Pavlovian fear memory circuits and phenotype models of PTSD

Soldiers With Posttraumatic Stress Disorder See a World Full of Threat: Magnetoencephalography Reveals Enhanced Tuning to Combat-Related Cues

“…Compared to those with PTSD, in soldiers without PTSD combat-word sparing was characterized by early and strong activation of midline frontal regions associated with fear regulation and extinction (22,31,32). In contrast, at mid-latencies, PTSD soldiers showed extensive activation of visual cortex.…”

Activation of Sigma-1 receptor ameliorates anxiety-like behavior and cognitive impairments in a rat model of post-traumatic stress disorder

“…pMAPK is a vital component in fear memory storage, and its activation is therefore an indicator of the neural network underlying the storage of fear memory [57]. It was reported that blockage of ERK on amygdala slices impaired LTP in the LA without affecting routine synaptic transmission, indicating an ERK -dependent process during memory consolidation and synaptic plasticity in the amygdala [55].…”

Epigenetic Mechanisms in Learned Fear: Implications for PTSD

“…In order for newly acquired information to develop into a stable memory, it must be consolidated through a complex set of molecular changes in distinct brain regions that support discrete forms of associative learning. Fear conditioning is a commonly used model of associative learning in rodents, in which memory for a context-shock association is stabilized via hippocampal-dependent consolidation processes, and memory for a cue-shock association is stabilized through amygdala-dependent consolidation processes (see Box 1 and Johnson et al, 2012). Previously consolidated memories can become labile upon recall, wherein an additional set of molecular changes are required for the recalled memory to become updated or re-stabilized in a process that has been termed reconsolidation (McKenzie and Eichenbaum, 2011).…”

“…Although PTSD has been associated with molecular changes in the hippocampus and the prefrontal cortex, the persistent symptoms of PTSD are most closely associated with alterations in the amygdala (Johnson et al, 2012), a region that has been implicated in the storage of remote memories for cued fear (Dudai, 2004;Gale et al, 2004;Medina et al, 2008). The transition of memories to a stable form is important for the persistence of PTSD and it is thus critical to understand the molecular mechanisms that underlie such memory stability in order to identify potential targets for pharmacological treatment.…”