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Les Satin

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Primary Appointment: Pharmacology Department
Other PIBS Depts.: Neuroscience
PubMed Name: Satin L.S. Satin L.
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 DESCRIPTION OF RESEARCH
  Research in my laboratory is concerned with two broad areas: 1) The role of ion channels and membrane excitability in the control of insulin exocytosis from pancreatic islets of Langerhans in health and disease, and 2) the cellular and molecular mechanisms which lead to synaptic dysfunction following traumatic brain injury (TBI). Techniques used in our research include patch clamp electrophysiology, intracellular free [Ca2+] measurements, PCR and RT-PCR, western blotting, FRET, immunocytochemistry, mathematical modeling, cell culture, confocal microscopy, gene transfection (including using adenovirus approaches) and secretion measurements.

We are currently particularly interested in understanding the ionic and metabolic origin of islet calcium and insulin oscillations, as these are disrupted in Type II diabetes mellitus. Ongoing studies include understanding how beta cell fuel metabolism, mitochondrial function, and islet electrophysiology interact using a new model of integrated islet function. A second major and related interest is in understanding cell-to-cell communication within the islet via gap junctions, and islet-islet communication within the pancreas as synchronized activity is crucial for integrated islet function and physiological secretion. A more detailed interest of the laboratory is in the K currents in beta cells, as a novel KCa current called Kslow is likely to be an important pacemaker current in the islet, and it is well known that ATP-sensitive K channels couple metabolism to islet electrical activity. With B. Corkey and L. Moitoso de Vargas of Boston University we are also trying to investigate how fatty acids such as palmitate and oleate specifically target pancreatic beta cells.

The second major area of interest in my lab concerns how membrane deformation of central neurons following traumatic brain injury (TBI) modulates synaptic receptors and contributes to defects in information processing after trauma. It is known that patients suffering from TBI have motor and memory impairments, and in vitro, synapses in the hippocampus are rendered incapable of longterm potentiation after TBI. However, we know little about the effects of trauma on single neurons in the CNS or on synapses. We use a novel in vitro model of neuronal injury to mimic TBI in cultured neurons. We have shown that mild injury leads to depressed NaKATPase function and cell depolarization (Tavalin et al, 1995; 1997), loss of Mg blockade of NMDA receptor function (Zhang et al, 1996), decreased AMPA receptor desensitization (Goforth et al, 1999; 2004), and increased GABA-A receptor function (Kao et al, 2004; all reviewed in Cohen et al, 2007). We are currently focusing on the effects of stretch on mEPSCs and mIPSCs, as well as on single channels. Work in my lab has been supported over many years by the NIDDK, NINDS, and we also have carried out a limited number of industrial studies for biotech and the pharmaceutical industry.