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NINDSNIMHNICHDNIDCDNEINIDCRNIANIAAANIDANHGRI NCCIHNIDDKNIEHSCCB

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Tenure-track Investigator

Yarimar Carrasquillo, Ph.D.

Behavioral, Neurocircuitry and Cellular Plasticity Section, NCCIH


Building 35A Room 1E-410
35 Convent Drive
Bethesda MD 20892
Office: (301) 451-8147

Fax: (301) 480-0772
yarimar.carrasquillo@nih.gov

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.



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.

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  • Jon MacLeod, B.A.
    Postbaccalaureate IRTA

  • 2) Yang, W., Carrasquillo, Y., Hooks, B.M., Nerbonne, J.M. and Burkhalter, A. (2013)
  • Distinct balance of excitation and inhibition in an interareal feedforward and feedback circuit of mouse visual cortex
  • Journal of Neuroscience, 33(44), 17373-84
  • 3) Carrasquillo, Y., Burkhalter, A. and Nerbonne, J.M. (2012)
  • A-type K+ channels encoded by Kv4.2, Kv4.3, and Kv1.4 differentially regulate intrinsic excitability in cortical pyramidal neurons
  • Journal of Physiology, 590, 3877-90
  • 4) Granados-Fuentes, D.*, Norris, A.J.*, Carrasquillo, Y., Herzog, E. and Nerbonne, J.M. (2012)
  • IA Channels Encoded by Kv1.4 and Kv4.2 Regulate Neuronal Firing in the Suprachiasmatic Nucleus and Circadian Rhythms in Locomotor Activity
  • Journal of Neuroscience, 32(29), 10045-10052
  • 5) Carrasquillo, Y.*, Marionneau, C.*, Norris, A.J., Townsend, R.R., Isom, L.L., Link, A.J. and Nerbonne, J.M. (2012)
  • The Sodium Channel Accessory Subunit Navβ1 Regulates Neuronal Excitability through Modulation of Repolarizing Voltage-Gated K+ Channels
  • Journal of Neuroscience, 32(17), 5716-5727
  • 6) Kolber, B., Montana, M., Carrasquillo, Y., Xu, J., Heinemann, S., Muglia, L. and Gereau IV, R.W. (2010)
  • Activation of metabotropic glutamate receptor 5 in the amygdala modulates pain-like behavior
  • Journal of Neuroscience, 30(24), 8203-13
  • 7) Carrasquillo, Y. and Gereau, R.W. (2008)
  • Pain Sensitization. In: Byrne, J.H. (ed.) Learning and Memory: A Comprehensive Reference
  • Oxford: Elsevier, 4, 65-90
  • 8) Carrasquillo, Y. and Gereau IV, R.W. (2008)
  • Hemispheric lateralization of a molecular signal for pain modulation in the amygdala
  • Molecular Pain, 4, 24
  • 9) Hu, H., Alter, B.J., Carrasquillo, Y., Qiu, C. and Gereau IV, R.W. (2007)
  • Metabotropic glutamate receptor 5 modulates nociceptive plasticity via extracellular signal-regulated kinase-Kv4.2 signaling in spinal cord dorsal horn neurons
  • Journal of Neuroscience, 27(48), 13181-91
  • 10) Carrasquillo, Y. and R. W. Gereau IV (2007)
  • Activation of the extracellular signal-regulated kinase in the amygdala modulates pain perception
  • Journal of Neuroscience, 27(7), 1543-51
  • 11) Hu, H.; Carrasquillo, Y., Karim, F., Jung, W., Nerbonne, J.M., Schwarz, T. and Gereau IV, R.W. (2006)
  • The Kv4.2 Potassium Channel Subunit Is Required for Pain Plasticity
  • Neuron, 50(1), 89-100
  • 12) Carrasquillo, Y. and Sweatt, JD. (2005)
  • Craving cocaine pERKs up the amygdala
  • Nature Neuroscience, 8(2), 129-130
  • 13) Carrasquillo, Y. and Gereau, R.W. (2004)
  • Rodent models clarify the role of cells expressing the substance P receptor in pain
  • Drug Discovery Today: Disease Models, 1(2), 107-113
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