We observed how a decrease of N1m source strength, taken to be a reflection of lateral inhibition in the auditory pathway, depended in part on the frequency spectrum of the preceding NFN masker. Our previous study indicated that N1m decrement was dependent on the bandwidth of stop-band frequency of the preceding masker [15
]. The present results demonstrated that lateral inhibitory effects from the lower and the higher spectral edges of NFN might be different along the auditory pathway. The most pronounced N1m decrement was obtained for the NFN1, which had a lower spectral edge of just 1/6 octave below the frequency of the test stimulus. Therefore, it can be assumed that the low frequency section of the NFN1 was the most influential on the N1m decrement. Similarly it could be assumed in case of NFN5 that the higher spectral edge of just 1/6 octave greater than the frequency of the test stimulus was mainly responsible for the N1m decrement. The N1m response elicited after exposure to NFN1 was significantly smaller than the one elicited after exposure to NFN5 even though both were equally distant from the test stimulus frequency. This result implies that the lower spectral edge of the NFN caused a larger N1m decrement than the higher spectral edge. The estimated source locations for N1m responses elicited by the TS with various preceding NFNs were not significantly different, a result suggesting that the neuronal group activated by the TS in NFN conditions did not differ, but rather the number of activated neurons and/or their level of synchrony did.
In this study, the TS and the stimulus timings remained constant in all conditions and only the preceding NFNs differed between the various conditions. Thus, only the type of the preceding NFN should be responsible for the difference in the N1m response elicited by the following TS. Of course, the preceding N1m response elicited by NFN-onset might also affect the N1m response elicited by the following TS-onset. However, the N1m responses to NFNs did not significantly differ in their source locations, source strengths, and latencies. Thus, we could hypothesize that the 3 s exposures to the NFN altered the responsiveness of the auditory neurons activated by the subsequent TS possibly via lateral connections, thus resulting in various N1m decrements.
The concept of lateral inhibition is similar to those suggested for other sensory systems showing excitatory and inhibitory interactions along the corresponding sensory pathway (c.f. figure ). Inhibitory lateral connections are a common model for contrast enhancement in sensory neural networks. In case of the auditory system, lateral inhibition seems to enhance spectral contrasts of sound inputs into the topographical frequency map, where neurons are systematically located with respect to specific frequency-tuning curves that exhibit a minimum threshold at a characteristic frequency (CF). Neurons with CFs outside the notch and close to the frequency slope of the NFN might receive less lateral inhibitory input from neighboring neurons with CFs inside the notch, since the latter are not excited by the NFN. This would result in an increased activation of the neurons with CFs around the edge frequency outside the notch. In contrast, neurons within the notch region are not excited, but still get strong inhibitory input via lateral connections from the neighboring neurons outside the notch, since the neighboring neurons are excited by the NFN. That results in a strongly inhibited activation of the neurons within the notch. Our previous study [14
] has shown that the N1m responses elicited by the neural group corresponding to the spectral notch frequencies of CFN were more strongly decreased than the N1m responses corresponding to the pass-band frequencies after the 3 s CFN exposure.
We could ask the question if the asymmetric N1m decrements might be explained by another mechanism, e.g. habituation. The displacement of the basilar membrane has a shallow tail in the base area corresponding to higher frequencies (figure ). Thus, low frequency sounds could activate and habituate neurons with higher CFs more easily than high frequency sounds activate neurons with lower CFs. In the present study, the lower spectral edge of the NFN may cause a stronger habituation effect on auditory neurons corresponding to the TS frequency than the higher spectral edge. However, previous electroencephalographic studies showed that the population level habituation effect on N1 decrements was symmetrical [6
]. These authors presented a test tone together with intervening tones with similar and different frequencies. The N1 decrement was maximal when the intervening tones were identical with the test stimulus, and the N1 became symmetrically larger as a function of the frequency difference between test tone and the intervening tone with higher or lower frequency. Therefore habituation alone could not explain the asymmetric N1m decrements observed in the present study.
Previous psychoacoustical study has shown that the effect of forward masking disappeared within 200 ms [24
]. In this study as well as in previous ones [14
] we have observed lateral inhibitory effects after the 500 ms silent interval between NFN and TS (figure ). Hence our results do not directly reflect the psychoacoustical forward masking effect. Also neurophysiological evidences obtained in animal studies indicated that the duration of the forward masking effect was less than 500 ms in the cochlea [25
], auditory nerve [26
], cochlear nucleus [28
], and primary auditory cortex [29
]. Mechanical lateral suppression caused by overlapping basilar membrane displacements and forward masking effects within the brainstem could not explain our results. Therefore we assume that the long lasting lateral inhibitory effect might be caused by inter-cortical inhibitory neural connections in the central auditory system [30
]. In summary, the asymmetric N1m decrements observed in the present study imply that the lateral inhibition from lower to higher frequencies might have stronger effect than the one from higher to lower frequencies in cortical structures such as lateral aspects of the Heschl's gyrus and the temporal plane, which are known to be the cortical generator sites of N1m [32