1. ERK, mTOR, and LTP
Panayiotis Tsokas, Tao Ma, Ravi Iyengar, Emmanuel M. Landau, and Robert D. Blitzer

The stable, late form of long-term potentiation (L-LTP) requires de novo protein synthesis. In this weeks Journal, Tsokas et al. dissected the signaling pathways that coordinate translation at the CA3CA1 synapse. Like LTP itself, translation required the coincident activation of two pathways. The kinase mammalian target of rapamycin (mTOR) enables translation of terminal oligopyrimidine messenger RNAs, which in turn encode translational machinery proteins such as elongation factor 1A. Expression of these proteins increased in an mTOR-dependent manner minutes after the authors induced L-LTP with high-frequency stimulation (HFS). Inhibitors of the extracellularly regulated kinase (ERK) pathway reduced expression. Conversely, inhibitors of phosphatidylinositide 3-kinase (PI3K), an upstream component of the mTOR pathway, reduced HFS-induced phosphorylation of ERK, suggesting a reciprocal regulation of the ERK and PI3KmTOR pathways in LTP. The interaction between the two pathways converged at PDK-1 (phosphoinositide-dependent kinase 1).

2. Targeting Regeneration
Xiao-Qing Tang, Paula Heron, Charles Mashburn, and George M. Smith

Getting injured axons to regenerate is only half the battle it seems, as they also have to get to the right target. In the case of sensory axons in the spinal cord, this means getting to, and staying within, the right lamina. Nociceptors that express calcitonin gene-related peptide (CGRP) and Substance P (SP) are normally restricted to lamina I and II. To target axons after a dorsal rhizotomy, Tang et al. used adenovirus to overexpress NGF in the dorsal spinal cord of rats. Three days later, they used more ventral injections to express the repellant guidance molecule semaphoring 3A (Sema3A). NGF-guided axons made it over the barrier of the dorsal root entry zone, but they grew t
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Contact: Sara Harris
sharris@sfn.org
202-962-4000
Society for Neuroscience
29-May-2007