Abstract
In Experiment 1, it was demonstrated that electrical stimulation of the medial division of the medial geniculate nucleus (mMGN) supports the acquisition of differential bradycardiac and corneo-retinal potential (CRP) conditioned response (CRs). In Experiment 2, the effect of electrolytic lesions in mMGN on differential conditioning was assessed. This study indicated that mMGN lesions prevent the acquisition of differential bradycardiac CRs but not CRP CRs to acoustic conditioned stimuli (CSs). In Experiment 3, it was found that ibotenic acid lesions in mMGN also prevent the acquisition of differential bradycardiac CRs by reducing the magnitude of the response to the paired stimulus (CS+). These findings indicate that intrinsic neurons in mMGN are involved in bradycardiac conditioning. In Experiment 4, it was demonstrated that either mMGN or auditory cortex lesions abolish retention of differential bradycardiac CRs by enhancing the magnitude of the response to the unpaired stimulus (CS-). However, lesions in the ventral division of MGN did not affect bradycardiac conditioning. The findings of these experiments suggest that mMGN is part of a "secondary" lemniscal system that plays an active role in conditioning. Auditory cortex appears to be involved in inhibition of responses to the CS-, perhaps via a corticothalamic pathway.