Computing the drainage discharge and assessing the impacts of tunnels drilled in Hard Rocks

International audienceMost Hard Rocks (HR) are or were exposed to deep weathering processes. It turns out that the hydraulic conductivity of HR is mostly inherited from these weathering processes (Lachassagne et al., 2011): (i) within their permeable Stratiform Fissured Layer (SFL) located below the low hydraulic conductivity unconsolidated weathered layer (saprolite). The thickness of both layers often reaches more than 100 m (Dewandel et al., 2006), (ii) and within the permeable vertical fissured layer developed at the periphery of or within preexisting geological discontinuities (joints, dykes, veins, lithological discontinuities, etc.) (Dewandel et al., 2011, Roques et al., 2012). From this conceptual model, the drainage discharge and the surface hydrogeological (piezometry in wells) and hydrological (discharge of streams) impacts of shallow highway tunnels drilled in a metamorphic series (metasedimentary and metavolcanic rocks) intruded by granitic bodies have been forecasted. These tunnels belong to the A89 highway recently opened (2012) in France between Balbigny and La Tour de Salvagny (Monts du Lyonnais, 50 km West of Lyon city). They are up to 4 km long, and their depth below ground level ranges between 0 and 300 m. The method is based on

Expression of Inwardly Rectifying Potassium Channels by an Inducible Adenoviral Vector Reduced the Neuronal Hyperexcitability and Hyperalgesia Produced by Chronic Compression of the Spinal Ganglion

BACKGROUND: A chronic compressed dorsal root ganglion (CCD) in rat produces pain behavior and an enhanced excitability of neurons within the compressed ganglion. Kir2.1 is an inwardly rectifying potassium channel that acts to stabilize the resting potential of certain cell types. We hypothesized that an inducible expression of Kir2.1 channels in CCD neurons might suppress neuronal excitability in the dorsal root ganglion (DRG) and reduce the associated pain behavior. RESULTS: We delivered, by microinjection into the fourth lumbar (L4) DRG, an adenoviral vector containing a reporter gene encoding the enhanced green fluorescent protein (GFP) and a Kir2.1 channel (AdKir). At the same time the ganglion was compressed by implantation of a rod through the intervertebral foramen (CCD). The in vivo expression of the transferred gene was controlled by an ecdysone analog via an ecdysone-inducible promoter in the viral vector. In comparison with the effects of vehicle or a control vector containing only the GFP gene, AdKir significantly reduced the neuronal hyperexcitability after CCD. Electrophysiological recordings, in vivo, from nociceptive and non-nociceptive DRG neurons expressing the virally produced Kir2.1 channels revealed a hyperpolarized resting membrane potential, an increased rheobase, and lack of spontaneous activity. Inducing the Kir2.1 gene at the beginning of CCD surgery partially prevented the development of mechanical hyperalgesia. However, a delayed induction of the Kir2.1 gene (3 days after CCD surgery) produced no significant effect on the pain behavior. CONCLUSIONS: We found that an inducible expression of Kir2.1 channels in chronically compressed DRG neurons can effectively suppress the neuronal excitability and, if induced at the beginning of CCD injury, prevent the development of hyperalgesia. We hypothesize that a higher level of neuronal hyperexcitability in the DRG is required to initiate than to maintain the hyperalgesia and that the hyperexcitability contributing to neuropathic pain is best inhibited as soon as possible after injury