Fear Memory

Abstract

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.

Major neurotransmitter systems in dorsal hippocampus and basolateral amygdala control social recognition memory

“…Given the connections between the various amygdala subnuclei (38), our data fit with those of Gur et al (39), showing that Ani given into the medial amygdala disrupts SRM, and with those of Wang et al (40), who showed that lesion of the medial or basolateral amygdala impairs social but not other types of recognition in mice.…”

“…Meanwhile, it can be concluded from the present data that the CA1 region of the dorsal hippocampus and the BLA are key participants in the regulation of SRM in rats, and that norepinephrine acting on β-receptors, dopamine acting on D1/D5 receptors, and histamine acting on H2 receptors in these two brain regions play a pivotal role in social recognition measured in a standard social discrimination paradigm. The roles of the catecholamines (14,18,38), and to an extent that of histamine (16,36), appear peculiarly interesting because they probably affect this (3) and other forms of memory (14) by actions in the hippocampus and BLA, mediated by the enhanced synthesis of the nuclear CREB (3,16,38), which is related to protein synthesis, here shown to be necessary for SRM, as previously posited by Kogan et al (3).…”

Delayed‐onset post‐traumatic stress disorder symptoms in dementia

“…13 The circuitry involves, in addition, cortical structures such as pre-and infralimbic ventromedial prefrontal cortex (see Figure 1). 14 'Fear extinction' is a form of learning thought to underlie the suppression of fear memories. 15 Emerging evidence suggests that stress impairs recovery from trauma by impairing fear extinction, with various functional as well as structural abnormalities identified in the hippocampus, prefrontal cortex and amygdala.…”

Selective post-training time window for memory consolidation interference of cannabidiol into the prefrontal cortex: Reduced dopaminergic modulation and immediate gene expression in limbic circuits

“…Inactivation of the prelimbic and infralimbic subfields reduces fear expression to context and memory extinction, respectively (Corcoran and Quirk, 2007;Sierra-Mercado et al, 2011). In fact, it has been postulated that memory consolidation involves a time-dependent reorganization of activity in the PFC and associated limbic structures (hippocampus, amygdala and entorhinal cortex) (Preston and Eichenbaum, 2013;Izquierdo et al, 2016). In support to this, intra-PFC infusion of dopamine D1, amino-hydroxymethyl-iso xazole propionate (AMPA) and glutamate N-methyl-Daspartate (NMDA) receptor antagonists or infusion of camino-butyrate type A (GABA A ) agonist were shown to interfere with aversive memory consolidation at distinct time windows.…”