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This Article Full Text Full Text (PDF) All Versions of this Article: 102/3/1821    most recent 00186.2009v1 Alert me when this article is cited 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 Google Scholar Articles by Milenkovic, I. Articles by Rübsamen, R. PubMed PubMed Citation Articles by Milenkovic, I. Articles by Rübsamen, R.

P2 Receptor–Mediated Signaling in Spherical Bushy Cells of the Mammalian Cochlear Nucleus

Institute of Biology II, Faculty of Biosciences, Pharmacy and Psychology, University of Leipzig, Leipzig, Germany

Submitted 3 March 2009; accepted in final form 28 June 2009

Abstract

Purinoreceptors of the P2 family contribute strongly to signaling in the cochlea, but little is known about the effects of purinergic neurotransmission in the central auditory system. Here we examine P2 receptor–mediated signaling in the large spherical bushy cells (SBCs) of Mongolian gerbils around the onset of acoustically evoked signal processing (P9–P14). Brief adenosine 5'-O-(3-thiotriphosphate) (ATPS) application evoked inward current, membrane depolarization, and somatic Ca²⁺ signals. Moreover, ATPS changed the SBCs firing pattern from phasic to tonic, when the application was synchronized with depolarizing current injection. This bursting discharge activity was dependent on [Ca²⁺]_i and Ca²⁺-dependent protein kinase (PKC) activity and is presumably caused by modulation of low-threshold K⁺ conductance. Activation of P2Y₁ receptors could not evoke these changes per se, thus it was concluded that the involvement of P2X receptors seems to be necessary. Ca²⁺ imaging data showed that both P2X and P2Y₁ receptors mediate Ca²⁺ signals in SBCs where P2Y₁ receptors most likely activate the PLC–IP₃ (inositol trisphosphate) pathway and release Ca²⁺ from internal stores. Immunohistochemical staining confirmed the expression of P2X₂ and P2Y₁ receptor proteins in SBCs, providing additional evidence for the involvement of both receptors in signal transduction in these neurons. Purinergic signaling might modulate excitability of SBCs and thereby contribute to regulation of synaptic strength. Functionally, the increase in firing rate mediated by P2 receptors could reduce temporal precision of the postsynaptic firing, e.g., phase locking, which has an immediate effect on signal processing related to sound localization. This might provide a mechanism for adaptation to the ambient acoustic environment.