Role of the Basolateral Amygdala in the Storage of Fear Memories across the Adult Lifetime of Rats

Abstract

The basolateral amygdala (BLA) is intimately involved in the development of conditional fear. Converging lines of evidence support a role for this region in the storage of fear memory but do not rule out a time-limited role in the memory consolidation. To examine this issue, we assessed the stability of BLA contribution to fear memories acquired across the adult lifetime of rats. Fear conditioning consisted of 10 tone-shock pairings in one context (remote memory), followed 16 months later by 10 additional tone-shock pairings with a novel tone in a novel context (recent memory). Twenty-four hours after recent training, rats were given NMDA or sham lesions of the BLA. Contextual and tone freezing were independently assessed in individual test sessions. Sham-lesioned rats showed high and comparable levels of freezing across all context and tone tests. In contrast, BLA-lesioned rats displayed robust freezing deficits across both recent and remote tests. Subsequent open-field testing revealed no effects of BLA lesions on activity patterns in a dark open field or during bright light exposure. Lesioned rats were able to reacquire normal levels of context-specific freezing after an overtraining procedure (76 unsignaled shocks). Together, these findings indicate that BLA lesions do not disrupt freezing behavior by producing hyperactivity, an inability to suppress behavior, or an inability to freeze. Rather, the consistent pattern of freezing deficits at both training-to-lesion intervals supports a role for the BLA in the permanent storage of fear memory.

Mechanisms of fear extinction

“…This is especially true with fear extinction because fear memories can last months or even years with little forgetting. 9 Extinction occurs under a variety of training protocols Generally speaking, any procedure in which the predictive value of the CS with respect to the occurrence of the US is compromised will result in some reduction of the conditioned fear response to the CS. This most obviously applies to the frequently used (and most effective) protocol in which a CS that previously was paired with the US on 100% of its occurrences subsequently is presented repeatedly without further US delivery.…”

Inhibition de l’apprentissage et de la mémoire par les anesthésiques généraux

“…Ablation or deactivation of the amygdala can prevent both the learning and expression of fear. [35][36][37][38][39][40][41] In addition, the amygdala modulates fear-related learning in other brain structures, such as the cortex and hippocampus. [42][43][44][45] Some types of fear conditioning, including the contextual and trace fear conditioning, also involve the hippocampus.…”

“…[46][47][48][49][50][51] Unlike the hippocampus, the amygdala is necessary for the acquisition of fearful memories and their long-term storage and retrieval. 38,[52][53][54] In summary, explicit memory requires structures in the medial temporal lobe, such as the hippocampal formation and several cortical regions. Implicit memory involves a number of diverse brain regions, including the cerebellum, striatum, and midbrain.…”

Developmental emergence of fear learning corresponds with changes in amygdala synaptic plasticity

“…Association of a conditioned stimulus and, for example, footshock in juvenile or adult rats causes activation of the amygdala, and induces a modification of conditioned stimulus-evoked responses of amygdala neurons (Rosenkranz and Grace, 2002). Lesions of the amygdala prevent or retard fear learning and memory (LaBar and LeDoux, 1996, Setlow et al, 2000, Gale et al, 2004. Furthermore, synaptic plasticity of cortical and thalamic inputs to the basolateral nucleus of the amygdala appears necessary for normal fear conditioning (Blair et al, 2001, Maren, 2005, such that manipulations that impair or enhance such plasticity also impair or enhance acquisition of behaviorally expressed learned fear (e.g., (Campeau et al, 1992, Davis et al, 1994, Szinyei et al, 2007.…”