Synaptic encoding of fear memories in the amygdala

Abstract

Over the years Pavlovian fear conditioning has proved to be a powerful model to investigate the neural underpinnings of aversive associative memory formation. Although it is well appreciated that plasticity occurring at excitatory synapses within the basolateral complex of the amygdala (BLA) plays a critical role in associative memory formation, recent evidence suggests that plasticity within the amygdala is more distributed than previously appreciated. In particular, studies demonstrate that plasticity in the central nucleus (CeA) is critical for the acquisition of conditioned fear. In addition, a variety of interneuron populations within the amygdala, defined by unique neurochemical markers, contribute to distinct aspects of stimulus processing and memory formation during fear conditioning. Here, we will review and summarize recent advances in our understanding of amygdala networks and how unique players within this network contribute to synaptic plasticity associated with the acquisition of conditioned fear.

Deletion of the creatine transporter gene in neonatal, but not adult, mice leads to cognitive deficits

“…Interestingly, conditioned fear behavior was not affected in either group of mice tested. Conditioned fear is thought to be based primarily in the amygdala, which reaches its peak development around gestational day 12 in the mouse . The lack of a conditioned fear phenotype and the presence of deficits in hippocampally based behaviors in the P5KO mice suggest that Cr may play an important role in the development of this brain region as well.…”

Neural circuit mechanism underlying the feeding controlled by insula-central amygdala pathway

“…Neurons in CeA have been widely reported to play important roles in fear conditioning, anxiety, pain, reward processing, and feeding behaviors (Duvarci et al, 2011;Fadok et al, 2018;Gilpin et al, 2015;Janak and Tye, 2015;Johansen et al, 2011;LeDoux, 2000;Ressler and Maren, 2019;Thompson and Neugebauer, 2017). Accordingly, it is not surprising that many different types of CeA neurons were identified based on their distinct electrophysiological properties, neuropeptides or other genetic markers (Day et al, 1999;Haubensak et al, 2010;Kim et al, 2017;van den Burg and Stoop, 2019).…”

Bridging Biological and Artificial Neural Networks with Emerging Neuromorphic Devices: Fundamentals, Progress, and Challenges

“…[248] This brings the investigation of learning and memory to the cell population and circuitry level. [248] This brings the investigation of learning and memory to the cell population and circuitry level.…”

“…[247] The existence of engrams is posited to explain the persistence of memory (Figure 11). [248] Recently, engram cells for particular memories have been demonstrated in the brain. [249] They are reactivated by specific cues associated with the training experience and has been shown to be able to mediate memory retrieval when activated artificially with optogenetic techniques.…”

“…Recent advances in neuroscience techniques have allowed us to observe and manipulate a population of neurons encoding a memory engram, the engram cells. [248] This brings the investigation of learning and memory to the cell population and circuitry level. Such memory might not be formed arbitrarily from a tabula rasa as typically done in computer memories, but might be highly regulated and organized according to innate principles.…”