Skip to main page content
U.S. flag

An official website of the United States government

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2011 Sep;279(1-2):131-9.
doi: 10.1016/j.heares.2011.04.018. Epub 2011 May 10.

Short-term plasticity and auditory processing in the ventral cochlear nucleus of normal and hearing-impaired animals

Yong Wang  1 , Heather O'Donohue, Paul Manis
Affiliations
Review

Short-term plasticity and auditory processing in the ventral cochlear nucleus of normal and hearing-impaired animals

Yong Wang et al. Hear Res. 2011 Sep.

Abstract

The dynamics of synaptic transmission between neurons plays a major role in neural information processing. In the cochlear nucleus, auditory nerve synapses have a relatively high release probability and show pronounced synaptic depression that, in conjunction with the variability of interspike intervals, shapes the information transmitted to the postsynaptic cells. Cellular mechanisms have been best analyzed at the endbulb synapses, revealing that the recent history of presynaptic activity plays a complex, non-linear, role in regulating release. Emerging evidence suggests that the dynamics of synaptic function differs according to the target neuron within the cochlear nucleus. One consequence of hearing loss is changes in evoked release at surviving auditory nerve synapses, and in some situations spontaneous release is greatly enhanced. In contrast, even with cochlear ablation, postsynaptic excitability is less affected. The existing evidence suggests that different modes of hearing loss can result in different dynamic patterns of synaptic transmission between the auditory nerve and postsynaptic neurons. These changes in dynamics in turn will affect the efficacy with which different kinds of information about the acoustic environment can be processed by the parallel pathways in the cochlear nucleus.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Schematic of synaptic depression at normal auditory synapses as modeled from measurements in mouse cochlear nucleus. Each plot shows the normalized EPSC amplitude during stimulation with regular trains at different frequencies from 20 to 400 Hz, with a linear time scale on the left, and recovery kinetics measured by single test pulses after the train with a logarithmic time scale on the right. A. Typical parameters for auditory nerve synapses onto VCN bushy cells. Note that there is substantial depression at high frequencies, but rapid recovery after the train, and that recovery occurs in 2 phases (see text). B. Typical parameters for auditory nerve synapses onto VCN T-stellate cells. Note that the magnitude of depression during the stimulus is less than for bushy cells, but that recovery is slower. The inset shows the early portion of the recovery on an expanded time scale. C. Direct comparison of the plots for bushy and stellate cells at 100 Hz. The kinetic models are based on the formalizations of Dittman et al. (2000) and Yang and Xu-Friedman (2008), and parameters were obtained from fits to data measured from auditory nerve root stimulation in identified cells in brain slices from CBA mice (R. Xie and P.B. Manis, unpublished data).
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Abbott LF, Regehr WG. Synaptic computation. Nature. 2004;431:796–803. - PubMed
    1. Barnes-Davies M, Forsythe ID. Pre- and postsynaptic glutamate receptors at a giant excitatory synapse in rat auditory brainstem slices. J Physiol. 1995;488:387–406. - PMC - PubMed
    1. Bellingham MC, Walmsley B. A novel presynaptic inhibitory mechanism underlies paired pulse depression at a fast central synapse. Neuron. 1999;23:159–70. - PubMed
    1. Belousov AB, O’Hara BF, Denisova JV. Acetylcholine becomes the major excitatory neurotransmitter in the hypothalamus in vitro in the absence of glutamate excitation. J Neurosci. 2001;21:2015–27. - PMC - PubMed
    1. Benowitz LI, Routtenberg A. GAP-43: an intrinsic determinant of neuronal development and plasticity. Trends Neurosci. 1997;20:84–91. - PubMed

Publication types