Anna Ingebretson

Postdoctoral Associate,

Anna Ingebretson

Contact Info

Postdoctoral Associate


Summary

My research in the Lemos lab focuses on characterizing how the stress-associated neuropeptide corticotropin releasing factor (CRF) regulates the function of cells and circuits within the striatum in both healthy physiological states and during stressful experiences. Within the nucleus accumbens, cholinergic interneurons are a key target for CRF: these cells express receptors for CRF and respond to CRF receptor activation by increasing their firing rate. I am interested in understanding not only the mechanisms underlying these dynamic rate changes but also the diverse patterns of neural activity in this cell population, which is thought to play a key role in cognition in vivo. I use ex vivo electrophysiology and imaging of neural activity to investigate activity and plasticity in this region. Additionally, within my research I incorporate examining sex as a biological variable and the role gonadal hormones may play in these circuits.

Research

Publications

Madayag A.C., Gomez D., Anderson E.M., Ingebretson A.E., Thomas M.J., and Hearing M.C. (2019). Cell-type and region-specific nucleus accumbens AMPAR plasticity associated with morphine reward, reinstatement, and spontaneous withdrawal. Brain Structure and Function, 224(7), 2311-2324.

Benneyworth M.A., Hearing M.C., Madayag A., Ingebretson A.E., Asp A.J., Schmidt C.E., Silvia K.A., Larson E.B., Ebner S.R., and Thomas, M.J. (2019). Synaptic depotentiation and mGluR5 activity in the nucleus accumbens drive cocaine-primed reinstatement of place preference. Journal of Neuroscience 39(24), 4785-4796.

Ebner S.R., Larson E.L., Hearing M.C., Ingebretson A.E., and Thomas, M.J. (2018). Extinction and reinstatement of cocaine-seeking in self-administering mice is associated with bidirectional AMPAR-mediated plasticity in the nucleus accumbens shell. Neuroscience 384, 340-349.

Ingebretson A.E., Hearing M.C., Huffington E.D., and Thomas, M.J. (2017). Endogenous dopamine and endocannabinoid signaling mediate cocaine-induced reversal of AMPAR synaptic potentiation in the nucleus accumbens shell. Neuropharmacology 131, 154-165.

Hearing M., Jedynak J., Ebner S.R., Ingebretson A., Asp A., Fischer R.A., Schmidt C., Larson E., and Thomas M.J. (2016). Reversal of morphine-induced cell-type specific synaptic plasticity in the nucleus accumbens blocks reinstatement. PNAS 113(3), 757-762.

Jedynak J., Hearing M., Ingebretson A., Ebner S.R., Kelly, M., Fischer, R.A., Kourrich, S., and Thomas M.J. (2016). Cocaine and amphetamine induce overlapping but distinct patterns of AMPAR plasticity in nucleus accumbens medium spiny neurons. Neuropsychopharmacology, 41(2), 464-476.

Olson, M.L., Ingebretson, A.E., and Harmelink, K.J. (2015). Hippocampal cortactin levels are reduced following spatial working memory formation, an effect blocked by chronic calpain inhibition. Brain Sciences 5(2), 541-557.