Both pre- and posttraining excitotoxic lesions of the basolateral amygdala abolish the expression of olfactory and contextual fear conditioning.

Abstract

The present study examined whether the basolateral amygdaloid complex (BLA) participates in the expression of fear conditioned to both an olfactory conditioned stimulus (CS) and the training context. In Experiment 1, pretraining excitotoxic lesions of the BLA abolished immediate postshock freezing, conditioned freezing to an olfactory CS, and conditioned freezing to the training context. Control experiments indicated that lesioned and sham-lesioned subjects did not differ in locomotor activity or in acquisition of a successive-cue odor discrimination task, suggesting that deficits in freezing behavior exhibited by BLA subjects were not due to an impairment in primary aspects of olfaction or to a general enhancement of locomotor activity. In Experiment 2, excitotoxic lesions of the BLA produced either 1 day or 15 days after olfactory fear conditioning abolished both odor-elicited and contextual freezing. Collectively, these data support the notion that the BLA participates in an enduring manner in the expression of conditioned freezing behavior elicited by both olfactory and contextual stimuli.

Differential Role of Muscarinic Transmission within the Entorhinal Cortex and Basolateral Amygdala in the Processing of Irrelevant Stimuli

“…In fact, animals with impaired muscarinic BLA transmission continue to behave according to the stimulus-no event association under conditions that normally do not support LI. Furthermore, although pharmacological and lesioninduced BLA perturbations, including intra-BLA scopolamine infusion (See et al, 2003), are known to impair conditioning (Cousens and Otto, 1998;Laurent and Westbrook, 2009;Schoenbaum et al, 2003;See et al, 2001), the dose of scopolamine used here did not impair conditioning in the NPE groups conditioned with either two or five trials. It should be noted that there was no behavioral difference between conditioning with two or five trials in the NPE groups suggesting a ceiling effect on performance, but in both cases suppression level was high leaving plenty of room for reduction by intra-BLA muscarinic blockade.…”

Temporary Inactivation of the Bed Nucleus of the Stria Terminalis But Not of the Amygdala Blocks Freezing Induced by Trimethylthiazoline, a Component of Fox Feces

“…Several recent studies have used an odor as a conditioned stimulus (CS) in a fear-conditioning paradigm (Otto et al, 1997;Richardson et al, 1999;Paschall and Davis, 2002). It has been shown that olfactory fear conditioning is mediated by the basolateral nucleus of the amygdala (Cousens and Otto, 1998). Therefore, we suggest that the amygdala would also be necessary for the learning of an association between a CS and TMT.…”

Neural circuits and mechanisms involved in Pavlovian fear conditioning: A critical review

“…In rats, amygdalar lesions impair both acquisition and expression of conditioned increase in blood pressure , potentiated startle (Hitchcock and Davis, 1986;Hitchcock and Davis, 1987), analgesia (Helmstetter, 1992), USV (Goldstein et al, 1996;Lee and Kim, 2004), and freezing (Blanchard and Blanchard, 1972;Cousens and Otto, 1998;Iwata et al, 1986;. Similarly, reversible inactivation of neurons in BLA prior to fear conditioning, via infusing the γ-aminobutyric acid (GABA A ) receptor agonist muscimol, blocks the acquisition of conditioned fear, while amygdalar muscimol infusions (prior to retention testing) in previously fear conditioned rats impair the expression of conditioned fear (Helmstetter and Bellgowan, 1994;Muller et al, 1997;Wilensky et al, 1999).…”