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A modeling study of the responses of the lateral superior olive to ipsilateral sinusoidally amplitude-modulated tones.

Wang L, Colburn HS - J. Assoc. Res. Otolaryngol. (2011)

Bottom Line: In the model, AHP channels alone were not sufficient to induce the observed rate decrease at high modulation frequencies.In contrast, both the small and large rate decreases were replicated when KLT channels were included in the LSO neuron model.These results support the conclusion that KLT channels may play a major role in the large rate decreases seen in some units and that background inhibition may be a contributing factor, a factor that could be adequate for small decreases.

View Article: PubMed Central - PubMed

Affiliation: Department of Biomedical Engineering, Center for Hearing Research, Boston University, Boston, MA 02215, USA.

ABSTRACT
The lateral superior olive (LSO) is a brainstem nucleus that is classically understood to encode binaural information in high-frequency sounds. Previous studies have shown that LSO cells are sensitive to envelope interaural time difference in sinusoidally amplitude-modulated (SAM) tones (Joris and Yin, J Neurophysiol 73:1043-1062, 1995; Joris, J Neurophysiol 76:2137-2156, 1996) and that a subpopulation of LSO neurons exhibit low-threshold potassium currents mediated by Kv1 channels (Barnes-Davies et al., Eur J Neurosci 19:325-333, 2004). It has also been shown that in many LSO cells the average response rate to ipsilateral SAM tones decreases with modulation frequency above a few hundred Hertz (Joris and Yin, J Neurophysiol 79:253-269, 1998). This low-pass feature is not directly inherited from the inputs to the LSO since the response rate of these input neurons changes little with increasing modulation frequency. In the current study, an LSO cell model is developed to investigate mechanisms consistent with the responses described above, notably the emergent rate decrease with increasing frequency. The mechanisms explored included the effects of after-hyperpolarization (AHP) channels, the dynamics of low-threshold potassium channels (KLT), and the effects of background inhibition. In the model, AHP channels alone were not sufficient to induce the observed rate decrease at high modulation frequencies. The model also suggests that the background inhibition alone, possibly from the medial nucleus of the trapezoid body, can account for the small rate decrease seen in some LSO neurons, but could not explain the large rate decrease seen in other LSO neurons at high modulation frequencies. In contrast, both the small and large rate decreases were replicated when KLT channels were included in the LSO neuron model. These results support the conclusion that KLT channels may play a major role in the large rate decreases seen in some units and that background inhibition may be a contributing factor, a factor that could be adequate for small decreases.

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Circuit diagram for the HH-type LSO cell model with four non-synapse channels: leak channel, sodium channel (Na), low-threshold potassium channel (KLT), and high-threshold potassium channel (KHT). The other two channels, Gexci and Ginhi, represent excitatory and inhibitory synaptic inputs.
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Fig2: Circuit diagram for the HH-type LSO cell model with four non-synapse channels: leak channel, sodium channel (Na), low-threshold potassium channel (KLT), and high-threshold potassium channel (KHT). The other two channels, Gexci and Ginhi, represent excitatory and inhibitory synaptic inputs.

Mentions: In the studies presented here, the basic structure for the HH-type LSO cell model (cf., Fig. 2) was fixed while channel parameters were varied. MATLAB (MathWorks, Natick, MA, USA) was used to initialize the LSO model parameters before each simulation and to organize the results after each simulation. In particular, the peak conductance of the KLT channel, gKLT, was varied to investigate its effect on the average firing rate in response to SAM tones. The overall membrane time constant τm and the membrane resistance rm, which are used to interpret some of the results, were computed as follows: The membrane resistance rm is equal to the combined resistance of all channels at rest. It was computed as the reciprocal of the sum of all the membrane conductances at resting potential (around −65 mV in the model). The resting conductance is principally attributed to the leak channel conductance gleak. A small amount of resting conductance is attributed to the slight KLT channel opening. Sodium channel and KHT channel conductance did not contribute because they were inactive at rest. The circuit diagram of the LSO cell model is shown in Figure 2 with default parameter values given in Table 2. The excitatory and inhibitory synaptic inputs shown in Figure 2 will be described in the following section.FIG. 2


A modeling study of the responses of the lateral superior olive to ipsilateral sinusoidally amplitude-modulated tones.

Wang L, Colburn HS - J. Assoc. Res. Otolaryngol. (2011)

Circuit diagram for the HH-type LSO cell model with four non-synapse channels: leak channel, sodium channel (Na), low-threshold potassium channel (KLT), and high-threshold potassium channel (KHT). The other two channels, Gexci and Ginhi, represent excitatory and inhibitory synaptic inputs.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3298618&req=5

Fig2: Circuit diagram for the HH-type LSO cell model with four non-synapse channels: leak channel, sodium channel (Na), low-threshold potassium channel (KLT), and high-threshold potassium channel (KHT). The other two channels, Gexci and Ginhi, represent excitatory and inhibitory synaptic inputs.
Mentions: In the studies presented here, the basic structure for the HH-type LSO cell model (cf., Fig. 2) was fixed while channel parameters were varied. MATLAB (MathWorks, Natick, MA, USA) was used to initialize the LSO model parameters before each simulation and to organize the results after each simulation. In particular, the peak conductance of the KLT channel, gKLT, was varied to investigate its effect on the average firing rate in response to SAM tones. The overall membrane time constant τm and the membrane resistance rm, which are used to interpret some of the results, were computed as follows: The membrane resistance rm is equal to the combined resistance of all channels at rest. It was computed as the reciprocal of the sum of all the membrane conductances at resting potential (around −65 mV in the model). The resting conductance is principally attributed to the leak channel conductance gleak. A small amount of resting conductance is attributed to the slight KLT channel opening. Sodium channel and KHT channel conductance did not contribute because they were inactive at rest. The circuit diagram of the LSO cell model is shown in Figure 2 with default parameter values given in Table 2. The excitatory and inhibitory synaptic inputs shown in Figure 2 will be described in the following section.FIG. 2

Bottom Line: In the model, AHP channels alone were not sufficient to induce the observed rate decrease at high modulation frequencies.In contrast, both the small and large rate decreases were replicated when KLT channels were included in the LSO neuron model.These results support the conclusion that KLT channels may play a major role in the large rate decreases seen in some units and that background inhibition may be a contributing factor, a factor that could be adequate for small decreases.

View Article: PubMed Central - PubMed

Affiliation: Department of Biomedical Engineering, Center for Hearing Research, Boston University, Boston, MA 02215, USA.

ABSTRACT
The lateral superior olive (LSO) is a brainstem nucleus that is classically understood to encode binaural information in high-frequency sounds. Previous studies have shown that LSO cells are sensitive to envelope interaural time difference in sinusoidally amplitude-modulated (SAM) tones (Joris and Yin, J Neurophysiol 73:1043-1062, 1995; Joris, J Neurophysiol 76:2137-2156, 1996) and that a subpopulation of LSO neurons exhibit low-threshold potassium currents mediated by Kv1 channels (Barnes-Davies et al., Eur J Neurosci 19:325-333, 2004). It has also been shown that in many LSO cells the average response rate to ipsilateral SAM tones decreases with modulation frequency above a few hundred Hertz (Joris and Yin, J Neurophysiol 79:253-269, 1998). This low-pass feature is not directly inherited from the inputs to the LSO since the response rate of these input neurons changes little with increasing modulation frequency. In the current study, an LSO cell model is developed to investigate mechanisms consistent with the responses described above, notably the emergent rate decrease with increasing frequency. The mechanisms explored included the effects of after-hyperpolarization (AHP) channels, the dynamics of low-threshold potassium channels (KLT), and the effects of background inhibition. In the model, AHP channels alone were not sufficient to induce the observed rate decrease at high modulation frequencies. The model also suggests that the background inhibition alone, possibly from the medial nucleus of the trapezoid body, can account for the small rate decrease seen in some LSO neurons, but could not explain the large rate decrease seen in other LSO neurons at high modulation frequencies. In contrast, both the small and large rate decreases were replicated when KLT channels were included in the LSO neuron model. These results support the conclusion that KLT channels may play a major role in the large rate decreases seen in some units and that background inhibition may be a contributing factor, a factor that could be adequate for small decreases.

Show MeSH