Yarimar Carrasquillo, Ph.D.
Behavioral, Neurocircuitry and Cellular Plasticity Section
Building 35, Room 1E-410
35 Convent Drive
Bethesda, Maryland 20892
The main goal of the lab is to identify anatomical, molecular and cellular mechanisms that underlie pathological pain states. Research will focus on the amygdala, a structure in the limbic brain system that plays critical roles in the modulation of tactile hypersensitivity, pain-related aversion learning and pain-induced changes in anxiety-related behaviors in rodent models of persistent pain.
Electrophysiological studies have demonstrated that increased excitability of amygdala neurons correlates with persistent pain, suggesting that hyperexcitability of neurons in the amygdala plays a critical role in the modulation of pain hypersensitivity. The specific conductance pathways affected and the molecular mechanisms underlying plasticity of the intrinsic excitability of amygdala neurons, however, are not known. In addition, the physiological role(s) of changes in the excitability of amygdala neurons to pain-related behaviors remain undefined. Research in the lab addresses these questions directly by combining behavioral, biochemical, electrophysiological, pharmacological and molecular genetic approaches.
Parallel studies in the lab use anatomical, behavioral, electrophysiological and optogenetic approaches to define how alterations in the excitability of amygdala neurons affect function at a circuit-level. These studies focus on evaluating the physiological impact of the modulation of neuronal excitability in distinct anatomical pathways to and from the amygdala on different components of persistent pain, including the sensory, affective and cognitive components.
Dr. Carrasquillo received her B.S. in Biology from the University of Puerto Rico, Rio Piedras and her Ph.D. in Neuroscience from Baylor College of Medicine. Her graduate work in the lab of Dr. Robert W. Gereau revealed critical roles for the amygdala in the modulation of persistent pain and also demonstrated that the extracellular signal regulated kinase (ERK) plays a role in this process. Her postdoctoral studies in the lab of Dr. Jeanne Nerbonne at Washington University School of Medicine revealed previously unappreciated molecular and functional diversity of repolarizing voltage-gated, A-type, (IA) K+ currents in central neurons. Dr. Carrasquillo joined the PAIN Branch at NCCIH as an investigator in 2014 where she directs a multifaceted, multidisciplinary research program focused on delineating the anatomical, molecular and cellular mechanisms that underlie pain perception and modulation.
Hu HJ, Carrasquillo Y, Karim F, Jung WE, Nerbonne JM, Schwarz TL, Gereau RW 4th. The kv4.2 potassium channel subunit is required for pain plasticity. Neuron. 2006;50(1):89-100.
Carrasquillo Y, Gereau RW 4th. Activation of the extracellular signal-regulated kinase in the amygdala modulates pain perception. J Neurosci. 2007;27(7):1543-51.
Carrasquillo Y, Gereau RW 4th. Hemispheric lateralization of a molecular signal for pain modulation in the amygdala. Mol Pain. 2008;4:24.
Marionneau C, Carrasquillo Y, Norris AJ, Townsend RR, Isom LL, Link AJ, Nerbonne JM. The sodium channel accessory subunit Navβ1 regulates neuronal excitability through modulation of repolarizing voltage-gated K⁺ channels. J Neurosci. 2012;32(17):5716-27.
Carrasquillo Y, Burkhalter A, Nerbonne JM. A-type K+ channels encoded by Kv4.2, Kv4.3 and Kv1.4 differentially regulate intrinsic excitability of cortical pyramidal neurons. J Physiol. 2012;590(Pt 16):3877-90.
Related Scientific Focus Areas
Molecular Biology and Biochemistry
Social and Behavioral Sciences
This page was last updated on November 4th, 2014