Basolateral amygdala is involved in modulating consolidation of memory for classical fear conditioning - PubMed (original) (raw)

Basolateral amygdala is involved in modulating consolidation of memory for classical fear conditioning

A Vazdarjanova et al. J Neurosci. 1999.

Abstract

Previous findings indicate that the basolateral amygdala complex of nuclei (BLC) is involved in modulating (i.e., enhancing or impairing) memory consolidation for aversive training such as inhibitory avoidance. The present study examined whether the BLC also modulates the consolidation of memory for classical fear conditioning in which a specific context is paired with footshock. Adult male rats with bilateral cannulae targeting the BLC were allowed, first, to habituate in a Y maze that had differently shaped and textured arms. On the next day the rats were placed in one maze arm (shock arm), and they received four unsignaled footshocks. In Experiment 1, immediately after the training some rats received BLC inactivation with lidocaine (10 microgram/0.2 microliter per side), and control rats received buffered saline. In Experiment 2, rats received immediate post-training intra-BLC infusions of the muscarinic receptor agonist oxotremorine (10 ng/0.2 microliter per side) or saline. On a 24 hr retention test each rat was placed in a "safe" arm of the maze and allowed to access all maze arms. Lidocaine-treated rats had impaired memory for the classical fear conditioning when they were compared with the saline-treated controls: they spent less time freezing, entered the shock arm more readily and more often, and spent more time in it. In contrast, oxotremorine-treated rats had a stronger memory for the context-footshock association as assessed by all measures of memory. Thus, post-training treatments affecting BLC function modulate memory for Pavlovian contextual fear conditioning in a manner similar to that found with other types of training.

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Figures

Fig. 1.

A, A schematic drawing illustrating the injector tip placements of saline-injected rats (circles) and lidocaine-injected rats (crosses). Numbers indicate relative position of the coronal sections in millimeters posterior to bregma (Paxinos and Watson, 1997). B, A microphotograph of a representative injector tip location. L, Lateral nucleus; CE, central nucleus; BL, basolateral/basal nucleus; Pir. Cx, piriform cortex. Scale bar, 0.5 mm.

Fig. 2.

Mean percentage of time spent freezing (±SEM) on day 2 before (PreShock) and during (1st–4th PostShock periods) training in rats that received infusions of saline (open circles) or lidocaine (filled squares) into the BLC after the training.

Fig. 3.

Impaired freezing of rats that had received post-training BLC inactivation. Shown is the mean time spent freezing (±SEM) during the retention test on day 3 in saline-treated rats (open bar) and lidocaine-treated rats (shaded bar). *p < 0.0001 compared with the saline group.

Fig. 4.

Impaired avoidance of rats that had received post-training BLC inactivation. A, Mean latencies, in seconds, to the first entry into the shock arm (±SEM) during the retention test on day 3 for the saline group (open bar) and the lidocaine group (shaded bar).B, Mean number of entries in the shock arm (±SEM) during the habituation period (dashed lines) and the retention test (bars). C, Mean percentage of time spent per arm during the habituation period on day 1 (dashed line) and the retention test on day 3 (bars; ±SEM). *p < 0.005 compared with the saline group; **p < 0.05 compared with the respective group’s percentage of time in either of the “safe” arms; +, p < 0.005 compared with the habituation period.

Fig. 5.

Injector tip placements for the subjects in the saline group (circles) and the subjects in the oxotremorine group (crosses). _Numbers_indicate relative position of the coronal sections in millimeters posterior to bregma (Paxinos and Watson, 1997).

Fig. 6.

Mean percentage of time spent freezing (±SEM) on day 2 before (PreShock) and during (1st–4th PostShock periods) training in rats that received infusions of saline (open circles) or oxotremorine (filled squares) into the BLC _after_the training.

Fig. 7.

Enhanced freezing of rats that had received muscarinic cholinergic receptor activation of the BLC after the training. Shown is the mean time spent freezing (±SEM) during the retention test on day 3 in rats that received post-training intra-BLC infusions of saline (open bar) or oxotremorine (shaded bar). *p < 0.005 compared with the saline group.

Fig. 8.

Enhanced avoidance of rats that had received muscarinic cholinergic receptor activation of the BLC after the training. A, Mean latencies, in seconds, to the first entry into the shock arm (±SEM) during the retention test on day 3 for rats in the saline group (open bar) and the oxotremorine group (shaded bar). B, Mean number of entries in the shock arm (±SEM) during the habituation period (dashed line) and the retention test (bars). C, Mean percentage of the time spent per arm during the habituation period on day 1 (dashed line) and the retention test on day 3 (bars; ±SEM). *p < 0.005 compared with the saline group; **p < 0.01 compared with the respective group’s percentage of time in either of the “safe” arms; +,p < 0.0001 compared with the habituation period.

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Basolateral amygdala is involved in modulating consolidation of memory for classical fear conditioning - PubMed (original) (raw)