Acid Phosphatase Activity in Spiral Ganglion Neurons of C57BL/6 Mice

1998 ◽  
Vol 4 (S2) ◽  
pp. 1104-1105
Author(s):  
Glenn M. Cohen
Keyword(s):  
Acid Phosphatase ◽  
Spiral Ganglion ◽  
Distribution Patterns ◽  
Electron Microscopic ◽  
Age Related ◽  
Sensory Hair Cells ◽  
Dense Deposits ◽  
Underlying Mechanisms ◽  
Ganglion Neurons ◽  
Marker Molecule

C57BL/6 mice, along with several other mouse genotypes, have served as models for human presbycusis (age-related hearing losses). C57BL/6 mice and their genetic substrain C57/M6 show progressively severe hearing losses, starting as early as 30 days postnatally. The hearing losses result from sweeping degeneration of sensory (hair) cells and neurons that begins in the basal end of the cochlea and advances apically. Although the underlying mechanisms orchestrating sensory and neural degeneration are not known, it is possible to correlate degenerative events with the cytoplasmic levels and distribution patterns of a marker molecule, such as acid phosphatase (AP). AP, a representative lysosomal enzyme, plays a role in both normal cellular metabolism and degenerative changes (trauma and senescence). AP activity is visualized histochemically at the light and electron microscopic levels by the presence of dense deposits within lysosomes.

scholarly journals Ultrastructural localization of Na,K-ATPase in the gerbil cochlea.

1995 ◽  
Vol 43 (10) ◽  
pp. 981-991 ◽  
Author(s):  
K Nakazawa ◽  
S S Spicer ◽  
B A Schulte
Keyword(s):  
Cell Membrane ◽  
Spiral Ganglion ◽  
Ultrastructural Localization ◽  
Cell Types ◽  
Spiral Ligament ◽  
Type I ◽  
Electron Microscopic ◽  
Enzyme Cytochemistry ◽  
Efferent Nerve ◽  
Ganglion Neurons

The transport enzyme Na,K-ATPase has been localized to several different cell types within the inner ear by enzyme cytochemistry, immunohistochemistry, and in situ hybridization. Although these histochemical procedures have provided a fairly consistent pattern of the enzyme's distribution, the precise location of Na,K-ATPase in the cell membrane of some polarized and non-polarized cell types remains uncertain. We addressed this problem in the gerbil cochlea using electron microscopic immunogold cytochemistry. The results confirmed prior ultrastructural localization of Na,K-ATPase along the basolateral plasma membrane of strial marginal and outer sulcus epithelial cells but differed from a previous report in failing to detect the enzyme at the surface of strial intermediate cells. The findings also concurred with and extended previous work in showing immunogold labeling along the entire cell membrane of non-polarized Type II fibrocytes in the inferior portion of the spiral ligament and of subpopulations of fibrocytes in the suprastrial and supralimbal regions. Our observations agreed further with light microscopic immunostaining in displaying uniform gold labeling for Na,K-ATPase in the neurilemma of Type I spiral ganglion neurons, even though these cells are completely ensheathed by myelin. Surprisingly, the enzyme was detectable in the neurilemma of afferent but not that of efferent nerve processes beneath hair cells.

scholarly journals Association of the Kv1 family of K+ channels and their functional blueprint in the properties of auditory neurons as revealed by genetic and functional analyses

2013 ◽  
Vol 110 (8) ◽  
pp. 1751-1764 ◽  
Author(s):  
Wenying Wang ◽  
Hyo Jeong Kim ◽  
Ping Lv ◽  
Bruce Tempel ◽  
Ebenezer N. Yamoah
Keyword(s):  
Membrane Potential ◽  
Developmental Plasticity ◽  
Spiral Ganglion ◽  
Membrane Properties ◽  
Resting Membrane Potential ◽  
Underlying Mechanisms ◽  
Null Mutant Mice ◽  
Ganglion Neurons

Developmental plasticity in spiral ganglion neurons (SGNs) ensues from profound alterations in the functional properties of the developing hair cell (HC). For example, prehearing HCs are spontaneously active. However, at the posthearing stage, HC membrane properties transition to graded receptor potentials. The dendrotoxin (DTX)-sensitive Kv1 channel subunits (Kv1.1, 1.2, and 1.6) shape the firing properties and membrane potential of SGNs, and the expression of the channel undergoes developmental changes. Because of the stochastic nature of Kv subunit heteromultimerization, it has been difficult to determine physiologically relevant subunit-specific interactions and their functions in the underlying mechanisms of Kv1 channel plasticity in SGNs. Using Kcna2 null mutant mice, we demonstrate a surprising paradox in changes in the membrane properties of SGNs. The resting membrane potential of Kcna2−/− SGNs was significantly hyperpolarized compared with that of age-matched wild-type (WT) SGNs. Analyses of outward currents in the mutant SGNs suggest an apparent approximately twofold increase in outward K+ currents. We show that in vivo and in vitro heteromultimerization of Kv1.2 and Kv1.4 α-subunits underlies the striking and unexpected alterations in the properties of SGNs. The results suggest that heteromeric interactions of Kv1.2 and Kv1.4 dominate the defining features of Kv1 channels in SGNs.

scholarly journals No dramatic age-related loss of hair cells and spiral ganglion neurons in Bcl-2 over-expression mice or Bax null mice

2010 ◽  
Vol 5 (1) ◽  
pp. 28 ◽  
Author(s):  
Haiyan Shen ◽  
Jonathan I Matsui ◽  
Debin Lei ◽  
Lirong Han ◽  
Kevin K Ohlemiller ◽  
...  
Keyword(s):  
Hair Cells ◽  
Spiral Ganglion ◽  
Spiral Ganglion Neurons ◽  
Over Expression ◽  
Age Related ◽  
Ganglion Neurons

scholarly journals Oxidative Stresses and Mitochondrial Dysfunction in Age-Related Hearing Loss

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Chisato Fujimoto ◽  
Tatsuya Yamasoba
Keyword(s):  
Hearing Loss ◽  
Mitochondrial Dysfunction ◽  
Stria Vascularis ◽  
Spiral Ganglion ◽  
Organ Of Corti ◽  
The Elderly ◽  
Laboratory Animals ◽  
Age Related ◽  
Ganglion Neurons ◽  
Age Related Hearing Loss

Age-related hearing loss (ARHL), the progressive loss of hearing associated with aging, is the most common sensory disorder in the elderly population. The pathology of ARHL includes the hair cells of the organ of Corti, stria vascularis, and afferent spiral ganglion neurons as well as the central auditory pathways. Many studies have suggested that the accumulation of mitochondrial DNA damage, the production of reactive oxygen species, and decreased antioxidant function are associated with subsequent cochlear senescence in response to aging stress. Mitochondria play a crucial role in the induction of intrinsic apoptosis in cochlear cells. ARHL can be prevented in laboratory animals by certain interventions, such as caloric restriction and supplementation with antioxidants. In this review, we will focus on previous research concerning the role of the oxidative stress and mitochondrial dysfunction in the pathology of ARHL in both animal models and humans and introduce concepts that have recently emerged regarding the mechanisms of the development of ARHL.

scholarly journals Biased Auditory Nerve Central Synaptopathy Exacerbates Age-related Hearing Loss

2020 ◽  
Author(s):  
Meijian Wang ◽  
Chuangeng Zhang ◽  
Shengyin Lin ◽  
Yong Wang ◽  
Benjamin J. Seicol ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Auditory Processing ◽  
Auditory Nerve ◽  
Spiral Ganglion ◽  
Central Auditory Processing ◽  
Endbulb Of Held ◽  
Age Related ◽  
Central Synapses ◽  
Ganglion Neurons ◽  
Age Related Hearing Loss

SUMMARYSound information is transmitted from the cochlea to the brain by different subtypes of spiral ganglion neurons (SGN), which show varying degrees of vulnerbility under pathological conditions. It remains unclear how information from these SGNs reassemble among target neurons in the cochlear nucleus (CN) at the auditory nerve (AN) central synapses, and how different synapses change during hearing loss. Combining immunohistochemistry with electrophysiology, we investigated the giant endbulb of Held synapses and their postsynaptic bushy neurons in mice under normal hearing and age-related hearing loss (ARHL). We found that calretinin-expressing and non-calretinin-expressing endbulbs converge at continuously different ratios onto bushy neurons with varying physiological properties. Endbulbs degenerate during ARHL, and the degeneration is more severe in non-calretinin-expressing synapses, which correlates with a gradual decrease in neuronal subpopulation predominantly innervated by these inputs. Our findings suggest that biased AN central synaptopathy and shifted CN neuronal composition underlie reduced auditory input and altered central auditory processing during ARHL.

scholarly journals Electron Microscopic Reconstruction of Neural Circuitry in the Cochlea

2020 ◽  
Author(s):  
Yunfeng Hua ◽  
Xu Ding ◽  
Haoyu Wang ◽  
Fangfang Wang ◽  
Yunge Gao ◽  
...  
Keyword(s):  
Glutamate Release ◽  
Spiral Ganglion ◽  
Organ Of Corti ◽  
Neural Circuitry ◽  
Fine Tuning ◽  
Electron Microscopic ◽  
Efferent Innervation ◽  
Wide Range ◽  
Medial Olivocochlear ◽  
Ganglion Neurons

AbstractRecent studies have revealed great diversity in the structure, function and efferent innervation of afferent synaptic connections between the cochlear inner hair cells (IHCs) and spiral ganglion neurons (SGNs), which likely enables audition to process a wide range of sound pressures. By performing an extensive electron microscopic reconstruction of the neural circuitry in the mature mouse organ of Corti, we demonstrate that afferent SGN-dendrites differ in strength and composition of efferent innervation in a manner dependent on their afferent synaptic connectivity with IHCs. SGNs that sample glutamate release from several presynaptic ribbons receive more efferent innervation from lateral olivocochlear projections than those driven by a single ribbon. Next to the prevailing unbranched SGN-dendrites, we found branched SGN-dendrites that can contact several ribbons of 1-2 IHCs. Unexpectedly, medial olivocochlear neurons provide efferent innervation of SGN-dendrites, preferring those contacting single-ribbon, pillar-side synapses. We propose a fine-tuning of afferent and efferent SGN-innervation.

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