scholarly journals Identification and modelling of fast and slow I h current components in vestibular ganglion neurons

2015 ◽  
Vol 42 (10) ◽  
pp. 2867-2877 ◽  
Author(s):  
Christophe B. Michel ◽  
Christine Azevedo Coste ◽  
Gilles Desmadryl ◽  
Jean‐Luc Puel ◽  
Jerome Bourien ◽  
...  
Keyword(s):  
Vestibular Ganglion ◽  
Ganglion Neurons

scholarly journals A biophysical model examining the role of low-voltage-activated potassium currents in shaping the responses of vestibular ganglion neurons

2016 ◽  
Vol 116 (2) ◽  
pp. 503-521 ◽  
Author(s):  
Ariel E. Hight ◽  
Radha Kalluri
Keyword(s):  
Low Voltage ◽  
Potassium Currents ◽  
Synaptic Conductance ◽  
Biophysical Model ◽  
Resting Potential ◽  
Interspike Intervals ◽  
Firing Patterns ◽  
Vestibular Ganglion ◽  
Ganglion Neurons ◽  
The Impact

The vestibular nerve is characterized by two broad groups of neurons that differ in the timing of their interspike intervals; some fire at highly regular intervals, whereas others fire at highly irregular intervals. Heterogeneity in ion channel properties has been proposed as shaping these firing patterns (Highstein SM, Politoff AL. Brain Res 150: 182–187, 1978; Smith CE, Goldberg JM. Biol Cybern 54: 41–51, 1986). Kalluri et al. ( J Neurophysiol 104: 2034–2051, 2010) proposed that regularity is controlled by the density of low-voltage-activated potassium currents ( IKL). To examine the impact of IKL on spike timing regularity, we implemented a single-compartment model with three conductances known to be present in the vestibular ganglion: transient sodium ( gNa), low-voltage-activated potassium ( gKL), and high-voltage-activated potassium ( gKH). Consistent with in vitro observations, removing gKL depolarized resting potential, increased input resistance and membrane time constant, and converted current step-evoked firing patterns from transient (1 spike at current onset) to sustained (many spikes). Modeled neurons were driven with a time-varying synaptic conductance that captured the random arrival times and amplitudes of glutamate-driven synaptic events. In the presence of gKL, spiking occurred only in response to large events with fast onsets. Models without gKL exhibited greater integration by responding to the superposition of rapidly arriving events. Three synaptic conductance were modeled, each with different kinetics to represent a variety of different synaptic processes. In response to all three types of synaptic conductance, models containing gKL produced spike trains with irregular interspike intervals. Only models lacking gKL when driven by rapidly arriving small excitatory postsynaptic currents were capable of generating regular spiking.

scholarly journals Muscarinic acetylcholine receptors modulate HCN channel properties in vestibular ganglion neurons

2022 ◽  
Author(s):  
Daniel Bronson ◽  
Radha Kalluri
Keyword(s):  
Signaling Cascades ◽  
Hcn Channels ◽  
Type I ◽  
Hcn Channel ◽  
Firing Patterns ◽  
Vestibular Ganglion ◽  
Muscarinic Acetylcholine ◽  
Efferent Neurons ◽  
Ganglion Neurons ◽  
Channel Properties

Vestibular efferent neurons play an important role in shaping vestibular afferent excitability and accordingly, on the information encoded by their spike patterns. Efferent-modulation is linked to muscarinic signaling cascades that affect ion channel conductances, most notably low-voltage gated potassium channels such as KCNQ. Here we tested and found that muscarinic signaling cascades also modulate hyperpolarization-activated cyclic-nucleotide gated channels (HCN). HCN channels play a key role in controlling spike-timing regularity and a non-chemical form of transmission between type I hair cells and vestibular afferents. The impact of cholinergic efferent input on HCN channels was assessed using voltage-clamp methods, which measure currents in the disassociated cell bodies of vestibular ganglion neurons (VGN). Membrane properties in VGN were characterized before and after administration of the muscarinic acetylcholine receptor (mAChR) agonist Oxotremorine-M (Oxo-M). We found that Oxo-M shifted the voltage-activation range of HCN channels in the positive direction by 4.1 +/- 1.1 mV, which more than doubled the available current when held near rest at -60 mV (a 184 +/- 90.1% increase, n=19). This effect was not blocked by pre-treating the cells with a KCNQ channel blocker, linopirdine, which suggests that this effect is not dependent on KCNQ currents. We also found that HCN channel properties in the baseline condition and sensitivity to mAChR activation depended on cell size and firing patterns. Large-bodied neurons with onset firing patterns had the most depolarized activation range and least sensitivity to mAChR activation. Together, our results highlight the complex and dynamic regulation of HCN channels in VGN.

Molecular identity, ontogeny, and cAMP modulation of the hyperpolarization-activated current in vestibular ganglion neurons

2012 ◽  
Vol 108 (8) ◽  
pp. 2264-2275 ◽  
Author(s):  
Angélica Almanza ◽  
Enoch Luis ◽  
Francisco Mercado ◽  
Rosario Vega ◽  
Enrique Soto
Keyword(s):  
Current Density ◽  
Small Cells ◽  
Resting Potential ◽  
Afferent Neuron ◽  
Intracellular Camp ◽  
Rt Pcr ◽  
Patch Clamp Technique ◽  
Vestibular Ganglion ◽  
Hyperpolarization Activated Current ◽  
Ganglion Neurons

Properties, developmental regulation, and cAMP modulation of the hyperpolarization-activated current ( Ih) were investigated by the whole cell patch-clamp technique in vestibular ganglion neurons of the rat at two postnatal stages (P7–10 and P25–28). In addition, by RT-PCR and immunohistochemistry the identity and distribution of hyperpolarization-activated and cyclic nucleotide-gated channel (HCN) isoforms that generate Ih were investigated. Ih current density was larger in P25–28 than P7–10 rats, increasing 410% for small cells (<30 pF) and 200% for larger cells (>30 pF). The half-maximum activation voltage ( V1/2) of Ih was −102 mV in P7–10 rats and in P25–28 rats shifted 7 mV toward positive voltages. At both ages, intracellular cAMP increased Ih current density, decreased its activation time constant (τ), and resulted in a rightward shift of V1/2 by 9 mV. Perfusion of 8-BrcAMP increased Ih amplitude and speed up its activation kinetics. Ih was blocked by Cs+, zatebradine, and ZD7288. As expected, these drugs also reduced the voltage sag caused with hyperpolarizing pulses and prevented the postpulse action potential generation without changes in the resting potential. RT-PCR analysis showed that HCN1 and HCN2 subunits were predominantly amplified in vestibular ganglia and end organs and HCN3 and HCN4 to a lesser extent. Immunohistochemistry showed that the four HCN subunits were differentially expressed (HCN1 > HCN2 > HCN3 ≥ HCN4) in ganglion slices and in cultured neurons at both P7–10 and P25–28 stages. Developmental changes shifted V1/2 of Ih closer to the resting membrane potential, increasing its functional role. Modulation of Ih by cAMP-mediated signaling pathway constitutes a potentially relevant control mechanism for the modulation of afferent neuron discharge.

AMPA Receptors in Cultured Vestibular Ganglion Neurons: Detection and Activation

1997 ◽  
Vol 9 (2) ◽  
pp. 221-228 ◽  
Author(s):  
Denis Rabejac ◽  
Gina Devau ◽  
Jacqueline Raymond
Keyword(s):  
Ampa Receptors ◽  
Vestibular Ganglion ◽  
Ganglion Neurons

Detection of calbindin-D 28k mRNA in rat vestibular ganglion neurons by in situ hybridization

1991 ◽  
Vol 9 (1-2) ◽  
pp. 153-156 ◽  
Author(s):  
Danielle Demêmes ◽  
Brigitte Moniot ◽  
Nour-eddine Lomri ◽  
Monique Thomasset ◽  
Alain Sans
Keyword(s):  
In Situ Hybridization ◽  
Vestibular Ganglion ◽  
Calbindin D ◽  
Ganglion Neurons

Unbiased quantification of Scarpa's ganglion neurons in aminoglycoside ototoxicity

2005 ◽  
Vol 15 (4) ◽  
pp. 197-202
Author(s):  
Gail Ishiyama ◽  
Michael Finn ◽  
Ivan Lopez ◽  
Yong Tang ◽  
Robert W. Baloh ◽  
...  
Keyword(s):  
Temporal Bone ◽  
Control Group ◽  
Vestibular Ganglion ◽  
Aminoglycoside Ototoxicity ◽  
Unbiased Stereology ◽  
History Of ◽  
Neuronal Number ◽  
Student’S T ◽  
Archival Human Temporal Bone ◽  
Ganglion Neurons

While most studies have demonstrated damage to the cochlear and vestibular endorgan as the primary site of aminoglycoside toxicity, the effect on the primary afferent neurons of the vestibular ganglion remains to be determined. This study used the unbiased stereology-optical fractionator method to obtain estimates of the vestibular ganglion neuronal number. Archival temporal bone specimens from seven subjects with a history of gentamicin (n = 3) and streptomycin (n = 4) aminoglycoside ototoxicity were used. The post-ototoxicity survival time ranged from two months to 8 years, with an average of 2.2 years. Seven archival human temporal bone specimens from age-matched subjects with no history of audiovestibular symptoms or ototoxicity served as controls. Group means were compared using unpaired, two-tailed student's t test. The average vestibular ganglion neuronal number in the aminoglycoside ototoxicity group was 20, 733 neurons (CV = 0.073), which was significantly lower (p < 0.005) than the average number in the age-matched control group of 24, 902 neurons (CV = 0.109). These findings may be consistent with either retrograde degeneration or a direct neurotoxic effect of the aminoglycosides on the vestibular ganglion neuron.

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