SYNAPTIC MECHANISMS IN AUDITORY CORTEX FUNCTION

Raju Metherate

Dept. of Psychobiology, University of California, Irvine, 2205 Biological Science II, Irvine, CA 92697-4550

Received 4/1/98 Accepted 4/20/98

8. PERSPECTIVE

It should be clear from this brief review that a considerable amount of information is known regarding the synaptic and cellular electrophysiology of auditory cortex. Equally clear is that there are obvious questions to be answered in future experiments. The short latency excitation and inhibition of AC neurons is due to the activation of fast EPSPs and IPSPs, most likely mediated by AMPA/KA and GABA-A receptors, respectively. However, it is not clear how slower EPSPs and IPSPs mediated by NMDA and GABA-B receptors, respectively, contribute to acoustic responses. These synaptic potentials are easily elicited in vitro, but their role in sensory processing in vivo remains unknown. Similarly, while reduction of spike activity has been associated with IPSPs in several instances, much work needs to be done to understand the range of functions performed by cortical inhibitory activity. Since sensory-evoked inhibitory activity is thought to originate primarily within the cortex, answering these questions also will provide information about cortical contributions to the processing of acoustic information. For example, the reduction of firing rates at high stimulus intensities for neurons with nonmonotonic intensity functions could result either from the recruitment of cortical inhibitory interneurons, and therefore be evident as enhanced IPSPs, or from reduction of afferent excitation due to activity in lower auditory pathways. The latter mechanism would result in smaller-amplitude evoked EPSPs in the cortex, with no evidence for IPSPs. Similar issues can be addressed regarding responses to binaural inputs.

The influence of neuromodulatory activity on acoustic-evoked synaptic potentials also should be determined. That brain arousal systems modify sensory processing is unquestioned, but the mechanisms involved are not clear. Recent demonstrations that the basal forebrain cholinergic system may dramatically regulate the response properties of AC neurons (56, 57, 58, 73) reinforces the need for systematic cellular studies.

Finally, several studies have classified AC and other neurons based on intrinsic electrophysiology and morphology. It remains to be determine how intrinsic properties shape responses to acoustic stimuli. Since intrinsic membrane properties determine the pattern and number of spikes elicited by excitatory inputs, they may combine with synaptic potentials to determine unique response properties of AC neurons.

Using electrophysiological and anatomical approaches in vivo and in vitro, a great deal of information has been acquired regarding the auditory physiology of AC neurons on the one hand, and cellular and synaptic physiology of AC neurons on the other. By combining these approaches, we draw closer to the goal of understanding the cellular bases of information processing in the auditory cortex.