Regulation ofd-Aspartate Release and Uptake in Adult Brain Stem Auditory Nuclei after Unilateral Middle Ear Ossicle Removal and Cochlear Ablation

Potashner, S.J.; Suneja, Sanoj K.; Benson, Christina G.

doi:10.1006/exnr.1997.6641

Cited by 102 publications

(106 citation statements)

References 60 publications

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“…Currently, there is no direct evidence to indicate that deafferenting NL dendrites in vitro decreases GluR signaling within the time frame examined in our studies. However, lesion-related losses in glutamate release have been observed at this level of the auditory system (Potashner et al, 1997), and therefore it seems likely that alterations in GluR signaling contribute to the deafferentationinduced dendritic losses observed for NL neurons.…”

Section: Is Afferent Input Necessary For Maintaining Nl Dendrites In mentioning

confidence: 99%

The Level and Integrity of Synaptic Input Regulates Dendrite Structure

Sorensen

Rubel

2006

J. Neurosci.

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How localized synaptic input regulates dendritic branch structure is not well understood. For these experiments, we used single-cell electroporation, live cell imaging, in vitro deafferentation, pharmacology, and electrophysiological stimulation to study how local alterations in synaptic input affect dendritic branch structure in nucleus laminaris (NL). We found that interrupting or modulating synaptic input to distinct sets of NL dendrites can regulate their structure on a very short timescale. Specifically, eliminating synaptic input by deafferenting only one set of the bitufted NL dendrites caused a selective reduction in the total dendritic branch length of the deafferented dendrites but relatively few changes in the normally innervated dendrites on the same cell. An analysis of individual dendritic branch changes demonstrated that both control and deafferented NL dendrites exhibit branch extension and retraction. However, the presence of intact synaptic inputs balanced these changes, maintaining the total dendritic branch length of control dendrites. When glutamate receptor signaling was blocked (DNQX and AP-5), NL neurons exhibited significant dendrite retraction, demonstrating that NL dendrite maintenance depends in part on presynaptic glutamatergic input. Electrophysiological experiments further confirmed that modulating the level of synaptic input regulates NL dendrite structure. Differential stimulation of the two sets of dendrites resulted in a selective reduction in the total dendritic branch length of the unstimulated dendrites and a selective increase in the total dendritic branch length of the stimulated dorsal dendrites. These results suggest that balanced activation of the two sets of NL dendrites is required to maintain the relative amount of dendritic surface area allotted to each input.

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Section: Is Afferent Input Necessary For Maintaining Nl Dendrites In mentioning

confidence: 99%

The Level and Integrity of Synaptic Input Regulates Dendrite Structure

Sorensen

Rubel

2006

J. Neurosci.

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“…Recent studies suggest that tinnitus may result from inappropriate plastic changes in the auditory pathway in response to acoustic trauma (Potashner et al, 1997;Milbrandt et al, 2000). Consistent with this hypothesis is evidence that aberrant neural activity in the dorsal cochlear nucleus (DCN) might underlie the generation of tinnitus.…”

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confidence: 90%

Elevated Fusiform Cell Activity in the Dorsal Cochlear Nucleus of Chinchillas with Psychophysical Evidence of Tinnitus

Brozoski¹,

Bauer²,

2002

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Chinchillas with psychophysical evidence of chronic tinnitus were shown to have significantly elevated spontaneous activity and stimulus-evoked responses in putative fusiform cells of the dorsal cochlear nuclei (DCN). Chinchillas were psychophysically trained and tested before and after exposure to a traumatic unilateral 80 dB (sound pressure level) 4 kHz tone. Before exposure, two groups were matched in terms of auditory discrimination performance (noise, and 1, 4, 6, and 10 kHz tones). After exposure, a single psychophysical difference emerged between groups. The exposed group displayed enhanced discrimination of 1 kHz tones ( p ϭ 0.00027). Postexposure discrimination of other stimuli was unaffected. It was hypothesized that exposed animals experienced a chronic subjective tone (i.e., tinnitus), resulting from their trauma, and that features of this subjective tone were similar enough to 1 kHz to affect discrimination of 1 kHz objective signals. After psychophysical testing, single-unit recordings were obtained from each animal's DCN fusiform cell layer. Putative fusiform cells of exposed animals showed significantly ( p ϭ 0.0136) elevated spontaneous activity, compared with cells of unexposed animals. Putative fusiform cells of exposed animals showed a greater stimulus-evoked response to tones at 1 kHz ( p ϭ 0.0000006) and at characteristic-frequency ( p ϭ 0.0000009). This increased activity was more pronounced on the exposed side. No increase in stimulus-evoked responses was observed to other frequencies or noise. These parallel psychophysical and electrophysiological results are consistent with the hypothesis that chronic tonal tinnitus is associated with, and may result from, trauma-induced elevation of activity of DCN fusiform cells.

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“…Author Manuscript changes in amino acid neurotransmitters and receptors (Bledsoe et al, 1995;Potashner et al, 1997Potashner et al, , 2000Milbrandt et al, 1997;Ryugo et al, 1998;Caspary et al, 1999;Helfert et al, 1999;Mossop et al, 2000;Nakagawa et al, 2000; Sato et al, 2000a,b;Holt et al, 2005), in ion channels (Macica et al, 2003;Lu et al, 2004;von Hehn et al, 2004), as well as in synapse-related proteins such as protein kinases, Gap43, calbindin, ERK, SAPK, NT3 and BDNF (Idrizbegovic et al, 1998;Garcia et al, 2000;Illing and Michler, 2001; Suneja and Potashner, 2003b). Thus, there is a resulting influence on the balance between excitation and inhibition reflected in changes in neuronal response profiles (Bledsoe et al, 1995;Caspary et al, 1995;Francis and Manis, 2000;Kaltenbach and Afman, 2000;Mossop et al, 2000;Salvi et al, 2000;Syka and Rybalko, 2000) as well as in changes in tonotopic maps (Willott et al, 1982(Willott et al, , 1993Robertson and Irvine, 1989;Schwartz et al, 1993;Rajan and Irvine, 1998;Salvi et al, 1999;Nagase et al, 2000).…”

Section: Author Manuscript Author Manuscriptmentioning

confidence: 99%

Changes in glycine immunoreactivity in the rat superior olivary complex following deafness

et al. 2005

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The balance between inhibitory and excitatory amino acid neurotransmitters contributes to the control of normal functioning of the auditory brainstem. Changes in the level of neuronal activity within the auditory brainstem pathways influence the balance between inhibition and excitation. Activity-dependent plasticity in the auditory pathways can be studied by creating a large decrease in activity through peripheral deafening. Deafness-related decreases in GABA have previously been shown in the inferior colliculus. However, glycine is a more prevalent inhibitory transmitter in the mature superior olivary complex (SOC). The present study therefore examined if there were deafness-related changes in glycine in the SOC using postembedding immunocytochemistry. Animals were bilaterally deafened by an intrascalar injection of neomycin. Five nuclei in the SOC, the lateral superior olive (LSO), superior paraolivary nucleus (SPoN), and the medial, lateral, and ventral nuclei of the trapezoid body (MNTB, LNTB, and VNTB) were examined 14 days following the deafening and compared to normal hearing age-matched controls. The LSO and SPoN were divided into high and low frequency regions. The number of glycine immunoreactive puncta on the somata of principal cells showed significant decreases in all regions assessed, with changes ranging from 50% in the VNTB to 23% in the LSO. J. Comp. Neurol. 494:179-189, 2006. Indexing termsauditory; brainstem; neomycin; superior olivary complex Increases or decreases in activity induce plastic changes in the mature auditory pathways (recently reviewed by Syka, 2002; and more generally by Møller 2001, 2005). There is deafness-associated plasticity at the synaptic level in the mature auditory brainstem, with HHS Public Access Author Manuscript Author ManuscriptAuthor ManuscriptAuthor Manuscript changes in amino acid neurotransmitters and receptors (Bledsoe et al., 1995;Potashner et al., 1997Potashner et al., , 2000Milbrandt et al., 1997;Ryugo et al., 1998;Caspary et al., 1999;Helfert et al., 1999;Mossop et al., 2000;Nakagawa et al., 2000; Sato et al., 2000a,b;Holt et al., 2005), in ion channels (Macica et al., 2003;Lu et al., 2004;von Hehn et al., 2004), as well as in synapse-related proteins such as protein kinases, Gap43, calbindin, ERK, SAPK, NT3 and BDNF (Idrizbegovic et al., 1998;Garcia et al., 2000;Illing and Michler, 2001; Suneja and Potashner, 2003b). Thus, there is a resulting influence on the balance between excitation and inhibition reflected in changes in neuronal response profiles (Bledsoe et al., 1995;Caspary et al., 1995;Francis and Manis, 2000;Kaltenbach and Afman, 2000;Mossop et al., 2000;Salvi et al., 2000;Syka and Rybalko, 2000) as well as in changes in tonotopic maps (Willott et al., 1982(Willott et al., , 1993Robertson and Irvine, 1989;Schwartz et al., 1993;Rajan and Irvine, 1998;Salvi et al., 1999;Nagase et al., 2000). A shift towards decreased inhibition and increased excitation has been reported in the CIC (Vale and Sanes, 2002) associated with decreases in GAB...

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Regulation ofd-Aspartate Release and Uptake in Adult Brain Stem Auditory Nuclei after Unilateral Middle Ear Ossicle Removal and Cochlear Ablation

Cited by 102 publications

References 60 publications

The Level and Integrity of Synaptic Input Regulates Dendrite Structure

The Level and Integrity of Synaptic Input Regulates Dendrite Structure

Elevated Fusiform Cell Activity in the Dorsal Cochlear Nucleus of Chinchillas with Psychophysical Evidence of Tinnitus

Changes in glycine immunoreactivity in the rat superior olivary complex following deafness

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