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Introduction to Acoustics

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446 Part D Hearing and Signal Processing<br />

Part D 12.2<br />

The recep<strong>to</strong>r potentials in an IHC responding <strong>to</strong><br />

<strong>to</strong>nesareshowninFig.12.10 [12.83]. The traces are<br />

the membrane potentials recorded in an IHC, each trace<br />

at a different stimulus frequency. These potentials are<br />

the driving force for the Ca 2+ signal <strong>to</strong> the synapse,<br />

and thus indirectly for the AN fibers connected <strong>to</strong> the<br />

cell. The properties of these potentials can be predicted<br />

from Fig. 12.9c by the thought experiment of moving<br />

a stimulus sinusoidally back and forth on the abscissa<br />

and following the potential traced out on the ordinate.<br />

The potential should be a dis<strong>to</strong>rted sinusoid, because<br />

25 mV<br />

AC comp.<br />

12.5 mV<br />

DC comp.<br />

0 10 20 30 40 50 60 ms<br />

100<br />

300<br />

500<br />

700<br />

900<br />

1000<br />

2000<br />

3000<br />

4000<br />

5000<br />

Fig. 12.10 Recep<strong>to</strong>r potentials in an IHC in the basal turn<br />

of a guinea-pig cochlea. The stimulus level was set at 80 dB<br />

SPL so that the cell would respond across a wide range of<br />

frequencies. Stimulus frequency is given at right. Notice the<br />

change in ordinate scale between the 900 Hz and 1000 Hz<br />

traces. (After [12.83], with permission)<br />

depolarizing responses are larger than hyperpolarizing<br />

ones, and it should have a steady (DC) offset, also because<br />

of the asymmetry favoring depolarization. At low<br />

frequencies, both components can be seen in Fig. 12.10;<br />

the response is a dis<strong>to</strong>rted sinusoid riding on a steady<br />

depolarization. At high frequencies (>1000 Hz), the sinusoidal<br />

component is reduced by low-pass filtering by<br />

the cell’s membrane capacitance and only the steady<br />

component is seen. The transition from sinusoidal recep<strong>to</strong>r<br />

potentials at low frequencies <strong>to</strong> rectified DC<br />

potentials at high frequencies corresponds <strong>to</strong> the loss<br />

of phase-locking at higher frequencies in AN fibers<br />

(Fig. 12.8c). At low frequencies, the IHC/AN synapse<br />

releases transmitter on the positive half cycles of the<br />

recep<strong>to</strong>r potential and the AN fiber is phase-locked; at<br />

high frequencies, there is a steady release of neurotransmitter<br />

and the AN fiber responds with a rate increase but<br />

without phase-locking.<br />

OHCs and the Cochlear Amplifier<br />

In the discussion of the basilar membrane, the need for<br />

a source of energy in the cochlea, a cochlear amplifier,<br />

was discussed. At present, two possible sources<br />

of the amplification have been suggested. The first is<br />

OHC motility [12.86,100] and the second is hair bundle<br />

motility [12.101]. Although hair bundle motility could<br />

function in both IHCs andOHCs, it seems likely that<br />

a) Treshold (dB SPL) b)<br />

100<br />

80<br />

60<br />

40<br />

20<br />

0<br />

0.1<br />

IHC<br />

damage<br />

Normal<br />

1 4<br />

OHC<br />

damage<br />

Normal<br />

0.1 1 4<br />

Frequency (kHz)<br />

Fig. 12.11a,b Schematic summary of AN tuning curves in<br />

normal ears and in ears with damaged cochleae. (a) In regions<br />

of the cochlea with remaining OHCs but damaged<br />

IHCs tuning curves mainly show a threshold elevation.<br />

(b) In regions with missing OHCs but intact IHCs there<br />

is an elevation of threshold at frequencies near BF and<br />

a substantial broadening of tuning. (After [12.51])

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