scholarly journals Fear Learning Enhances Prefrontal Cortical Suppression of Auditory Thalamic Inputs to the Amygdala in Adults, but Not Adolescents

2020 ◽  
Vol 21 (8) ◽  
pp. 3008 ◽  
Author(s):  
Nicole C. Ferrara ◽  
Eliska Mrackova ◽  
Maxine K. Loh ◽  
Mallika Padival ◽  
J. Amiel Rosenkranz

Adolescence is characterized by increased susceptibility to the development of fear- and anxiety-related disorders. Adolescents also show elevated fear responding and aversive learning that is resistant to behavioral interventions, which may be related to alterations in the circuitry supporting fear learning. These features are linked to ongoing adolescent development of medial prefrontal cortical (PFC) inputs to the basolateral amygdala (BLA) that regulate neural activity and contribute to the refinement of fear responses. Here, we tested the hypothesis that the extent of PFC inhibition of the BLA following fear learning is greater in adults than in adolescents, using anesthetized in vivo recordings to measure local field potentials (LFPs) evoked by stimulation of PFC or auditory thalamic (MgN) inputs to BLA. We found that BLA LFPs evoked by stimulation of MgN inputs were enhanced in adults following fear conditioning. Fear conditioning also led to reduced summation of BLA LFPs evoked in response to PFC train stimulation, and increased the capacity of PFC inhibition of MgN inputs in adults. These data suggest that fear conditioning recruits additional inhibitory capacity by PFC inputs to BLA in adults, but that this capacity is weaker in adolescents. These results provide insight into how the development of PFC inputs may relate to age differences in memory retention and persistence following aversive learning.

2016 ◽  
Vol 96 (2) ◽  
pp. 695-750 ◽  
Author(s):  
Ivan Izquierdo ◽  
Cristiane R. G. Furini ◽  
Jociane C. Myskiw

Fear memory is the best-studied form of memory. It was thoroughly investigated in the past 60 years mostly using two classical conditioning procedures (contextual fear conditioning and fear conditioning to a tone) and one instrumental procedure (one-trial inhibitory avoidance). Fear memory is formed in the hippocampus (contextual conditioning and inhibitory avoidance), in the basolateral amygdala (inhibitory avoidance), and in the lateral amygdala (conditioning to a tone). The circuitry involves, in addition, the pre- and infralimbic ventromedial prefrontal cortex, the central amygdala subnuclei, and the dentate gyrus. Fear learning models, notably inhibitory avoidance, have also been very useful for the analysis of the biochemical mechanisms of memory consolidation as a whole. These studies have capitalized on in vitro observations on long-term potentiation and other kinds of plasticity. The effect of a very large number of drugs on fear learning has been intensively studied, often as a prelude to the investigation of effects on anxiety. The extinction of fear learning involves to an extent a reversal of the flow of information in the mentioned structures and is used in the therapy of posttraumatic stress disorder and fear memories in general.


2020 ◽  
Author(s):  
Maryne Dupin ◽  
Samuel Garcia ◽  
Belkacem Messaoudi ◽  
Valérie Doyère ◽  
Anne-Marie Mouly

ABSTRACTIn fear conditioning, where a conditioned stimulus predicts the arrival of an aversive stimulus, the animal encodes the time interval between the two stimuli. Freezing, the most used index to assess learned fear, lacks the temporal resolution required to investigate interval timing at the early stages of learning. Here we monitored respiration to visualize anticipatory behavioral responses in an odor fear conditioning in rats, while recording theta (5-15Hz) and gamma (40-80Hz) brain oscillatory activities in the medial prefrontal cortex (mPFC), basolateral amygdala (BLA), dorsomedial striatum (DMS) and olfactory piriform cortex (PIR). We investigated the temporal patterns of respiration frequency and of theta and gamma activity power during the odor-shock interval. We found that akin to respiration patterns, theta temporal curves were modulated by the duration of the odor-shock interval in the four recording sites, and respected scalar property in mPFC and DMS. In contrast, gamma temporal curves were modulated by the interval duration only in the mPFC, and in a manner that did not respect scalar property. This suggests a preferential role for theta rhythm in interval timing. In addition, our data bring the novel idea that the respiratory rhythm might take part in the setting of theta activity dynamics.


2019 ◽  
Author(s):  
John Morris ◽  
Francois Windels ◽  
Pankaj Sah

AbstractThe partial reinforcement extinction effect (PREE) is a paradoxical learning phenomenon in which omission of reinforcement during acquisition results in more persistent conditioned responding in extinction. Here, we report a significant PREE with an inverted-U, entropy-like distribution against reinforcement probability following tone foot shock fear conditioning in rats, which was associated with increased neural activity in hippocampus and amygdala as indexed by p-ERK and c-fos immunolabelling. In vivo electrophysiological recordings of local field potentials (LFPs) showed that 50% reinforcement was associated with increases in the frequency and power of tone-evoked theta oscillations in both the subiculum region of hippocampus and in basolateral amygdala (BLA) during both acquisition (Day 1) and extinction (Day 2) sessions. Tone-evoked LFPs in 50% reinforced animals also showed increases in coherence and bidirectional Granger Causality between hippocampus and amygdala. The results support a Bayesian interpretation of the PREE, in which the phenomenon is driven by increases in the entropy or uncertainty of stimulus contingencies, and indicate a crucial role for hippocampus in mediating this uncertainty-dependent effect.


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Marie-France Marin ◽  
Alexe Bilodeau-Houle ◽  
Simon Morand-Beaulieu ◽  
Alexandra Brouillard ◽  
Ryan J. Herringa ◽  
...  

Abstract The biological mechanisms involved in fear transmission within families have been scarcely investigated in humans. Here we studied (1) how children acquired conditioned fear from observing their parent, or a stranger, being exposed to a fear conditioning paradigm, and (2) the subsequent fear extinction process in these children. Eighty-three child-parent dyads were recruited. The parent was filmed while undergoing a conditioning procedure where one cue was paired with a shock (CS + Parent) and one was not (CS −). Children (8 to 12 years old) watched this video and a video of an adult stranger who underwent conditioning with a different cue reinforced (CS + Stranger). Children were then exposed to all cues (no shocks were delivered) while skin conductance responses (SCR) were recorded. Children exhibited higher SCR to the CS + Parent and CS + Stranger relative to the CS −. Physiological synchronization between the child’s SCR during observational learning and the parent’s SCR during the actual process of fear conditioning predicted higher SCR for the child to the CS + Parent. Our data suggest that children acquire fear vicariously and this can be measured physiologically. These data lay the foundation to examine observational fear learning mechanisms that might contribute to fear and anxiety disorders transmission in clinically affected families.


2019 ◽  
Author(s):  
Yosif Zaki ◽  
William Mau ◽  
Christine Cincotta ◽  
Anahita Hamidi ◽  
Emily Doucette ◽  
...  

AbstractThe formation and extinction of fear memories represent two forms of learning that each engage the hippocampus and amygdala. How cell populations in these areas contribute to fear relapse, however, remains unclear. Here, we demonstrate that, in mice, cells active during fear conditioning in the dentate gyrus of hippocampus and basolateral amygdala exhibit decreased activity during extinction and are re-engaged after fear reinstatement. In vivo calcium imaging reveals that reinstatement drives population dynamics in the basolateral amygdala to revert to a network state similar to the state present during fear conditioning. Finally, we find that optogenetic inactivation of neuronal ensembles active during fear conditioning in either the hippocampus or amygdala is sufficient to disrupt fear expression after reinstatement. These results suggest that fear reinstatement triggers a partial re-emergence of the original fear memory representation, providing new insight into the neural substrates of fear relapse.


eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Mohammed Mostafizur Rahman ◽  
Sonal Kedia ◽  
Giselle Fernandes ◽  
Sumantra Chattarji

Although mGluR5-antagonists prevent fear and anxiety, little is known about how the same receptor in the amygdala gives rise to both. Combining in vitro and in vivo activation of mGluR5 in rats, we identify specific changes in intrinsic excitability and synaptic plasticity in basolateral amygdala neurons that give rise to temporally distinct and mutually exclusive effects on fear-related behaviors. The immediate impact of mGluR5 activation is to produce anxiety manifested as indiscriminate fear of both tone and context. Surprisingly, this state does not interfere with the proper encoding of tone-shock associations that eventually lead to enhanced cue-specific fear. These results provide a new framework for dissecting the functional impact of amygdalar mGluR-plasticity on fear versus anxiety in health and disease.


2017 ◽  
Author(s):  
Jordan M. Ross ◽  
Max L. Fletcher

SummaryAssociative fear learning produces fear toward the conditioned stimulus (CS) and often generalization, the expansion of fear from the CS to similar, unlearned stimuli. However, how fear learning affects early sensory processing of learned and unlearned stimuli in relation to behavioral fear responses to these stimuli remains unclear. We subjected mice to a classical olfactory fear conditioning paradigm and used awake, in vivo calcium imaging to quantify learning-induced changes in glomerular odor responses, which constitutes the first site of olfactory processing in the brain. The results demonstrate that olfactory fear learning non-specifically enhances glomerular odor representations in a learning-dependent manner and increases representational similarity between the CS and non-conditioned odors. This mechanism may prime the system towards generalization of learned fear. Additionally, CS-specific enhancements remain even when associative learning is blocked; suggesting two separate mechanisms lead to enhanced glomerular responses following odor-shock pairings.


2022 ◽  
Author(s):  
Leonardo M Cardozo ◽  
Blythe C Dillingham ◽  
Andre F Sousa ◽  
Westley Dang ◽  
Nicholas Job ◽  
...  

The nature and distribution of the synaptic changes that underlie memory are not well understood. We examined the synaptic plasticity behind context fear learning and found that conditioning produced potentiation of excitatory synapses specifically onto the basolateral amygdala neurons activated during learning. This synaptic potentiation lasted at least 7 days, and its disruption impaired memory recall. High frequency optogenetic stimulation of the CS and US-activated ensembles or biochemical induction of synaptic potentiation in US-responsive neurons alone was sufficient to produce a context fear association without prior associative training. These results suggest that plasticity of CS inputs onto US-responsive amygdala neurons is a necessary and sufficient step in forming context fear associations, and that context discrimination is determined by the CS-specific amygdala inputs activated during retrieval.


Sign in / Sign up

Export Citation Format

Share Document