Post-training intrabasolateral amygdala infusions of dopamine modulate consolidation of inhibitory avoidance memory: involvement of noradrenergic and cholinergic systems

Authors

  • Ryan T. LaLumiere,

    1. Center for the Neurobiology of Learning and Memory, Department of Neurobiology and Behavior, University of California, Irvine, CA 92697–3800, USA
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  • Linda T. Nguyen,

    1. Center for the Neurobiology of Learning and Memory, Department of Neurobiology and Behavior, University of California, Irvine, CA 92697–3800, USA
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  • James L. McGaugh

    1. Center for the Neurobiology of Learning and Memory, Department of Neurobiology and Behavior, University of California, Irvine, CA 92697–3800, USA
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Ryan T. LaLumiere, as above.
E-mail: rlalumie@uci.edu

Abstract

There is extensive evidence that several neurotransmitter systems within the basolateral amygdala (BLA) influence memory consolidation. The present study investigated the influence of dopamine (DA) in the BLA on the consolidation of memory for inhibitory avoidance (IA) training. Male Sprague–Dawley rats (≈300 g) were trained on a step-through IA task and, 48 h later, tested for retention as indexed by their latencies to enter the shock compartment on the test day. Drugs were infused into the BLA or central amygdala nucleus (CEA) immediately or 3 h after training via bilateral cannulae. DA infused into the BLA immediately after training enhanced retention, whereas DA infused into the BLA 3 h after training or into the CEA did not affect retention. Infusions of the dopaminergic antagonist cis-Flupenthixol together with DA blocked the DA-induced memory enhancement. Immediate post-training intra-BLA infusions of the D1 receptor antagonist SCH 23390 or the D2 receptor antagonist sulpiride impaired retention. β-adrenergic or muscarinic cholinergic receptor antagonists coinfused into the BLA with DA blocked the memory enhancing effects of DA. These findings indicate that dopaminergic activation within the BLA modulates memory consolidation and that the modulation involves activation of both D1 and D2 receptors and concurrent activation of β-adrenergic and cholinergic influences within the BLA.

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