Loss of heterozygosity on the long arm of chromosome 11 in orbital embryonal rhabdomyosarcoma (OERMS): a microsatellite study of seven cases.

OBJECTIVES. To investigate, by means of microsatellite analysis, regions of chromosome 11 involved in the genesis of embryonal rhabdomyosarcoma (ERMS) localized to the orbit. METHODS. Microsatellite analysis was carried out on seven cases of orbital ERMS by comparing the electrophoretic migration patterns of PCR-amplified microsatellites of chromosome 11 from both constitutional (blood) and tumor genotypes. Five of the tumors analyzed were samples frozen at the time of surgery, and two were paraffin embedded. RESULTS. Overall, microsatellites D11S1396 (11q13.1-q22.3) and D11S976 (11q) showed loss of heterozygosity (LOH) in all tumor samples, thus indicating the presence, on the long arm of chromosome 11, of one or more tumor suppressor genes with a possible role in the genesis of the disease. CONCLUSION. While the role of genes on the short arm of chromosome 11 in the genesis of ERMS is well established, much less is known of the possible involvement of tumor suppressor genes on the long arm of the same chromosome. This is the first report showing the possible involvement of tumor suppressor genes in this portion of the chromosome in ERMS localized to the orbit.

Low-calcium-induced enhancement of chemical synaptic transmission from photoreceptors to horizontal cells in the vertebrate retina.

According to the classical calcium hypothesis of synaptic transmission, the release of neurotransmitter from presynaptic terminals occurs through an exocytotic process triggered by depolarization-induced presynaptic calcium influx. However, evidence has been accumulating in the last two decades indicating that, in many preparations, synaptic transmitter release can persist or even increase when calcium is omitted from the perfusing saline, leading to the notion of a "calcium-independent release" mechanism. Our study shows that the enhancement of synaptic transmission between photoreceptors and horizontal cells of the vertebrate retina induced by low-calcium media is caused by an increase of calcium influx into presynaptic terminals. This paradoxical effect is accounted for by modifications of surface potential on the photoreceptor membrane. Since lowering extracellular calcium concentration may likewise enhance calcium influx into other nerve cells, other experimental observations of "calcium-independent" release may be reaccommodated within the framework of the classical calcium hypothesis without invoking unconventional processes.