Transplantation approaches using cellular bridges, fetal central nervous system cells, fibroblasts expressing neurotrophin-3 (ref. 6), hybridoma cells expressing inhibitory protein-blocking antibodies, or olfactory nerves ensheathing glial cells transplanted into the acutely injured spinal cord have produced axonal regrowth or functional benefits. Transplants of rat or cat fetal spinal cord tissue into the chronically injured cord survive and integrate with the host cord, and may be associated with some functional improvements. In addition, rats transplanted with fetal spinal cord cells have shown improvements in some gait parameters, and the delayed transplantation of fetal raphe cells can enhance reflexes. We transplanted neural differentiated mouse embryonic stem cells into a rat spinal cord 9 days after traumatic injury. Histological analysis 2-5 weeks later showed that transplant-derived cells survived and differentiated into astrocytes, oligodendrocytes and neurons, and migrated as far as 8 mm away from the lesion edge. Furthermore, gait analysis demonstrated that transplanted rats showed hindlimb weight support and partial hindlimb coordination not found in 'sham-operated' controls or control rats transplanted with adult mouse neocortical cells.

Biochemistry. In the article ''Identification by mass spectrometry of the phosphorylated residue responsible for activation of the catalytic domain of myosin I heavy chain kinase, a member of the PAK͞STE20 family'' by Joanna Szczepanowska, Xiaolong Zhang, Christopher J. Herring, Jun Qin, Edward D. Korn, and Hanna Brzeska, which appeared in number 16, August 5, 1997, of Proc. Natl. Acad. Sci. USA (94,(8503)(8504)(8505)(8506)(8507)(8508), the authors wish to note that in Fig. 3, the ions of m͞z 1345.3 and 1247.1 were incorrectly identified as b 13 and b 13 ⌬ , respectively, produced by cleavage of the peptide AS(Pi)VVGTTYW-MAPEVVK between E and V (Fig. 3 Inset). In fact, these ions are b 12 and b 12 ⌬ , produced by cleavage of the peptide between P and E. This correction has no effect on the conclusion that the phosphorylated residue is serine. Also, in Table 2, reference numbers 22-24 should be 21-23 (the reference in the legend is cited correctly) and the MIHCK sequence is from residue 624 to residue 638.Cell Biology. In the article ''Subtraction hybridization identifies a transformation progression-associated gene PEG-3 with sequence homology to a growth arrest and DNA damageinducible gene'' by Zao

AMPA receptors play a central role in basal excitatory synaptic transmission as well as synaptic maturation and plasticity. The transmembrane AMPA receptor regulatory protein (TARP) stargazin (␥2) serves multiple roles in trafficking and stabilizing synaptic AMPA receptors and may be incorporated as an auxiliary subunit. We wanted to determine whether stargazin altered channel function of neuronal AMPA receptors. Transfection of cultured hippocampal neurons with stargazin produced two distinct effects on AMPA receptor functional properties: a sixfold reduction in glutamate-evoked desensitization and a twofold increase in the relative size of responses to the partial agonist kainate. Kinetic and dose-response analyses suggest that the effect of stargazin on glutamate desensitization results from an allosteric interaction that destabilizes the desensitized state of the receptor and that potentiation of kainate responses reflects increased efficacy rather than a change in affinity. These functional effects were also observed in human embryonic kidney 293 cells transfected with various heteromeric and homomeric AMPA receptors, with distinct subunit-dependent effects on glutamate desensitization, kainate efficacy, and trafficking. Two regions of stargazin mediate its functional effects: the C-terminal intracellular domain seems to be more important for effects on glutamate-evoked desensitization and receptor trafficking, whereas the first extracellular domain makes a larger contribution to effects on kainate efficacy. These data indicate that TARPs are involved both in trafficking and direct modulation of channel function and, as auxiliary subunits of neuronal AMPA receptors, must be considered in the functional heterogeneity of neuronal AMPA receptors.

Toxic zinc influx may contribute to selective neuronal death after transient global ischemia. We previously used the high-affinity (K(D) = 27 nm) fluorescent dye mag-fura-5 to detect initial increases in neuronal intracellular free Zn(2+) ([Zn(2+)](i)) associated with brief Zn(2+) exposure. Here we used the specific low-affinity Zn(2+) indicator Newport Green (K(D) = 1 microm) to measure the peak levels of [Zn(2+)](i) attained during prolonged, toxic exposures to extracellular Zn(2+). Murine cortical cell cultures exposed for 5-10 min to 300 microm Zn(2+) in the presence of kainate or elevated extracellular K(+) developed widespread neuronal death over the next 24 hr. Such Zn(2+) exposure under depolarizing conditions was accompanied by a large increase in [Zn(2+)](i) reaching several hundred nanomolar, which gradually recovered over the next 20-40 min after termination of Zn(2+) exposure. Both the level of [Zn(2+)](i) elevation and the extent of subsequent neuronal death depended on the concentration of extracellular Zn(2+) between 30 microm and 1 mm. In contrast, exposure to 300 microm Zn(2+) in the presence of 300 microm NMDA resulted in little increase in [Zn(2+)](i) and little neuronal death, suggesting that NMDA receptor-gated channels are less important as a route of toxic Zn(2+) entry than voltage-gated calcium channels.