2/3 and layer 5 rat neocortical pyramidal neurons J. Physiol., June 1, 2003; 549(2): 471 - 488. [Abstract] [Full Text] [PDF]

				G. E. Stutzmann, F. M. LaFerla, and I. Parker Ca2+ Signaling in Mouse Cortical Neurons Studied by Two-Photon Imaging and Photoreleased Inositol Triphosphate J. Neurosci., February 1, 2003; 23(3): 758 - 765. [Abstract] [Full Text] [PDF]

Home  |   Search  |   Archive  |   Subscribe  |   Contact  |   Help