YKavli May Lunch (Zoom)
Please Note: This meeting will be held online via Zoom.
The Kavli Institute for Brain and Mind (KIBM) hosts meetings for early career researchers to help foster their research community at UCSD. Our goal is to bring early career researchers (non-faculty) together so they can meet, network and share research. This event is open only to EARLY CAREER RESEARCHERS (grad student/ postdoc/ project scientist).
Youtong Huang - Microglia use TAM receptors to detect and engulf amyloid beta plaques in Alzheimer’s disease
Bio: I’m a 5th year Ph.D. candidate in Biological Sciences, doing my thesis work happily in the lab of Greg Lemke at the Salk Institute (lab website: http://lemkelab.org)
Abstract: Many Alzheimer’s disease (AD) risk genes are predominantly expressed in microglia, the primary immune cells in the CNS. Two microglial TAM receptor tyrosine kinases - Axl and Mer – have been linked to AD but their roles in disease have not been tested experimentally. We find that in AD and its mouse models, induced expression of Axl and Mer in amyloid plaque-associated microglia is coupled to induced plaque decoration by the TAM ligand Gas6 and its co-ligand phosphatidylserine. Genetic ablation of Axl and Mer results in microglia that are unable to normally detect, respond to, organize, or phagocytose amyloid beta plaques, a hallmark of AD pathology. These major deficits notwithstanding, TAM-deficient AD mice develop fewer dense-core plaques than AD mice. Our findings reveal that the TAM system is an essential mediator of microglial recognition and engulfment of plaques, and that TAM-driven microglial phagocytosis does not constrain, but rather promotes, plaque development.
Shijia Liu - A key hub that orchestrates breathing, pain and anxiety
Bio: Shijia is a PhD candidate in the Biology Program and works at Dr. Sung Han’s lab at the Salk Institute. She is interested in studying the neural circuitry of motivational behaviors and physiology to better understand the brain-body connection.
Abstract: Breathing and pain seem to be unrelated critical brain functions, yet they influence each other. Severe pain induces hyperventilation, whereas paced slow breathing alleviates pain perception. However, a neural circuit-based understanding of this pain-breathing interaction is lacking. Here, we report a neural circuit that controls breathing together with pain and anxiety. We identify breathing rhythm-regulating neurons in the lateral parabrachial nucleus (PBL), which express the µ-opioid receptor (Oprm1). PBLOprm1 neurons rapidly modulate breathing through their projections to the breathing rhythm generator, pre-Bötzinger complex. Moreover, PBLOprm1 neurons are required for noxious stimuli-induced hyperventilation, and inhibiting their activity not only decreases breathing rate but also attenuates affective-motivational pain perception and anxiety-like behaviors. These results suggest that PBLOprm1 neurons are a key hub in the regulation of breathing, pain and anxiety, which may provide a neurobiological understanding of slow-breathing induced hypoalgesia.
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Chair: Robert Gallant, Carmine Chavez-Martinez