Connections and synaptic function in the posteroventral cochlear nucleus of deaf jerker mice.

Mutations in the gene that encodes espins can cause deafness and vestibular disorders; mice that are homozygous for the autosomal recessive jerker mutation in the espin gene never hear. Extracellular injections of biocytin into the anteroventral cochlear nucleus (AVCN) revealed that although the cochlear nuclei are smaller in je/je mice, the topography in its innervation resembles that in wild-type mice. Auditory nerve fibers innervate narrow, topographically organized, "isofrequency" bands in deaf animals over the ages examined, P18-P70. The projection of tuberculoventral cells was topographic in je/je as in wild-type mice. Terminals of auditory nerve fibers in the multipolar cell area included both large and small endings, whereas in the octopus cell area they were exclusively small boutons in je/je as in wild-type mice, but end bulbs near the nerve root of je/je animals were smaller than in hearing animals. In whole-cell recordings from targets of auditory nerve fibers, octopus and T stellate cells, miniature excitatory postsynaptic currents (mEPSCs) had similar shapes as in +/+, indicating that the properties of AMPA receptors were not affected by the mutation. In je/je animals the frequency of spontaneous mEPSCs was elevated, and synaptic depression in responses to trains of shocks delivered at between 100 and 333 Hz was greater than in wild-type mice, indicating that the probability of neurotransmitter release was increased. The frequency of spontaneous mEPSCs and extent of synaptic depression were greater in octopus than in T stellate cells, in both wild-type and in je/je mice.