Ibotenic acid lesions in the amygdaloid central nucleus but not in the lateral subthalamic area prevent the acquisition of differential Pavlovian conditioning of bradycardia in rabbits.

The present study examined the effect of ibotenic acid lesions in the amygdaloid central nucleus (ACe) or in the lateral zona incerta of the subthalamus (LZI) on the acquisition of differential Pavlovian conditioning of bradycardia in rabbits. Previous work has shown that bilateral electrolytic lesions in either ACe or LZI abolished the retention of conditioned heart rate (HR) responses. In order to determine whether these findings were due to destruction of cells intrinsic to ACe or LZI, ibotenic acid lesions were placed bilaterally in either structure or in control sites. Following recovery, animals were subjected to differential Pavlovian conditioning in which one tone (CS+) was paired with periorbital shock and a second tone (CS-) was presented alone. It was found that destruction of cell bodies in ACe, but not LZI, prevented the acquisition of the differential bradycardiac conditioned response. In addition, ACe lesions did not interfere with baseline HR, the HR orienting response, the HR unconditioned response to shock, or the concomitantly conditioned corneoretinal potential. The results of this study suggest that destruction of cells intrinsic to ACe selectively prevents the acquisition of differentially conditioned HR, and perhaps other conditioned responses related to conditioned arousal, but does not affect unlearned HR responses or specific somatomotor conditioned responses.

Role of auditory cortex in the acquisition of differential heart rate conditioning.

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.

Involvement of cortical and thalamic auditory regions in retention of differential bradycardiac conditioning to acoustic conditioned stimuli in rabbits.

Our previous findings indicate that lesions in the medial division of the medial geniculate nucleus (mMGN) prevent the acquisition of differential conditioning of bradycardia to acoustic stimuli in rabbits. In the present experiment, the effect of lesions in mMGN on retention of differential bradycardiac conditioning was examined. In addition, the possible involvement of auditory cortex in differential conditioning was investigated. Electrodes were chronically implanted in mMGN, the ventral division of the medial geniculate nucleus (vMGN), or auditory cortex. After 7 days of recovery, animals received one differential Pavlovian conditioning session. At the end of the session, lesions were produced through the implanted electrodes. All animals demonstrated differential bradycardiac conditioning during the prelesion session. Animals with vMGN lesions also demonstrated differential conditioning during the postlesion session. However, mMGN and auditory cortex lesion animals failed to demonstrate differential conditioning during the postlesion session due to an increased response magnitude to the unpaired tone (CS-). These data support the hypothesis that mMGN plays a role in differential conditioning of bradycardia to tonal stimuli. In addition, these findings suggest that a possible corticothalamic pathway may be involved in the inhibition of the response to the CS-.

Ibotenic acid lesions in the medial geniculate region prevent the acquisition of differential Pavlovian conditioning of bradycardia to acoustic stimuli in rabbits.

The present study examined the effect of ibotenic acid lesions in the medial portion of the medial geniculate nucleus (mMGN) on differential heart rate (HR) conditioning to acoustic stimuli in rabbits. Lesions in mMGN prevented the acquisition of differential HR conditioned responses but not bradycardiac responses to the conditioned stimuli. The data suggest that cells in this region play an important role in the discriminative component of HR conditioning.

Sinoaortic denervation does not prevent differential Pavlovian conditioning of bradycardia in rabbits.

Recent findings suggest that descending projections from the amygdaloid central nucleus (ACE) to the nucleus of the solitary tract (NTS) may modulate the baroreceptor reflex and thereby facilitate the expression of the bradycardiac conditioned response (CR) in rabbits. The purpose of the present study was to examine the role of the afferent limb of the baroreceptor reflex in differential Pavlovian conditioning of bradycardia in rabbits. Animals received either aortic denervation, sinoaortic denervation or sham denervation. After recovery from surgery, animals received one differential Pavlovian conditioning session per day over the next 6 days. Sinoaortic denervation abolished the baroreceptor reflex as assessed by intravenous injections of phenylephrine. In addition, sinoaortic denervation increased baseline heart rate (HR), altered the topography of the HR unconditioned response, but did not abolish the HR orienting response or prevent the acquisition of bradycardiac CRs. The findings of the present study suggest that afferent barosensory input is necessary for the expression of the HR CR in rabbits. However, descending ACE projections may still play a role in the HR CR by directly affecting NTS neurons.

The role of amygdaloid central nucleus in the retention of differential pavlovian conditioning of bradycardia in rabbits.

The present study examined the role of the amygdaloid central nucleus (ACE) in the retention of differential pavlovian conditioning of bradycardia in rabbits. Electrodes were implanted bilaterally in ACE or in control sites just dorsal and rostral to ACE. Following recovery, animals were subjected to differential pavlovian conditioning in which one tone (CS+) was paired with periorbital shock and a second tone (CS-) was presented alone. Subsequent electrolytic lesions abolished the heart rate (HR) conditioned response (CR), yet had no effect on HR orienting response, unconditioned response, or baseline. In a follow-up experiment, corneoretinal potential (CRP) and HR were recorded. Bilateral ACE lesions profoundly attenuated or abolished the HR CR without abolishing CRP CRs. The major finding of this study is that bilateral lesions of ACE selectively attenuate the HR CR while not necessarily abolishing other CRs.

The role of the medial geniculate region in differential Pavlovian conditioning of bradycardia in rabbits.

The present study examined the role of the medial geniculate region (MGN) in differential Pavlovian conditioning of bradycardia and corneo-retinal potential (CRP) to acoustic stimuli in rabbits. Injections of horseradish peroxidase into the amygdala central nucleus, an area that mediates the bradycardia-conditioned response (CR), produced cell body and fiber labeling at the ventral and medial borders of the MGN. Then, bilateral electrolytic lesions were made at the medial border of the MGN or in control sites dorsal and/or rostral to the MGN. Ten days after surgery, lesioned and unoperated control animals were subjected to 7 days of differential Pavlovian conditioning. In the control lesion and unoperated groups, the CS+ consistently elicited larger bradycardia responses than the CS-. However, animals with bilateral lesions in the medial MGN did not demonstrate differential bradycardia CRs. Bradycardia response magnitude in MGN lesion animals was not affected. Evidence of CRP differential conditioning was present in each group. The present findings suggest that a region just medial to the MGN is involved in bradycardia differential conditioning in rabbits. The fact that bradycardia responses were still present after medial MGN lesions suggests that other auditory regions may also be involved in the mediation of the bradycardia CR.

Lateral subthalamic area as mediator of classically conditioned bradycardia in rabbits.

This study was conducted to examine whether a central efferent pathway passing through the lateral zona incerta (LZI) of the subthalamus selectively mediates the bradycardia conditioned response (CR) in rabbits. Electrodes were implanted bilaterally in LZI or in control sites just dorsal or ventral to LZI. Two days following surgery, animals were subjected to Pavlovian conditioning or to pseudoconditioning. Subsequent bilateral electrolytic lesions did not influence the heart rate (HR) orienting response, unconditioned response, baseline, or lack of response to pseudoconditioning. Bilateral LZI lesions alone abolished the HR CR. In a follow-up experiment, the corneoretinal potential (CRP) CR and HR were recorded. Bilateral LZI lesions following conditioning to a criterion of 65% CRP CRs abolished the HR CR without affecting CRP CRs. The present findings indicate that LZI is part of an efferent pathway that selectively mediates the HR CR in rabbits.