Fear conditioning enhances short-latency auditory responses of lateral amygdala neurons: Parallel recordings in the freely behaving rat

Quirk, Gregory J.; Repa, J. Christopher; LeDoux, Joseph E.

doi:10.1016/0896-6273(95)90092-6

Cited by 732 publications

(660 citation statements)

References 55 publications

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“…This is comparable to the percentage of correlated BLA neurons recorded in prior conditioning studies (Muramoto et al, 1993;Quirk et al, 1995). Twenty-eight neurons showed correlates that centered on reward acquisition at the 1 2 3 4…”

Section: Cell Classificationsupporting

confidence: 79%

Characteristics of basolateral amygdala neuronal firing on a spatial memory task involving differential reward.

Pratt¹,

Mizumori²

1998

Behavioral Neuroscience

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Previous research has shown that spatial, movement, and reward information is integrated within the ventral striatum (VS). The present study examined the possible contribution of the basolateral nuclei of the amygdala (BLA) to this interaction by examining behavioral correlates of BLA neurons while rats performed multiple memory trials on an 8-arm radial maze. Alternate arms consistently held 1 of 2 different amounts of reward. Recorded cells were correlated with motion, auditory input, space, and reward acquisition. Reward-related units were found that anticipated reward encounter, that responded during reward consumption, and that differentiated between high and low reward magnitude. This is consistent with the hypothesis that BLA neurons may provide the VS with reward-related information that could then be integrated with spatial information to ultimately affect goal-directed behavior. Past research into the role of the amygdala in animal behavior has demonstrated that it is an important substrate for the association of cues with their affective significance.

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Section: Cell Classificationsupporting

confidence: 79%

Characteristics of basolateral amygdala neuronal firing on a spatial memory task involving differential reward.

Pratt¹,

Mizumori²

1998

Behavioral Neuroscience

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“…As synaptic plasticity in the LA is thought to underlie fear memories (Quirk et al, 1995;Collins and Pare, 2000;Repa et al, 2001;Bauer et al, 2002), we also tested for LTP in VPA-treated rats. We found that the potentiation caused by a classical pairing protocol with an extracellular electrode placed just medial to the LA was significantly increased in treated rats (t 12 ¼ 3.12 p ¼ 0.009; n ¼ 15 for control, 10 for treated; Figure 4c).…”

Section: In Vitro Slice Electrophysiology In the Basolateral Amygdalamentioning

confidence: 99%

“…Synaptic plasticity is also boosted suggesting that the amygdala turned hyperplastic following a single exposure of the embryo to VPA. Considering that LTP in the basolateral amygdala is thought to be the key cellular mechanism underlying fear memory formation (Quirk et al, 1995;Rogan et al, 1997;Collins and Pare, 2000;Repa et al, 2001;Bauer et al, 2002), hyperreactivity and hyperplasticity are strong candidates mediating the enhanced and overgeneralized fear memories in the VPA-treated rats.…”

Section: A Novel Role Suggested For the Amygdala In Autismmentioning

confidence: 99%

Abnormal Fear Conditioning and Amygdala Processing in an Animal Model of Autism

Markram

Rinaldi

Mendola

et al. 2007

Neuropsychopharmacol

337

262

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A core feature of autism spectrum disorders is the impairment in social interactions. Among other brain regions, a deficit in amygdala processing has been suggested to underlie this impairment, but whether the amygdala is processing fear abnormally in autism, is yet not clear. We used the valproic acid (VPA) rat model of autism to (a) screen for autism-like symptoms in rats, (b) test for alterations in amygdala-dependent fear processing, and (c) evaluate neuronal reactivity and synaptic plasticity in the lateral amygdala by means of in vitro single-cell electrophysiological recordings. VPA-treated animals displayed several symptoms common to autism, among them impaired social interactions and increased repetitive behaviors. Furthermore, VPA-treated rats were more anxious and exhibited abnormally high and longer lasting fear memories, which were overgeneralized and harder to extinguish. On the cellular level, the amygdala was hyperreactive to electrical stimulation and displayed boosted synaptic plasticity as well as a deficit in inhibition. We show for the first time enhanced, overgeneralized and resistant conditioned fear memories in an animal model of autism. Such hyperfear could be caused by the hyperreactivity and hyperplasticity found in the lateral amygdala, which may in turn be due to a deficit in the inhibitory system of the amygdala. We hypothesize an 'aversive world' syndrome that could, even if not a primary cause of the disorder itself, underlie some core symptoms in autism, such as impairments in social interactions and resistance to rehabilitation.

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“…The association formed between the CS and US can elicit a conditioned fear response (CR) when the CS is presented alone. In rodents the most readily observable CRs include freezing, response suppression (Quirk et al, 1995;Killcross et al, 1997;Fendt and Fanselow, 1999;Gewirtz and Davis, 2000;LeDoux, 2000), and autonomic changes such as tachycardia (Young and Leaton, 1994;Nijsen et al, 1998) and increased body temperature (Noble and Delini-Stula, 1976). Although the neural and molecular mechanisms underlying the formation of CS-US associations are well established (for reviews, see Davis, 2000;Rodrigues et al, 2004), those mechanisms that mediate the suppression of an established fear response in extinction are less clear.…”

Section: Introductionmentioning

confidence: 99%

“…Quirk et al (1995) reported that the acquisition of learned fear was associated with LTP-like increases in firing in neurons in the lateral amygdala. However, when these animals were subjected to extinction training in the same session, these neurons exhibited a gradual decrease in firing in response to CS presentations.…”

Section: Introductionmentioning

confidence: 99%

Disruption of AMPA Receptor Endocytosis Impairs the Extinction, but not Acquisition of Learned Fear

Dalton

Wang

Floresco

et al. 2007

Neuropsychopharmacol

145

135

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Synaptic plasticity in the form of long-term potentiation (LTP) plays a critical role in the formation of a Pavlovian fear association. However, the role that synaptic plasticity plays in the suppression of a learned fear response remains to be clarified. Here, we assessed the role that long-term depression (LTD) plays in the acquisition, expression, and extinction of a conditioned fear response. We report that blockade of LTD with a GluR2-derived peptide (Tat-GluR2 3Y ; 1.5 mmol/kg, i.v.) that blocks regulated a-amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid (AMPA) receptor endocytosis during an initial extinction training session disrupted both the expression and recall of extinction learning. A similar impairment of extinction during training, but not recall, was observed when NMDA receptor-dependent LTD was inhibited through the selective blockade of NMDA NR2B receptors with Ro 25-6981. In contrast, blockade of LTD with Tat-GluR2 3Y during fear conditioning or during a fear recall test did not effect the expression or recall of either contextual or cue-induced conditioned fear. Similarly, administration of Tat-GluR2 3Y prior to an extinction recall test did not affect spontaneous recovery or rate of re-extinction in previously extinguished rats. These data demonstrate that AMPA receptor endocytosis does not mediate acquisition or expression of conditioned fear, but may play a role in the extinction of fear memories. Furthermore, these findings suggest that LTD may be a molecular mechanism that facilitates the selective modification of a learned association while leaving intact the ability to form a new memory.

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Fear conditioning enhances short-latency auditory responses of lateral amygdala neurons: Parallel recordings in the freely behaving rat

Cited by 732 publications

References 55 publications

Characteristics of basolateral amygdala neuronal firing on a spatial memory task involving differential reward.

Characteristics of basolateral amygdala neuronal firing on a spatial memory task involving differential reward.

Abnormal Fear Conditioning and Amygdala Processing in an Animal Model of Autism

Disruption of AMPA Receptor Endocytosis Impairs the Extinction, but not Acquisition of Learned Fear

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