Introduction to the Special Issue on the 2011 Tohoku Earthquake and Tsunami

The 11 March 2011 Tohoku earthquake (05:46:24 UTC) involved a massive rupture of the plate‐boundary fault along which the Pacific plate thrusts under northeastern Honshu, Japan. It was the fourth‐largest recorded earthquake, with seismic‐moment estimates of 3–5×10^(22)  N•m (M_w 9.0). The event produced widespread strong ground shaking in northern Honshu; in some locations ground accelerations exceeded 2g. Rupture extended ∼200  km along dip, spanning the entire width of the seismogenic zone from the Japan trench to below the Honshu coastline, and the aftershock‐zone length extended ∼500  km along strike of the subduction zone. The average fault slip over the entire rupture area was ∼10  m, but some estimates indicate ∼25  m of slip located around the hypocentral region and extraordinary slip of up to 60–80 m in the shallow megathrust extending to the trench. The faulting‐generated seafloor deformation produced a devastating tsunami that resulted in 5–10‐km inundation of the coastal plains, runup of up to 40 m along the Sanriku coastline, and catastrophic failure of the backup power systems at the Fukushima Daiichi nuclear power station, which precipitated a reactor meltdown and radiation release. About 18,131 lives appear to have been lost, 2829 people are still missing, and 6194 people were injured (as reported 28 September 2012 by the Fire and Disaster Management Agency of Japan) and over a half million were displaced, mainly due to the tsunami impact on coastal towns, where tsunami heights significantly exceeded harbor tsunami walls and coastal berms

Effects of mecamylamine on the Golgi recurrent collateral--Renshaw-cell synapse in the spinal cord

The fact that mecamylamine is a secondary amine with "nicotinic" blocking properties suggested it would act at the Golgi recurrent collateral--Renshaw-cell synapse in the spinal cord. Glass micropipettes were used to obtain extracellular Renshaw-cell discharges due to antidromic ventral root stimulation in cats anesthetized with pentobarbital. The effects of mecamylamine, hexamethonium, physostigmine, and nicotine given intravenously were determined in this preparation. It was found that mecamylamine reduced the terminal portions of the repetitive discharge of Renshaw cells to antidromic stimulation. The stimulant effect of physostigmine and nicotine on Renshaw cells was blocked by mecamylamine. Hexamethonium in similarly effective ganglionic blocking doses had no effect.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/32383/1/0000458.pd