Both medial prefrontal and amygdala central nucleus lesions abolish heart rate classical conditioning, but only prefrontal lesions impair reversal of eyeblink differential conditioning

Chachich, Mark E.; Powell, D. A.

doi:10.1016/s0304-3940(98)00832-5

Cited by 48 publications

(46 citation statements)

References 15 publications

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“…Preserved acquisition of conditioned fear in animals with damage to vmPFC agrees with previous findings for conditioned freezing (Morgan et al, 1993;Morrow et al, 1999), blood pressure changes (Fryztak and Neafsey, 1994), eyeblink responses (Buchanan and Powell, 1982;Chachich and Powell, 1998), and skin conductance changes (Bechara et al, 1999). Powell and colleagues have shown that mPFC lesions block heart rate conditioning in rabbits (Buchanan and Powell, 1982;Powell, 1994), but ventral mPFC lesions similar to ours had no effect .…”

Section: Discussionsupporting

confidence: 90%

The Role of Ventromedial Prefrontal Cortex in the Recovery of Extinguished Fear

et al. 2000

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Conditioned fear responses to a tone paired with footshock extinguish when the tone is presented repeatedly in the absence of shock. Rather than erase the tone-shock association, extinction is thought to involve new learning accompanied by inhibition of conditioned responding. Despite much interest in extinction from a clinical perspective, little is known about the neural circuits that are involved. Although the prefrontal cortex has a well established role in the inhibition of inappropriate behaviors, previous reports have disagreed as to the role of the ventromedial prefrontal cortex (vmPFC) in extinction. We have reexamined the effects of electrolytic vmPFC lesions made before training on the acquisition, extinction, and recovery of conditioned fear responses in a 2 d experiment. On Day 1 vmPFC lesions had no effect on acquisition or extinction of conditioned freezing and suppression of bar pressing. On Day 2 sham rats recovered only 27% of their acquired freezing, whereas vmPFC-lesioned rats recovered 86%, which was indistinguishable from a control group that never received extinction. The high recovery in lesioned rats could not be attributed to decreased motivation or altered sensitivity to footshock. vmPFC lesions that spared the caudal infralimbic (IL) nucleus had no effect. Thus, the vmPFC (particularly the IL nucleus) is not necessary for expression of extinction, but it is necessary for the recall of extinction learning after a long delay. These data suggest a role of the vmPFC in consolidation of extinction learning or the recall of contexts in which extinction took place.Key words: extinction; infralimbic; prelimbic; fear conditioning; amygdala; inhibition Prefrontal cortex has long been implicated in inhibition of inappropriate responses. Lesions of medial prefrontal cortex (mPFC) cause perseverative responding in animals and humans and cause deficits in reversal tasks (for review, see Kolb, 1984;Fuster, 1997). Perseverative responding in prefrontal animals was extended to conditioned fear when it was shown that rats with mPFC lesions could acquire freezing responses to a tone paired with a footshock, but they required many more days to extinguish those responses when the tone was presented alone (Morgan et al., 1993). More recent data support the hypothesis that mPFC is involved in the inhibition of fear responses (Bremner et al., 1999;Herry et al., 1999;Morrow et al., 1999), and it has been suggested that deficits in extinction of conditioned fear may cause certain anxiety disorders (Charney and Deutch, 1996;Pitman, 1997).Many questions remain, however, concerning the role of the ventromedial prefrontal cortex (vmPFC) in extinction of fear. Following the original report by Morgan et al. (1993), Gewirtz et al. (1997 found no effect of vmPFC lesions on extinction of conditioned fear responses. To explain this discrepancy, Gewirtz et al. (1997) suggested that the prolonged extinction might have been attributable to increased acquisition in the lesioned animals, which was masked by asymptotic freezi...

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Section: Discussionsupporting

confidence: 90%

The Role of Ventromedial Prefrontal Cortex in the Recovery of Extinguished Fear

et al. 2000

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“…It has been shown previously by Kronforst-Collins and Disterhoft (1998), Weible et al (2000), and McLaughlin et al (2002) that pretraining mPFC lesions have a more dramatic effect on trace than delay conditioning. mPFC lesions also dramatically affect reversal conditioning but have no effect on initial differential discrimination of the EB CR (Chachich and Powell, 1999). Hippocampal lesions have a similar effect.…”

Section: Discussionmentioning

confidence: 93%

Post-Training Lesions of the Medial Prefrontal Cortex Interfere with Subsequent Performance of Trace Eyeblink Conditioning

Simon¹,

Knuckley²,

Churchwell³

et al. 2005

J. Neurosci.

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Rabbits were trained on trace eyeblink (EB) conditioning until they reached a criterion of 10 consecutive EB conditioned responses (CRs). Electrolytic lesions were made in the medial prefrontal cortex (mPFC) centered on the prelimbic area (Brodmann's area 32), at five different intervals after training. These included immediately, 24 h, 1 and 2 weeks, and 1 month after training. Separate groups of animals received sham lesions at these same intervals after training. After a 2 week postoperative recovery period, all animals were retested for 3 d on trace conditioning, using the same parameters used during preoperative training. Mean EB conditioning performance deficits occurred in the animals with mPFC lesions compared with sham-lesioned animals on the first day of retesting in all five groups. However, by the second or third day of retesting, the rabbits with lesions were performing at a level that was comparable with that of sham animals. Rabbits that received more posterolateral lesions of the neocortex did not, however, show postoperative conditioning deficits. A comparison of percentage EB CRs of animals with postoperative training with that of animals that received mPFC lesions before training suggests that the mPFC post-training lesions produce damage to a retrieval process and not to a storage site or an acquisition process.

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“…Studies using rabbits have revealed that animals exhibit conditioned bradycardia (decreased heart rate) responses during the early phase of eyeblink conditioning (Yehle, 1968; Lavond et al, 1984). Amygdala lesions have been shown to abolish conditioned bradycardia and reflex facilitation of nictitating membrane responses and retard the learning of eyeblink CR (Weisz et al, 1992;Chachich and Powell, 1998). Conversely, electrical stimulation of amygdalar central nucleus has been found to decrease heart rate and increase nictitating membrane response amplitudes (Whalen and Kapp, 1991).…”

Section: Discussionmentioning

confidence: 99%

Differential Effects of Cerebellar, Amygdalar, and Hippocampal Lesions on Classical Eyeblink Conditioning in Rats

Lee¹,

Kim²

2004

J. Neurosci.

133

150

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Eyeblink conditioning has been hypothesized to engage two successive stages of nonspecific emotional (fear) and specific musculature (eyelid) learning, during which the nonspecific component influences the acquisition of the specific component. Here we test this notion by investigating the relative contributions of the cerebellum, the amygdala, and the hippocampus to the emergence of conditioned eyelid and fear responses during delay eyeblink conditioning in freely moving rats. Periorbital electromyography (EMG) and 22 kHz ultrasonic vocalization (USV) activities were measured concurrently from the same subjects and served as indices of conditioned eyeblink and fear responses, respectively. In control animals, conditioned EMG responses increased across training sessions, whereas USV responses were initially robust but decreased across training sessions. Animals with electrolytic lesions to their cerebellum (targeting the interpositus nucleus) were completely unable to acquire conditioned EMG responses but exhibited normal USV behavior, whereas animals with lesions to the amygdala showed decelerated acquisition of conditioned EMG responses and displayed practically no USV behavior. In contrast, hippocampal lesioned rats demonstrated facilitated acquisition of conditioned EMG responses, whereas the USV behavior was unaffected. The amygdalar involvement in eyeblink conditioning was examined further by applying the GABA A agonist muscimol directly into the amygdala either before or immediately after training sessions. Although pretraining muscimol infusions impaired conditioned EMG responses, post-training infusions did not. Together, these results suggest that, even during a simple delay eyeblink conditioning, animals learn about different aspects associated with the behavioral task that are subserved by multiple brain-memory systems that interact to produce the overall behavior.

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Both medial prefrontal and amygdala central nucleus lesions abolish heart rate classical conditioning, but only prefrontal lesions impair reversal of eyeblink differential conditioning

Cited by 48 publications

References 15 publications

The Role of Ventromedial Prefrontal Cortex in the Recovery of Extinguished Fear

The Role of Ventromedial Prefrontal Cortex in the Recovery of Extinguished Fear

Post-Training Lesions of the Medial Prefrontal Cortex Interfere with Subsequent Performance of Trace Eyeblink Conditioning

Differential Effects of Cerebellar, Amygdalar, and Hippocampal Lesions on Classical Eyeblink Conditioning in Rats

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