302
W.E Dolphin
Assuming that ABR waves are generated in a similar manner and from
similar structures as in other mammals, these relatively reduced latencies
indicate a higher conduction velocity, that is, the spread of neural excitation through the auditory system, from periphery to more central structures,
proceeds more rapidly in cetaceans than in other mammals. Although faster
processing within nuclei (i.e., decreased synaptic delays) is a possibility that
cannot be ruled out, a more probable explanation for the decreased conduction time is an increase in axonal conduction velocity. Conduction velocity in myelinated mammalian axons is approximately proportional to fiber
diameter. Axons within the cetacean auditory pathway are the largest diameter fibers reported in mammals. Eighth nerve diameters have been measured up to 5 to 7/lm in T. truncatus (Bullock and Gurevich 1979) more
than twice as large as found in other species such as humans having a mean
fiber diameter of 2 to 3/lm. Fibers up to 50/lm have been traced from the
cochlear nucleus to the lateral lemniscus (De Graaf 1967; Goa and Zhou
1991).
The greatly enlarged axons and significant hypertrophy of auditory structures strongly imply an adaptation of cetaceans for the extremely rapid
conduction of auditory information.
2.4 Stimulus Levels and the Preservation of
Timing Information
2.4.1 ABR Intensity Series
The entry of Ca++ into a neuron, necessary for transmitter vesicle release,
is known to be voltage-, and therefore, intensity-dependent. Transmitter
binding and subsequent neurotransmitter release is a probabilistic function of Ca++ entry and is, therefore, also intensity-dependent. Thus, an
increase in stimulus intensity results in (1) an increased probability that
any given auditory neuron will discharge in response to the stimulus
presentation with the result that a greater number of neurons are likely to
discharge, (2) depolarization of each neuron, which is likely to proceed
more rapidly, thus decreasing the time to reach threshold and, therefore,
decreasing the latency of discharge relative to stimulus onset, and (3) an
increased probability that a large proportion of excited neurons will discharge synchronously. Thus, increased stimulus intensity should result in
both an increase in response amplitude as well as a decrease in response
latency.
In cetaceans, as in all other animals tested, with an increase in stimulus
intensity there is a corresponding, but nonmonotonic, increase in peak-topeak ABR amplitude. For low-to-moderate sound pressure levels, response
amplitudes show a near-linear dependency on stimulus intensity. This
growth function, as shown in Figure 7.4, asymptotes for sound pressure
levels greater than approximately 120 to 130dB re 1/lPa (i.e., 60 to 70dB
W.E Dolphin
Assuming that ABR waves are generated in a similar manner and from
similar structures as in other mammals, these relatively reduced latencies
indicate a higher conduction velocity, that is, the spread of neural excitation through the auditory system, from periphery to more central structures,
proceeds more rapidly in cetaceans than in other mammals. Although faster
processing within nuclei (i.e., decreased synaptic delays) is a possibility that
cannot be ruled out, a more probable explanation for the decreased conduction time is an increase in axonal conduction velocity. Conduction velocity in myelinated mammalian axons is approximately proportional to fiber
diameter. Axons within the cetacean auditory pathway are the largest diameter fibers reported in mammals. Eighth nerve diameters have been measured up to 5 to 7/lm in T. truncatus (Bullock and Gurevich 1979) more
than twice as large as found in other species such as humans having a mean
fiber diameter of 2 to 3/lm. Fibers up to 50/lm have been traced from the
cochlear nucleus to the lateral lemniscus (De Graaf 1967; Goa and Zhou
1991).
The greatly enlarged axons and significant hypertrophy of auditory structures strongly imply an adaptation of cetaceans for the extremely rapid
conduction of auditory information.
2.4 Stimulus Levels and the Preservation of
Timing Information
2.4.1 ABR Intensity Series
The entry of Ca++ into a neuron, necessary for transmitter vesicle release,
is known to be voltage-, and therefore, intensity-dependent. Transmitter
binding and subsequent neurotransmitter release is a probabilistic function of Ca++ entry and is, therefore, also intensity-dependent. Thus, an
increase in stimulus intensity results in (1) an increased probability that
any given auditory neuron will discharge in response to the stimulus
presentation with the result that a greater number of neurons are likely to
discharge, (2) depolarization of each neuron, which is likely to proceed
more rapidly, thus decreasing the time to reach threshold and, therefore,
decreasing the latency of discharge relative to stimulus onset, and (3) an
increased probability that a large proportion of excited neurons will discharge synchronously. Thus, increased stimulus intensity should result in
both an increase in response amplitude as well as a decrease in response
latency.
In cetaceans, as in all other animals tested, with an increase in stimulus
intensity there is a corresponding, but nonmonotonic, increase in peak-topeak ABR amplitude. For low-to-moderate sound pressure levels, response
amplitudes show a near-linear dependency on stimulus intensity. This
growth function, as shown in Figure 7.4, asymptotes for sound pressure
levels greater than approximately 120 to 130dB re 1/lPa (i.e., 60 to 70dB