The Lemos Laboratory investigates how stress is processed and encoded in the brain. Importantly, the lab is interested in understanding how stressors impinge on the brain to alter behavioral responses and outcomes. We are particularly interested in examining how stress-associated neuropeptides regulate the function of neural circuits important for motivation and emotion. My work has focuses on the interaction between neuropeptides such as corticotropin releasing factor (CRF) and dynorphin with monoamine systems such as serotonin and dopamine. In the coming years we will continue to look at these interactions as well as the actions of CRF and dynorphin on network function of motivational circuits such as the striatum. We are also invested in understanding how chronic or traumatic stress renders the brain vulnerable to disease states such as depression, anxiety and addiction.
We use a multidisciplinary technical approach to tackle these questions. Specifically, the lab uses and has expertise in the following techniques: ex vivo slice electrophysiology, ex vivo slice voltammetry, fluorescent in situ hybridization, fluorescent immunohistochemistry, confocal imaging, optogenetics, chemogenetics, transgenics and behavior. Furthermore, we are in the process of setting up in vivo fiber photometry techniques to record activity of specific cell-types in awake behaving animals.
(For a comprehensive list of recent publications, refer to PubMed, a service provided by the National Library of Medicine.)
- Lemos JC, Shin JH, Alvarez VA Corticotropin releasing factor enhances dopamine transients via indirect activation of M5 muscarinic acetylcholine receptors. 2017. In preparation
- Dobbs LK*, Lemos JC,* Alvarez VA. Restructuring of basal ganglia circuitry and associated behaviors triggered by low striatal D2 receptor expression: implications for substance use disorders. Genes Brain Behav. 2017;16(1):56-70. *co-first author listed in alphabetical order
- Lemos JC, Friend DM, Kaplan AR, Shin JH, Rubinstein M, Kravitz AV, Alvarez VA. Enhanced GABA transmission drives bradykinesia following loss of dopamine D2 receptor signaling. Neuron;90(4):824-38.
- Dobbs LK, Kaplan AR, Lemos JC, Matsui A, Rubinstein MR, Alvarez VA. Dopamine regulation of lateral inhibition between striatal neurons gates the stimulant actions of cocaine. Neuron. 2016;90(5):1100-13.
- Wang W, Nitulescu I, Lewis JS, Lemos JC, Bamford IJ, Posielski NM, Storey GP, Phillips PEM, Bamford NS. Overinhibition of corticostriatal activity following prenatal cocaine exposure. Annals of Neurology. 2013;73(3):355-69.