Memory-enhancing intra-basolateral amygdala infusions of clenbuterol increase Arc and CaMKIIα protein expression in the rostral anterior cingulate cortex

Crystal M Holloway-Erickson,Jayme R Mcreynolds,Christa K Mcintyre

doi:10.3389/fnbeh.2012.00017

Crystal M Holloway-Erickson, Jayme R Mcreynolds + Show 1 more

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https://doi.org/10.3389/fnbeh.2012.00017

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Journal: Frontiers in Behavioral Neuroscience	Publication Date: Jan 1, 2012
Citations: 39	License type: cc-by

Abstract

Activation of β-adrenoceptors in the basolateral complex of the amygdala (BLA) modulates memory through interactions with multiple memory systems. The cellular mechanisms for this interaction remain unresolved. Memory-modulating BLA manipulations influence expression of the protein product of the immediate early gene activity-regulated cytoskeletal-associated protein (Arc) in the dorsal hippocampus, and hippocampal expression of Arc protein is critically involved in memory consolidation and long-term potentiation. The present studies examined whether this influence of the BLA is specific to the hippocampus and to Arc protein. Like the hippocampus, the rostral portion of the anterior cingulate cortex (rACC) is involved in the consolidation of inhibitory avoidance (IA) memory, and IA training increases Arc protein in the rACC. Because the BLA interacts with the rACC in the consolidation of IA memory, the rACC is a potential candidate for further studies of BLA modulation of synaptic plasticity. The alpha isoform of the Calcium/Calmodulin-dependent protein kinase II (CaMKIIα) and the immediate early gene c-Fos are involved in long-term potentiation and memory. Both Arc and CaMKIIα proteins can be translated in isolated synapses, where the mRNA is localized, but c-Fos protein remains in the soma. To examine the influence of memory-modulating manipulations of the BLA on expression of these memory and plasticity-associated proteins in the rACC, male Sprague–Dawley rats were trained on an IA task and given intra-BLA infusions of either clenbuterol or lidocaine immediately after training. Findings suggest that noradrenergic stimulation of the BLA may modulate memory consolidation through effects on both synaptic proteins Arc and CaMKIIα, but not the somatic protein c-Fos. Furthermore, protein changes observed in the rACC following BLA manipulations suggest that the influence of the BLA on synaptic proteins is not limited to those in the dorsal hippocampus.

Highlights

Stressful or emotionally arousing events are typically remembered better than emotionally neutral events
We found a significant increase in Arc protein expression in tissue taken from the rostral portion of the anterior cingulate cortex (rACC) of rats that were trained on a single-trial inhibitory avoidance (IA) task, compared to the rACC of naive rats
The main finding of these experiments is that post-training infusions of a memory-enhancing dose of clenbuterol into the basolateral complex of the amygdala (BLA) increase expression of the plasticity-associated proteins Arc and CaMKIIα in the rACC

Summary

Introduction

Stressful or emotionally arousing events are typically remembered better than emotionally neutral events. Extensive evidence indicates that this sympathetic response contributes to the enhancement of memory consolidation through actions on β-adrenoceptors in the basolateral complex of the amygdala (BLA) (Liang et al, 1986; Quirarte et al, 1997; McIntyre et al, 2002; McReynolds et al, 2010). A single footshock is sufficient to produce a longterm contextual memory in rats and increases norepinephrine (NE) levels in the amygdala (Quirarte et al, 1998; McIntyre et al, 2002). Administration of an antagonist to β-adrenoceptors in the BLA blocks the memory enhancement produced by systemic administration of epinephrine (Liang et al, 1986) or the glucocorticoid corticosterone (Quirarte et al, 1997; McReynolds et al, 2010). Direct activation of the noradrenergic system in the amygdala, through infusions of NE or the β-adrenoceptor agonist clenbuterol enhance memory of inhibitory avoidance (IA) training, passive avoidance tasks, contextual fear conditioning, conditioned taste aversion, and object recognition training (Gold and van Buskirk, 1975; Gallagher et al, 1977; Ferry and McGaugh, 1999; Hatfield and McGaugh, 1999; LaLumiere et al, 2003; Miranda et al, 2003; McIntyre et al, 2005; Roozendaal et al, 2008)

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