Key result
Auditory cortex lesions abolish differential HR conditioning vs visual lesions due to increased CS- response.
Why the study?
The role of the auditory cortex in the acquisition of differential bradycardiac conditioning to tonal stimuli was unclear.
Supports auditory cortex role in autonomic conditioning; leaves open translation to human cardiovascular research.
Previous findings from our laboratory indicate that lesions of the auditory cortex disrupt the retention of differentially conditioned bradycardiac responses to tonal stimuli in rabbits. In the present experiment, the effect of lesions of the auditory cortex on the acquisition of differential bradycardiac conditioning was examined. The effect of lesions in the auditory cortex were compared to the effect produced by control lesions in the visual cortex. After 7 days of recovery, animals received 7 days of differential Pavlovian bradycardiac conditioning in which one tone (CS+) was paired with the unconditioned stimulus, and another tone (CS-) was never paired with the unconditioned stimulus. All animals demonstrated differential conditioning during the first 3 days of conditioning. On days 4-7, however, auditory cortex lesioned animals did not exhibit significant differential heart rate (HR) conditioning, whereas control animals with lesions in the visual cortex showed no loss of conditioning during this period. The loss of differential conditioning in animals with lesions in the auditory cortex appears to be due to an increase in the magnitude of the response to the CS-. These data support the hypothesis that the auditory cortex serves to inhibit the response to the CS- in differential conditioning of bradycardia to acoustic stimuli, and that the inhibition may be mediated by a descending corticothalamic or corticolimbic pathway.
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Teich et al. (1988) studied Differential heart rate conditioning. Lesions of the auditory cortex vs. Control lesions in the visual cortex was evaluated on Differential heart rate (HR) conditioning. Lesions of the auditory cortex resulted in a loss of differential heart rate conditioning on days 4-7 compared to visual cortex lesions, due to an increased response to the CS-.
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