Amplitude modulation (AM) is a temporal feature of most natural acoustic signals. A long psychophysical tradition has shown that AM is important in a variety of perceptual tasks, over a range of time scales. Technical possibilities in stimulus synthesis have reinvigorated this field and brought the modulation dimension back into focus. We address the question whether specialized neural mechanisms exist to extract AM information, and thus whether consideration of the modulation domain is essential in understanding the neural architecture of the auditory system. The available evidence suggests that this is the case. Peripheral neural structures not only transmit envelope information in the form of neural activity synchronized to the modulation waveform but are often tuned so that they only respond over a limited range of modulation frequencies. Ascending the auditory neuraxis, AM tuning persists but increasingly takes the form of tuning in average firing rate, rather than synchronization, to modulation frequency. There is a decrease in the highest modulation frequencies that influence the neural response, either in average rate or synchronization, as one records at higher and higher levels along the neuraxis. In parallel, there is an increasing tolerance of modulation tuning for other stimulus parameters such as sound pressure level, modulation depth, and type of carrier. At several anatomical levels, consideration of modulation response properties assists the prediction of neural responses to complex natural stimuli. Finally, some evidence exists for a topographic ordering of neurons according to modulation tuning. The picture that emerges is that temporal modulations are a critical stimulus attribute that assists us in the detection, discrimination, identification, parsing, and localization of acoustic sources and that this wide-ranging role is reflected in dedicated physiological properties at different anatomical levels.

Previous studies have shown that the tonotopic organization of primary auditory cortex is altered subsequent to restricted cochlear lesions (Robertson and Irvine, 1989) and that the topographic reorganization of the primary somatosensory cortex is correlated with changes in the perceptual acuity of the animal (Recanzone et al., 1992a-d). Here we report an increase in the cortical area of representation of a restricted frequency range in primary auditory cortex of adult owl monkeys that is correlated with the animal's performance at a frequency discrimination task. Monkeys trained for several weeks to discriminate small differences in the frequency of sequentially presented tonal stimuli revealed a progressive improvement in performance with training. At the end of the training period, the tonotopic organization of Al was defined by recording multiple-unit responses at 70-258 cortical locations. These responses were compared to those derived from three normal monkeys and from two monkeys that received the same auditory stimuli but that were engaged in a tactile discrimination task. The cortical representation, the sharpness of tuning, and the latency of the response were greater for the behaviorally relevant frequencies of trained monkeys when compared to the same frequencies of control monkeys. The cortical area of representation was the only studied parameter that was correlated with behavioral performance. These results demonstrate that attended natural stimulation can modify the tonotopic organization of Al in the adult primate, and that this alteration is correlated with changes in perceptual acuity.

A synaptic memory trace for cortical receptive field plasticity. Neuromodulation is required for cortical plasticity, but it is uncertain how subcortical neuromodulatory systems, such as the cholinergic nucleus basalis ( A major subcortical nucleus critical for receptive field plasticity is NB, the main source of cortical acetylcholine (ACh) 4,9,[14][15][16][17][19][20][21] . How are neuromodulators such as ACh involved in plasticity, and what circuit elements do they act upon? One possibility is that neuromodulation creates a cellular tag or memory trace for synaptic events that occurred in conjunction with neuromodulator release. However, the effects of ACh on cortical