Issue Cover (August 2015)

Front cover : Argon inhalation after retinal ischemia and reperfusion injury rescued retinal ganglien cells from death. Argons neuroprotective properties thereby comprise the induction of ERK‐1/2 phosphorylation. Immunohistochemistry with anti‐pERK‐1/2 (green fluorescence) and anti‐GFAP (red fluorescence) unveiled that pERK‐1/2 was upregulated in Müller cells (cell bodies in the inner nuclear layer and processes expanding the whole retina) 24 h after ischemiaand reperfusion and Argon treatment. The mechanism, by which Argon exerts ist neuroprotective effects are ‐ at least in part ‐ mediated by the mitogen activated protein kinase ERK‐1/2. Inhibition of ERK‐1/2 results in a reduction of the anti‐apoptotic effects of Argon. Focussing the crucial neuron‐glia‐crosstalk, Argon may be considered as a treatment opportunity in ischemia induced neurodegeneration.Read the full article ‘ Neuroprotective effects of Argon are mediated via an ERK‐1/2 dependent regulation of hemeoxygenase‐1 in retinal ganglion cells ’ by F. Ulbrich, K. B. Kaufmann, M. Coburn, W. Alexander Lagrèze, M. Roesslein, J. Biermann, H. Buerkle, T. Loop and U. Goebel ( J. Neurochem. 2015, vol. 134 (4), pp. 717–727) on doi: 10.1111/jnc.13115