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. 2008 Apr 3;15(4):238-43.
doi: 10.1101/lm.760908. Print 2008 Apr.

Involvement of basolateral amygdala alpha2-adrenoceptors in modulating consolidation of inhibitory avoidance memory

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Involvement of basolateral amygdala alpha2-adrenoceptors in modulating consolidation of inhibitory avoidance memory

Barbara Ferry et al. Learn Mem. .

Abstract

These experiments investigated the role of the alpha(2)-adrenoceptors of the basolateral nucleus of the amygdala (BLA) in modulating the retention of inhibitory avoidance (IA). In Experiment 1, male Sprague Dawley rats implanted with bilateral cannulae in the BLA received microinfusions of a selective alpha(2)-adrenoceptor antagonist idazoxan 20 min either before or immediately after training. Retention was tested 48 h later. Idazoxan induced a dose-dependent enhancement of retention performance and was more effective when administered post-training. In Experiment 2, animals received pre- or post-training intra-BLA infusions of a selective alpha(2)-adrenoceptor agonist UK 14,304. The agonist induced a dose-dependent impairment of retention performance and, as with the antagonist treatments, post-training infusions were more effective. These results provide additional evidence that consolidation of inhibitory avoidance memory depends critically on prolonged activation of the noradrenergic system in the BLA and indicate that this modulatory influence is mediated, in part, by pre-synaptic alpha(2)-adrenoceptors.

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Figures

Figure 1.
Figure 1.
(Top) Schematic representation of the amygdaloid complex. The solid lines indicate the position of the photomicrograph (bottom) representing the cannula (upper arrow) and the injection tip (lower arrow) placement. BLA, basolateral nucleus of the amygdala; CN, central nucleus of the amygdala.
Figure 2.
Figure 2.
The effects of pre- and post-training infusions of various doses of idazoxan (a selective α2-adrenoceptor antagonist) into the basolateral amygdala on inhibitory avoidance retention latencies. Error bars represent mean ± SEM latency (in seconds) to enter the dark compartment on the retention test. Pre-training groups were infused 20 min before training whereas post-training groups were infused immediately after the footshock administration. *P < 0.05 compared with the corresponding group of the other condition; ***P < 0.001 compared with vehicle-injected group; •P < 0.05; •••P < 0.001; ••P < 0.01 compared with 0.3 μg of idazoxan-injected group in the same condition. n = 9–13 per group.
Figure 3.
Figure 3.
The effects of immediate post-training infusions of various doses of UK 14,304 (a selective α2-adrenoceptor agonist) into the basolateral amygdala on inhibitory avoidance retention latencies. Error bars represent mean ± SEM latency (in seconds) to enter the dark compartment on the retention test. Pre-training groups were infused 20 min before training whereas post-training groups were infused immediately after the footshock administration. **P < 0.01 compared with the corresponding group of the other condition; ***P < 0.001 compared with vehicle-injected group; •••P < 0.001 compared with 0.1 and 1.0 ng of UK 14,304-injected group; ◆◆P < 0.01 compared with 1.0 and 3.0 ng of UK 14,304-injected group. n = 9–12 per group.

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