Synaptotagmins 1 and 7 in vesicle release from rods of mouse retina.

Synaptotagmins are the primary Ca2+ sensors for synaptic exocytosis. Previous work suggested synaptotagmin-1 (Syt1) mediates evoked vesicle release from cone photoreceptor cells in the vertebrate retina whereas release from rods may involve another sensor in addition to Syt1. We found immunohistochemical evidence for syntaptotagmin-7 (Syt7) in mouse rod terminals and so performed electroretinograms (ERG) and single-cell recordings using mice in which Syt1 and/or Syt7 were conditionally removed from rods and/or cones. Synaptic release was measured in mouse rods by recording presynaptic anion currents activated during glutamate re-uptake and from exocytotic membrane capacitance changes. Deleting Syt1 from rods reduced glutamate release evoked by short depolarizing steps but not long steps whereas deleting Syt7 from rods reduced release evoked by long but not short steps. Deleting both sensors completely abolished depolarization-evoked release from rods. Effects of various intracellular Ca2+ buffers showed that Syt1-mediated release from rods involves vesicles close to ribbon-associated Ca2+ channels whereas Syt7-mediated release evoked by longer steps involves more distant release sites. Spontaneous release from rods was unaffected by eliminating Syt7. While whole animal knockout of Syt7 slightly reduced ERG b-waves and oscillatory potentials, selective elimination of Syt7 from rods had no effect on ERGs. Furthermore, eliminating Syt1 from rods and cones abolished ERG b-waves and additional elimination of Syt7 had no further effect. These results show that while Syt7 contributes to slow non-ribbon release from rods, Syt1 is the principal sensor shaping rod and cone inputs to bipolar cells in response to light flashes.

Mammomonogamus laryngeus (Railliet, 1899) infection in buffaloes in Rio Grande do Sul, Brazil.

Parasites of the genus Mammomonogamus affect the respiratory tract of domestic animals. The present study was carried out to determine the presence of Mammomonogamus laryngeus infection and to analyze its lesions in infected buffaloes in Rio Grande do Sul, Brazil, between April and November 1999. The infection rate was 30.5%. In 32 infected buffaloes, the worm pairs collected per animal did not exceed 20. The microscopic diagnosis showed intense polypoid to intramucosal proliferation at the entrance to the pharynx, to which the parasites had adhered, with foci of multifocal hydropic degeneration of the epithelium or individual degeneration of epithelial cells with mild intraepithelial inflammatory infiltrate. The submucosa revealed intense lymphocyte infiltrate extending into the salivary glands. The submucosa also showed formation of structures that resemble lymphoid follicles.