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RAPID REPORT |
1 Synapse and Hearing Laboratory, The John Curtin School of Medical Research, The Australian National University, Canberra, ACT 0200, Australia
2 Department of Cell Physiology and Pharmacology University of Leicester, PO Box 138, Leicester LE1 9HN, UK
We have investigated changes in the neuronal excitability of the auditory brainstem in a congenitally deaf mouse (deafness dn/dn). Whole cell patch recordings from principal neurones of the medial nucleus of the trapezoid body (MNTB) showed strikingly enhanced excitability in the deaf mice when compared to control CBA mice at 12–14 days postnatal. MNTB neurones in normal CBA mice showed the phenotypic single action potential response on depolarization in current clamp; however, recordings from CBA mice carrying the homozygous deafness mutation fired trains of action potentials on depolarization. We show here that these changes are associated with reduced functional expression of dendrotoxin-sensitive Kv1 potassium channels. In contrast, no differences were found in voltage-gated calcium currents between control and deaf mice. These results reveal that loss of hair cell function in the cochlea leads to changes in ion channel expression in the central nervous system and suggests that this deafness model will be an important tool in understanding central changes occurring in human congenital deafness and in exploring activity-dependent regulation of ion channel expression.
(Received 2 May 2004;
accepted after revision 28 June 2004;
first published online 2 July 2004)
Corresponding author B. Walmsley: Synapse and Hearing Laboratory, Division of Neuroscience, John Curtin School of Medical Research, Australian National University, PO Box 334, Canberra, ACT 0200, Australia. Email: bruce.walmsley{at}anu.edu.au
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