Synaptophysin immunoreactivity in the cochlear nucleus after unilateral cochlear or ossicular removal

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

doi:10.1002/(sici)1098-2396(199703)25:3<243::aid-syn3>3.0.co;2-b

Cited by 94 publications

(51 citation statements)

References 65 publications

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“…Interestingly, a similar reduction in g KLV has been reported in cochlear-ablated chick NM neurons (protein expression) (Lu et al 2004) and in congenitally deaf mouse MNTB neurons (current density) (Leao et al 2004). The different aspects of changes in intrinsic excitability observed in this study as compared to previous reports may reflect the different nature of Bhearing loss.^The progressive hearing loss studied here should cause a gradual change in auditory nerve activity, and at these ages, does not cause synaptic degeneration (Willott and Bross 1996) nucleus (Tucci et al 1987;Born and Rubel 1988;Born et al 1991;Benson et al 1997). The systematic latency difference between young and old high-frequency bushy cells in DBA mice was quite striking.…”

Section: Discussionmentioning

confidence: 55%

“…The dorsal third of the nucleus was defined by the trajectory of the ANFs from the nerve root region (Wang and Manis 2005). Based on the mouse cochlear frequency map and its projection onto the AVCN (Ehret 1983;Berglund and Brown 1994;Muller et al 2005), cells in the region we targeted would be expected to have best frequencies above 25 kHz.…”

Section: Slice Preparationmentioning

confidence: 99%

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Temporal Coding by Cochlear Nucleus Bushy Cells in DBA/2J Mice with Early Onset Hearing Loss

Wang

Manis

2006

JARO

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The bushy cells of the anterior ventral cochlear nucleus (AVCN) preserve or improve the temporal coding of sound information arriving from auditory nerve fibers (ANF). The critical cellular mechanisms entailed in this process include the specialized nerve terminals, the endbulbs of Held, and the membrane conductance configuration of the bushy cell. In one strain of mice (DBA/2J), an early-onset hearing loss can cause a reduction in neurotransmitter release probability, and a smaller and slower spontaneous miniature excitatory postsynaptic current (EPSC) at the endbulb synapse. In the present study, by using a brain slice preparation, we tested the hypothesis that these changes in synaptic transmission would degrade the transmission of timing information from the ANF to the AVCN bushy neuron. We show that the electrical excitability of bushy cells in hearing-impaired old DBA mice was different from that in young, normal-hearing DBA mice. We found an increase in the action potential (AP) firing threshold with current injection; a larger AP afterhyperpolarization; and an increase in the number of spikes produced by large depolarizing currents. We also tested the temporal precision of bushy cell responses to high-frequency stimulation of the ANF. The standard deviation of spikes (spike jitter) produced by ANF-evoked excitatory postsynaptic potentials (EPSPs) was largely unaffected in old DBA mice. However, spike entrainment during a 100-Hz volley of EPSPs was significantly reduced. This was not a limitation of the ability of bushy cells to fire APs at this stimulus frequency, because entrainment to trains of current pulses was unaffected. Moreover, the decrease in entrainment is not attributable to increased synaptic depression. Surprisingly, the spike latency was 0.46 ms shorter in old DBA mice, and was apparently attributable to a faster conduction velocity, since the evoked excitatory postsynaptic current (EPSC) latency was shorter in old DBA mice as well. We also tested the contribution of the low-voltage-activated K+ conductance (g (KLV)) on the spike latency by using dynamic clamp. Alteration in g (KLV) had little effect on the spike latency. To test whether these changes in DBA mice were simply a result of continued postnatal maturation, we repeated the experiments in CBA mice, a strain that shows normal hearing thresholds through this age range. CBA mice exhibited no reduction in entrainment or increased spike jitter with age. We conclude that the ability of AVCN bushy neurons to reliably follow ANF EPSPs is compromised in a frequency-dependent fashion in hearing-impaired mice. This effect can be best explained by an increase in spike threshold.

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Section: Discussionmentioning

confidence: 55%

Section: Slice Preparationmentioning

confidence: 99%

Temporal Coding by Cochlear Nucleus Bushy Cells in DBA/2J Mice with Early Onset Hearing Loss

Wang

Manis

2006

JARO

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“…Synaptophysin is a 38 kDa calcium-binding glycoprotein widely found in presynaptic membranes and vesicles (Jahn et al, 1985;Wiedenmann and Franke, 1985) and is used as a marker for synaptic reorganization after denervation (Benson et al, 1997;Brock and O'Callaghan, 1987;Masliah et al, 1991;Walaas et al, 1988) and for quantification of synapses (Calhoun et al, 1996). Decreased expression of synaptophysin was found in the VCN following AAT or cochlear ablation (Benson et al, 1997;FuentesSantamaría et al, 2007;Muly et al, 2002).…”

Section: Effects Of Noise Exposure and Antioxidant Treatment On Synapmentioning

confidence: 99%

“…Decreased expression of synaptophysin was found in the VCN following AAT or cochlear ablation (Benson et al, 1997;FuentesSantamaría et al, 2007;Muly et al, 2002). Precerebellin (Cbln1), the precursor of the brain-specific neuropeptide cerebellin, is a synapse organizer for both pre-and post-synaptic components and is involved in synaptic integrity, plasticity, as well as synapse maintenance in the cerebellum (Hirai et al, 2005;Ito-Ishida et al, 2008;Matsuda et al, 2010;Miura et al, 2009).…”

Section: Effects Of Noise Exposure and Antioxidant Treatment On Synapmentioning

confidence: 99%

Selective degeneration of synapses in the dorsal cochlear nucleus of chinchilla following acoustic trauma and effects of antioxidant treatment

Chen

Choi

et al. 2012

Hearing Research

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“…In addition, glycine receptor subunit phosphorylation levels may have altered glycine receptor clustering and trafficking (Meier et al, 2001). Thus, one explanation of the present deficits after UCA would include a diminished expression of glycine receptor subunit expression and trafficking through an induced down regulation of protein phosphorylations (proposed in Suneja et al, 1997). If so, the recovery of ligand binding activity after reducing CaMKII activity or increasing PKC and PKA activity implies that exogenous control of protein phosphorylations may alleviate these deficits.…”

Section: Discussionmentioning

confidence: 93%

Protein kinases regulate glycine receptor binding in brain stem auditory nuclei after unilateral cochlear ablation

2007

Self Cite

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Glycinergic synaptic inhibition is part of acoustic information processing in brain stem auditory pathways and contributes to the regulation of neuronal excitation. We found previously that unilateral cochlear ablation (UCA) in young adult guinea pigs decreased [ 3 H]strychnine binding activity in several brain stem auditory nuclei. This study determined if the UCA-induced deficit could be regulated by protein kinase C (PKC), protein kinase A (PKA) or Ca 2+ /calmodulin-dependent protein kinase II (CaMKII). The specific binding of [ 3 H]strychnine was measured in slices of the dorsal (DCN), posteroventral (PVCN) and anteroventral (AVCN) cochlear nucleus (CN), the lateral (LSO) and medial (MSO) superior olive, and the inferior colliculus (IC) 145 days after UCA. Tissues from age-matched unlesioned animals served as controls. UCA induced deficits in specific binding in the AVCN, PVCN and LSO on the ablated side and in the MSO bilaterally. These deficits were reversed by 3 μM phorbol 1,2-dibutyrate, a PKC activator, or 0.2 mM dibutyryl-cAMP, a PKA activator. However, 50 nM Ro31-8220, a PKC inhibitor, and 2 μM H-89, a PKA inhibitor, had no effect in unlesioned controls and after UCA. In contrast, 4 μM KN-93, a CaMKII inhibitor, relieved or reversed the UCA-induced binding deficits and elevated binding in the IC. These findings suggest a UCA-induced down regulation of glycine receptor synthesis may have occurred via reduced phosphorylation of proteins that control receptor synthesis; this effect was reversed by diminishing CaMKII activity or increasing PKC and PKA activity.

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Synaptophysin immunoreactivity in the cochlear nucleus after unilateral cochlear or ossicular removal

Cited by 94 publications

References 65 publications

Temporal Coding by Cochlear Nucleus Bushy Cells in DBA/2J Mice with Early Onset Hearing Loss

Temporal Coding by Cochlear Nucleus Bushy Cells in DBA/2J Mice with Early Onset Hearing Loss

Selective degeneration of synapses in the dorsal cochlear nucleus of chinchilla following acoustic trauma and effects of antioxidant treatment

Protein kinases regulate glycine receptor binding in brain stem auditory nuclei after unilateral cochlear ablation

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