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CMBN double seminar

Organized in collaboration with Sunnaas Hospital (Dr. Tor Haugstad)

Tuesday 23rd March 2010 at 1200

Dept of Anatomy (lunch room), Domus Medica, University of Oslo, Gaustad

Refreshments will be served (coffee, biscuits, fruit)


Ellen A. Lumpkin12:00-12:45 Prof. Ellen Lumpkin, Baylor College of Medicine, Houston TX

The cellular and molecular basis of touch sensation in mammals

The goal of our research is to discover mechanotransduction molecules that initiate touch sensation in mammals. Much of our effort focuses on mammalian Merkel cell-neurite complexes, which are exquisitely sensitive touch receptors that encode object shape and fine textures. Merkel cells are enigmatic epidermal cells first described in 1875. The role that these cells play in touch reception has been the subject of controversy for 40 years. Based on morphology, Merkel cells are proposed to be mechanosensory cells that transduce force into membrane-potential changes, and then signal afferent neurons through synaptic transmission. To test this hypothesis, we use mouse genetics, in vitro systems and intact electrophysiological recordings. Our in vitro studies have demonstrated that Merkel cells are force-sensitive and that voltage-activated channels open downstream of mechanical stimuli. To determine whether Merkel cells are necessary for touch responses in the intact skin, we generated mice that selectively lack Merkel cells in the body skin. With intact electrophysiological recordings, we demonstrated a complete absence of one class of light-touch responses in these mice. Collectively, these results suggest that Merkel cells are required for appropriate sensory coding of light touch and pave the way to discover touch transduction mechanisms.


Michael J. Friedlander13:00-13:45 Prof. Michael J. Friedlander, Baylor College of Medicine, Houston TX

Differential synaptic plasticity responses across neurons in the cerebral cortex

Hebbian synaptic plasticity requires proscribed temporal activation of pre- and postsynaptic sites. Spike timing dependent plasticity (STDP) rules predict that postsynaptic spiking that leads presynaptic activation results in long term synaptic depression. We explored the validity of this prediction within the microcircuitry of the neocortex in acute brain slices. Surprisingly, individual sets of synaptic connections of otherwise like type showed dramatic variability in their synaptic plasticity responses to such fixed temporally paired post-presynaptic activation with outcomes of LTP, LTD or no plasticity. Using paired individual cell recording and quantal analysis, we determined that postsynaptic sites followed the PTSD "rule" consistent with AMPA receptor internalization and LTD for postsynaptic spiking leading presynaptic stimulation but presynaptic sites sometimes violated the STDP "rule" by increasing release probability, leading to LTP at identical post-presynaptic pairing delays. These findings are considered in the context of underling molecular mechanisms and impact on information processing within neocortex.

Centre for Molecular Biology and Neuroscience (CMBN)
PO Box 1105 Blindern, NO-0317 Oslo, Norway. Tel: +47 22851528. Fax: +47 22851488