Neuronal ensembles encoding distinct modalities in the mouse somatosensory cortex
Cortical circuits which represent and encode distinct somatosensory modalities, such as heat, cold and pressure, and delineate them from each other are not well understood. Modality-specificity could come about via distinct hard-wired cortical circuits or via distinct spatiotemporal patterns of activity generated within common set of cortical neurons.
We further aim to address the role of cortical inhibition in generating and modulating these ensembles via background suppression. Do all interneurons sculpt the respective spatiotemporal activity patterns in the same way, or are distinct modalities related to distinct classes of interneurons which form the respective sensory codes?
These integrative approaches are expected to provide insights into neuronal ensembles mediating specific modalities of perceptions, which in turn guide specific behaviors. In a broader perspective, we use our model system to ask how functional specificity is generated in cortical circuits.
Luo C, Gangadharan V, Bali KK, Xie RG, Agarwal N, Kurejova M, Tappe-Theodor A, Tegeder I, Feil S, Lewin G, Polgar E, Todd AM, Schlossmann J, Hofmann F, Liu DL, Hu SJ, Feil R, Kuner T*, Kuner R (2012) Presynaptically localized cyclic GMP-dependent Protein Kinase 1 is a key determinant of spinal synaptic potentiation and pain hypersensitivity. PLoS Biol 10(3):e1001283.
Gangadharan V, Wang R, Ulzhöfer B, Luo C, Bardoni R, Bali KK, Agarwal N, Tegeder I, Hildebrandt U, Nagy GG, Todd AJ, Ghirri A, Häussler A, Sprengel R*, Seeburg PH, Macdermott AB, Lewin GR, Kuner R (2011) Peripheral calcium-permeable AMPA receptors regulate chronic inflammatory pain in mice. J Clin Invest 121(4):1608-23.
Luo C, Seeburg PH, Sprengel R*, Kuner R (2008) Activity-dependent potentiation of calcium signals in spinal sensory networks in inflammatory pain states. Pain 140: 358-367.
Hartmann B, Ahmadi S, Heppenstall P, Zeilhofer HU, Lewin G, Schott C, Seeburg PH, Sprengel R*, Kuner R (2004) The AMPA receptor subunits, GluR-A and GluR-B reciprocally modulate spinal synaptic plasticity and inflammatory pain. Neuron 44: 637-650.
*Principal investigators of other projects within the CRC