The long-term objective of this research program is to increase understanding of neurobiological systems involved in regulating the storage of information in the brain.
The specific aims are to investigate 1) the involvement of amygdala nuclei in mediating hormone and drug influences on memory storage; 2) the influence of training, drug and hormone administration on the release of norepinephrine (NE) and acetylcholine (ACh) in the amygdala; and 3) the interaction of the amygdala with other brain regions in modulating memory storage. A first set of experiments will determine whether lesions of the central (CE) or basolateral nucleus (BLA) of the amygdala block adrenergic, opiate, GABAergic and cholinergic influences on memory storage. The experiments will also examine the effects, on memory, of infusions of drugs affecting these systems administered posttraining into the CE or BLA. A second series of experiments will use in vitro microdialysis and high-performance liquid chromatography to examine the release of NE and ACh in the amygdala induced by training and by drugs affecting adrenergic, opiate, GABAergic cholinergic and glucocorticoid systems. A third set of experiments will determine whether lesions of the CE or BLA or drug infusions administered into these amygdala nuclei alter the memory-modulating effects of drugs infused into the striatum, hippocampus or medial septum. The experiments will also determine whether temporary impairment of hippocampal and striatal functioning blocks the modulating effects of drugs infused into the BLA or CE posttraining. The findings of these experiments will significantly increase our understanding of the influences of drugs and hormones on memory storage as well as the role of amygdala nuclei in modulating memory storage. Additionally, the findings should contribute to our knowledge of disorders of learning and memory resulting from damage to hormonal and brain systems and influence the development of therapeutic strategies for the treatment of disorders of learning and 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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