Correction: In an article that appeared in the June 1998 issue of Nature Neuroscience (Vol 1:124–131), the authors, Martin E. Schwab, Michaela Thallmair, Werner Z’Graggen, and Gerlinde Metz, reported that the monoclonal antibody IN-1 promotes collateral sprouting in the rat spinal cord, red nucleus, and pons following a lesion to the corticospinal tract. The sprouting was accompanied by functional recovery. The authors also published a paper in the June 15, 1998 issue of The Journal of Neuroscience (“Functional Recovery and Enhanced Corticofugal Plasticity after Unilateral Pyramidal Tract Lesion and Blockade of Myelin-Associated Neurite Growth Inhibitors in Adult Rats,” pages 4744–4757), which described experiments that were performed in parallel in their laboratory and reached similar conclusions; specifically, whereas the Nature Neuroscience (NN) article concentrated on spinal effects, the Journal of Neuroscience (JNS) paper used identical lesions and antibody treatments and described in detail sprouting in red nucleus and pons as well as functional recovery. Although the data sets are largely unique to each paper, the experimental design and results were very similar. Moreover, some of the data presented in the two papers are also identical (Fig. 5B in NN and Fig. 4A inJNS), whereas other data represent different time points from the same animals (Fig. 6B in NN and Fig. 6A in JNS).
The authors greatly regret that neither of these papers cites the other and that the authors failed to inform the editors of eitherNN or NNS of the existence of another closely related paper that was under consideration elsewhere. The authors also regret that an important result presented in the JNS paper (the effect of a second lesion rostral to the first) was mistakenly described in the NN paper as “W.J.Z., in preparation”) while it was already in press at JNS.
The authors apologize to the editors, referees, and readers of both Nature Neuroscience and The Journal of Neuroscience for these errors and any confusion that they may have caused.