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This Article Full Text Full Text (PDF) All Versions of this Article: 98/3/1634    most recent 01150.2006v2 01150.2006v1 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 Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Milenkovic, I. Articles by Rübsamen, R. Search for Related Content PubMed PubMed Citation Articles by Milenkovic, I. Articles by Rübsamen, R.

Development of Chloride-Mediated Inhibition in Neurons of the Anteroventral Cochlear Nucleus of Gerbil (Meriones unguiculatus)

Ivan Milenkovi¹, Mirko Witte¹, Rostislav Tureek², Marco Heinrich¹, Thomas Reinert¹ and Rudolf Rübsamen¹

¹Institute of Biology II, Faculty of Biosciences, Pharmacy and Psychology, University of Leipzig, Leipzig, Germany; and ²Institute of Experimental Biomedicine, Academy of Sciences, Prague, Czech Republic

Submitted 30 October 2006; accepted in final form 27 June 2007

At the initial stages in neuronal development, GABAergic and glycinergic neurotransmission exert depolarizing responses, assumed to be of importance for maturation, which in turn shift to hyperpolarizing in early postnatal life due to development of the chloride homeostasis system. Spherical bushy cells (SBC) of the mammalian cochlear nucleus integrate excitatory glutamatergic inputs with inhibitory (GABAergic and glycinergic) inputs to compute signals that contribute to sound localization based on interaural time differences. To provide a fundamental understanding of the properties of GABAergic neurotransmission in mammalian cochlear nucleus, we investigated the reversal potential of the GABA-evoked currents (E_GABA) by means of gramicidin-perforated-patch recordings in developing SBC. The action of GABA switches from depolarizing to hyperpolarizing by the postnatal day 7 due to the negative shift in E_GABA. Furthermore, we studied the expression pattern of the K⁺-Cl^–-extruding cotransporter KCC2, previously shown to induce a switch from neonatal Cl^– efflux to the mature Cl^– influx in various neuron types, thereby causing a shift from depolarizing to hyperpolarizing GABA action. The KCC2 protein is expressed in SBC already at birth, yet its activity is attained toward the end of the first postnatal week as indicated by pharmacological inhibition. Interruption of the Cl^– extrusion by [(dihydroindenyl)oxy] alkanoic acid or furosemide gradually shifted E_GABA in positive direction with increasing maturity, suggesting that KCC2 could be involved in maintaining low [Cl^–]_i after the postnatal day 7 thereby providing the hyperpolarizing Cl^–-mediated inhibition in SBC.

This article has been cited by other articles:

				I. Milenkovic, I. Rinke, M. Witte, B. Dietz, and R. Rubsamen P2 Receptor-Mediated Signaling in Spherical Bushy Cells of the Mammalian Cochlear Nucleus J Neurophysiol, September 1, 2009; 102(3): 1821 - 1833. [Abstract] [Full Text] [PDF]