Fear conditioning and LTP in the lateral amygdala are sensitive to the same stimulus contingencies

10.1038/89465 ◽  
2001 ◽  
Vol 4 (7) ◽  
pp. 687-688 ◽  
Author(s):  
Elizabeth P. Bauer ◽  
Joseph E. LeDoux ◽  
Karim Nader
Keyword(s):  
Fear Conditioning ◽  
Lateral Amygdala

scholarly journals Overexpression of Homer1a in the basal and lateral amygdala impairs fear conditioning and induces an autism-like social impairment

2016 ◽  
Vol 7 (1) ◽  
Author(s):  
Anwesha Banerjee ◽  
Jonathan A. Luong ◽  
Anthony Ho ◽  
Aeshah O. Saib ◽  
Jonathan E. Ploski
Keyword(s):  
Fear Conditioning ◽  
Social Impairment ◽  
Lateral Amygdala

scholarly journals Fear signaling in the prelimbic-amygdala circuit: a computational modeling and recording study

2013 ◽  
Vol 110 (4) ◽  
pp. 844-861 ◽  
Author(s):  
Sandeep Pendyam ◽  
Christian Bravo-Rivera ◽  
Anthony Burgos-Robles ◽  
Francisco Sotres-Bayon ◽  
Gregory J. Quirk ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Fear Conditioning ◽  
Large Scale ◽  
Conditioned Fear ◽  
Individual Variability ◽  
Biophysical Model ◽  
Human Homolog ◽  
Lateral Amygdala ◽  
Internal Inhibition ◽  
Β Blocker

The acquisition and expression of conditioned fear depends on prefrontal-amygdala circuits. Auditory fear conditioning increases the tone responses of lateral amygdala neurons, but the increase is transient, lasting only a few hundred milliseconds after tone onset. It was recently reported that that the prelimbic (PL) prefrontal cortex transforms transient lateral amygdala input into a sustained PL output, which could drive fear responses via projections to the lateral division of basal amygdala (BL). To explore the possible mechanisms involved in this transformation, we developed a large-scale biophysical model of the BL-PL network, consisting of 850 conductance-based Hodgkin-Huxley-type cells, calcium-based learning, and neuromodulator effects. The model predicts that sustained firing in PL can be derived from BL-induced release of dopamine and norepinephrine that is maintained by PL-BL interconnections. These predictions were confirmed with physiological recordings from PL neurons during fear conditioning with the selective β-blocker propranolol and by inactivation of BL with muscimol. Our model suggests that PL has a higher bandwidth than BL, due to PL's decreased internal inhibition and lower spiking thresholds. It also suggests that variations in specific microcircuits in the PL-BL interconnection can have a significant impact on the expression of fear, possibly explaining individual variability in fear responses. The human homolog of PL could thus be an effective target for anxiety disorders.

scholarly journals Basolateral amygdala neurons are activated during threat expectation

2019 ◽  
Vol 121 (5) ◽  
pp. 1761-1777 ◽  
Author(s):  
Alon Amir ◽  
Pinelopi Kyriazi ◽  
Seung-Chan Lee ◽  
Drew B. Headley ◽  
Denis Paré
Keyword(s):  
Brain Stem ◽  
Fear Conditioning ◽  
Linear Model ◽  
Unit Activity ◽  
Generalized Linear Model ◽  
Basolateral Amygdala ◽  
Unit Recording ◽  
Lateral Amygdala ◽  
Defensive Behaviors ◽  
Foraging Task

Fear conditioning studies have led to the view that the amygdala contains neurons that signal threat and in turn elicit defensive behaviors through their brain stem and hypothalamic targets. In agreement with this model, a prior unit-recording study in rats performing a seminaturalistic foraging task revealed that many lateral amygdala (LA) neurons are predator responsive. In contrast, our previous study emphasized that most basolateral (BL) amygdala neurons are inhibited at proximity of the predator. However, the two studies used different methods to analyze unit activity, complicating comparisons between them. By applying the same method to the sample of BL neurons we recorded previously, the present study revealed that most principal cells are inhibited by the predator and only 4.5% are activated. Moreover, two-thirds of these cells were also activated by nonthreatening stimuli. In fact, fitting unit activity with a generalized linear model revealed that the only task variables associated with a prevalent positive modulation of BL activity were expectation of the predator’s presence and whether the prior trial had been a failure or success. At odds with the threat-coding model of the amygdala, actual confrontation with the predator was usually associated with a widespread inhibition of principal BL neurons. NEW & NOTEWORTHY The basolateral amygdala (BL) is thought to contain neurons that signal threat, in turn eliciting defensive behaviors. In contrast, the present study reports that very few principal BL cells are responsive to threats and that most of them are also activated by nonthreatening stimuli. Yet, expectation of the threat’s presence was associated with a prevalent positive modulation of BL activity; actual confrontation with the threat was associated with a widespread inhibition.

scholarly journals A Biologically Realistic Network Model of Acquisition and Extinction of Conditioned Fear Associations in Lateral Amygdala Neurons

2009 ◽  
Vol 101 (3) ◽  
pp. 1629-1646 ◽  
Author(s):  
Guoshi Li ◽  
Satish S. Nair ◽  
Gregory J. Quirk
Keyword(s):  
Fear Conditioning ◽  
Network Model ◽  
Basolateral Amygdala ◽  
Conditioned Fear ◽  
Pyramidal Cells ◽  
Model Learning ◽  
Lateral Amygdala ◽  
Single Structure ◽  
Firing Properties

The basolateral amygdala plays an important role in the acquisition and expression of both fear conditioning and fear extinction. To understand how a single structure could encode these “opposite” memories, we developed a biophysical network model of the lateral amygdala (LA) neurons during auditory fear conditioning and extinction. Membrane channel properties were selected to match waveforms and firing properties of pyramidal cells and interneurons in LA, from published in vitro studies. Hebbian plasticity was implemented in excitatory AMPA and inhibitory GABAA receptor-mediated synapses to model learning. The occurrence of synaptic potentiation versus depression was determined by intracellular calcium levels, according to the calcium control hypothesis. The model was able to replicate conditioning- and extinction-induced changes in tone responses of LA neurons in behaving rats. Our main finding is that LA activity during both acquisition and extinction can be controlled by a balance between pyramidal cell and interneuron activations. Extinction training depressed conditioned synapses and also potentiated local interneurons, thereby inhibiting the responses of pyramidal cells to auditory input. Both long-term depression and potentiation of inhibition were required to initiate and maintain extinction. The model provides insights into the sites of plasticity in conditioning and extinction, the mechanism of spontaneous recovery, and the role of amygdala NMDA receptors in extinction learning.

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