The overall objective of this research program is to understand the neurobiological systems regulating the consolidation of long-term memory. Previous research has shown that stress hormones and activation of the amygdala enhance the consolidation of recent experiences. Such evidence suggests that the amygdala regulates the strength of memory in relation to the significance of experiences.
The specific aims of the experiments are to determine: 1) neuromodulatory interactions within the basolateral region of the amygdala (BLA) that are critically involved in regulating memory consolidation, 2) BLA regulation of the consolidation of different aspects or forms of memory, and 3) BLA influences on other brain regions involved in consolidation of different aspects or forms of memory. Experiments will use intra-BLA infusions administered to rats after inhibitory avoidance training to test the specific hypothesis that muscarinic cholinergic activation in the BLA is critical for the effects, on memory consolidation, of drugs affecting other neuromodulatory systems, including noradrenergic and GABAergic systems. Experiments will also use in vivo microdialysis and high performance liquid chromatography to determine the effects of inhibitory avoidance training on the release of norepinephrine and acetyicholine in the BLA. Other experiments will use intra-BLA infusions of memory-enhancing doses of noradrenergic and muscarinic cholinergic drugs administered after either context exposure or a brief footshock to determine whether the infusions differentially affect memory for the context or shock experiences. Experiments using intra-BLA drug infusions administered after exposure to context or footshock will determine BLA influences on memory processing in other brain regions. The findings of these experiments will significantly increase our understanding of the functioning of BLA activation in regulating the consolidation of long-term memory. Additionally, as the BLA mediates stress hormone-induced enhancement of memory consolidation, the findings may have important implications for understanding and treating disorders of emotionally influenced memory.
| Ferry, Barbara; Parrot, Sandrine; Marien, Marc et al. (2015) Noradrenergic influences in the basolateral amygdala on inhibitory avoidance memory are mediated by an action on ?2-adrenoceptors. Psychoneuroendocrinology 51:68-79 |
| McGaugh, James L (2015) Consolidating memories. Annu Rev Psychol 66:1-24 |
| Chavez, Candice M; McGaugh, James L; Weinberger, Norman M (2013) Activation of the basolateral amygdala induces long-term enhancement of specific memory representations in the cerebral cortex. Neurobiol Learn Mem 101:8-18 |
| Patihis, Lawrence; Frenda, Steven J; LePort, Aurora K R et al. (2013) False memories in highly superior autobiographical memory individuals. Proc Natl Acad Sci U S A 110:20947-52 |
| McGaugh, James L (2013) Making lasting memories: remembering the significant. Proc Natl Acad Sci U S A 110 Suppl 2:10402-7 |
| LePort, Aurora K R; Mattfeld, Aaron T; Dickinson-Anson, Heather et al. (2012) Behavioral and neuroanatomical investigation of Highly Superior Autobiographical Memory (HSAM). Neurobiol Learn Mem 98:78-92 |
| McIntyre, Christa K; McGaugh, James L; Williams, Cedric L (2012) Interacting brain systems modulate memory consolidation. Neurosci Biobehav Rev 36:1750-62 |
| Roozendaal, Benno; McGaugh, James L (2011) Memory modulation. Behav Neurosci 125:797-824 |
| McReynolds, Jayme R; Donowho, Kyle; Abdi, Amin et al. (2010) Memory-enhancing corticosterone treatment increases amygdala norepinephrine and Arc protein expression in hippocampal synaptic fractions. Neurobiol Learn Mem 93:312-21 |
| Barsegyan, Areg; Mackenzie, Scott M; Kurose, Brian D et al. (2010) Glucocorticoids in the prefrontal cortex enhance memory consolidation and impair working memory by a common neural mechanism. Proc Natl Acad Sci U S A 107:16655-60 |
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