David Chung

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David recently graduated from the University of California, Los Angeles (UCLA), with a major in Applied Mathematics and a minor in Biomedical Research. He has been a part of Dr. Carlos Portera-Cailliau’s lab since April 2019, researching tactile defensiveness behaviors in mice with Fragile X Syndrome. Fragile X syndrome is a neurodevelopmental disorder that often presents with atypical sensory processing and tactile defensiveness. Recently, the Portera-Cailliau Lab reported that the Fmr1 knockout (Fmr1-/-) mouse model exhibits similar avoidance responses to repetitive whisker stimulation. This is accompanied with a lack of adaptation of layer (L) 2/3 neurons in the primary somatosensory cortex (S1) to repetitive whisker stimulation and a lower proportion of whisker-responsive neurons from postnatal day 15. Whisker-evoked activity in L2/3 of S1 is shaped by feedforward inhibition from GABAergic parvalbumin (PV) expressing interneurons, and these PV cells are hypofunctional in primary sensory cortices of Fmr1-/- mice. To test if PV cell hypoactivity is associated with tactile defensiveness, David is investigating the potential of a novel allosteric modulator of Kv3.1 channels to increase PV cell activity in Fmr1-/- mice. These represent the first preclinical studies in a mouse model of autism that investigate the pharmacological manipulation of PV cells to rescue avoidance behaviors. David would like to thank the Portera-Cailliau lab and the Biomedical Research Minor for all the mentorship and guidance in helping him improve as a scientist, and would also like to thank the Amgen Foundation for providing the opportunity to focus on his research.    

David recently graduated from the University of California, Los Angeles (UCLA), with a major in Applied Mathematics and a minor in Biomedical Research. He has been a part of Dr. Carlos Portera-Cailliau’s lab since April 2019, researching tactile defensiveness behaviors in mice with Fragile X Syndrome.

Fragile X syndrome is a neurodevelopmental disorder that often presents with atypical sensory processing and tactile defensiveness. Recently, the Portera-Cailliau Lab reported that the Fmr1 knockout (Fmr1-/-) mouse model exhibits similar avoidance responses to repetitive whisker stimulation. This is accompanied with a lack of adaptation of layer (L) 2/3 neurons in the primary somatosensory cortex (S1) to repetitive whisker stimulation and a lower proportion of whisker-responsive neurons from postnatal day 15. Whisker-evoked activity in L2/3 of S1 is shaped by feedforward inhibition from GABAergic parvalbumin (PV) expressing interneurons, and these PV cells are hypofunctional in primary sensory cortices of Fmr1-/- mice. To test if PV cell hypoactivity is associated with tactile defensiveness, David is investigating the potential of a novel allosteric modulator of Kv3.1 channels to increase PV cell activity in Fmr1-/- mice. These represent the first preclinical studies in a mouse model of autism that investigate the pharmacological manipulation of PV cells to rescue avoidance behaviors.

David would like to thank the Portera-Cailliau lab and the Biomedical Research Minor for all the mentorship and guidance in helping him improve as a scientist, and would also like to thank the Amgen Foundation for providing the opportunity to focus on his research.