Brain and Cognition Division

The goal of this research is to understand the neurobiological mechanisms of memory formation. Much of the work examines mechanisms that regulate - turn on and off, amplify and attenuate - the processes that initiate and maintain neural changes representing memory. For example, why do we remember salient events more readily than minor events? This lab has found that certain hormonal responses to an experience, particularly release of epinephrine into the circulation, control how well the memory for that experience will be remembered. Release of epinephrine initiates a physiological cascade that regulates neural plasticity, including increases in blood and brain glucose levels, release of neurotransmitters in the brain, and activation of transcription factors.

Currently, the laboratory is examining neurochemical, cellular and molecular events subsequent to the increases in circulating epinephrine and glucose levels that regulate neural plasticity, with focus on the hippocampus, amygdala, and striatum. These experiments include studies of protein synthesis, signal transduction molecules, transcription factors, and genomic and proteomic responses to the physiological mechanisms that regulate neural plasticity. One goal of the research is to identify drugs that enhance memory, particularly in conditions such as aging, Alzheimer's Disease, and Down syndrome. Another research stream examines effects of stress on multiple memory systems with application to drug abuse.

The laboratory uses interdisciplinary methods ranging from systems to molecular neuroscience: Behavior (learning and memory tasks for rats and mice); Neurophysiology (long-term potentiation); Neurochemistry (microdialysis and HPLC assessments of release of neurotransmitters (e.g., ACh, NE, DA) while rats and mice are learning; Cell and molecular biology (immunocytochemistry, quantitative western analyses, e.g., CREB, pCREB), ELISAs (steroid assays); Genomic and proteomic analyses (via collaborations with other neuroscience laboratories and centers at UIUC).

Representative Publications:

• Qi, Z. and Gold, P.E. (2009). Intrahippocampal infusions of anisomycin produce amnesia: contributions of increased release of norepinephrine, dopamine and acetylcholine. Learning and Memory, 16, 308-314.
• Morris, K.A., Chang, Q., Mohler, E.G., and Gold, P.E. (2009). Age-related memory impairments resulting from decreases in blood glucose responses to epinephrine in Fischer-344 rats. Neurobiology of Aging, in press [preprint available on line].
• Canal, C.E., Chang, Q., and Gold, P.E. (2008). Intra-amygdala injections of CREB antisense impair inhibitory avoidance memory: Role of norepinephrine and acetylcholine. Learning and Memory, 15, 677-686.
• Korol, D.L. and Gold, P.E. (2008). Epinephrine converts LTP from transient to durable form in awake rats. Hippocampus, 18, 81-91.
• Chang, Q. and Gold, P.E. (2008). Age-related changes in memory and in acetylcholine functions in the hippocampus in the Ts65Dn mouse, a model of Down syndrome. Neurobiology of Learning and Memory, 89, 167-177.

Classes Recently Taught:

• Brain, learning and memory (PSYC 414, NEUR 414]
• Dialogues in Neuroscience [MCB 529, NEUR 507, PSYCH 593pg]
• Rotating seminars on topics such as: Molecular biology of memory; Signal transduction mechs of mem; Neurobiol aging; Neural bases of cog pathologies; Hippocampus anat and physiol;...