RESUMEN
The consensus view of olfactory processing is that the axons of receptor-specific primary olfactory sensory neurons (OSNs) converge to a small subset of glomeruli, thus preserving the odour identity before the olfactory information is processed in higher brain centres. In the present study, we show that two different subsets of ciliated OSNs with different odorant specificities converge to the same glomeruli. In order to stain different ciliated OSNs in the crucian carp Carassius carassius we used two different chemical odorants, a bile salt and a purported alarm substance, together with fluorescent dextrans. The dye is transported within the axons and stains glomeruli in the olfactory bulb. Interestingly, the axons from the ciliated OSNs co-converge to the same glomeruli. Despite intermingled innervation of glomeruli, axons and terminal fields from the two different subsets of ciliated OSNs remained mono-coloured. By 4-6 days after staining, the dye was transported trans-synaptically to separately stained axons of relay neurons. These findings demonstrate that specificity of the primary neurons is retained in the olfactory pathways despite mixed innervation of the olfactory glomeruli. The results are discussed in relation to the emerging concepts about non-mammalian glomeruli.
Asunto(s)
Carpas/fisiología , Bulbo Olfatorio/metabolismo , Vías Olfatorias/fisiología , Neuronas Receptoras Olfatorias/efectos de los fármacos , Olfato , Animales , Colorantes , Dextranos , Hipoxantinas/farmacología , Bulbo Olfatorio/efectos de los fármacos , Vías Olfatorias/efectos de los fármacos , Neuronas Receptoras Olfatorias/metabolismo , Sinapsis/metabolismo , Ácido Taurolitocólico/farmacologíaRESUMEN
An enormous number of B cells with different B-cell receptors (BCRs) are continuously produced in the bone marrow. BCRs are further diversified during the germinal center reaction. Due to extensive recirculation, B cells with mutually binding BCR are likely to meet in lymphoid organs. We have addressed possible outcomes of such an encounter in vitro. B lymphoma cells were transfected with complementary BCR, one transfectant expressing an Idiotype⺠(Idâº) BCR and the other an anti-Id BCR. To exclude confounding effects of secreted Ig, the transfected B lymphoma cells only expressed membrane IgD. Coincubation of paired Idâº/anti-Id lymphoma cells results in conjugate formation, signaling, activation of Caspase 3/7, and apoptosis of at least one of the two cells in the pair. Our data provide suggestive evidence for a mechanism whereby the B-cell compartment is partly purged of B cells with complementary BCRs.
Asunto(s)
Linfocitos B/inmunología , Tolerancia Inmunológica , Inmunoglobulina D/metabolismo , Región Variable de Inmunoglobulina/inmunología , Receptores de Antígenos de Linfocitos B/inmunología , Animales , Anticuerpos Antiidiotipos/genética , Anticuerpos Antiidiotipos/metabolismo , Apoptosis/genética , Apoptosis/inmunología , Médula Ósea/inmunología , Caspasa 3/metabolismo , Caspasa 7/metabolismo , Diferenciación Celular/genética , Diferenciación Celular/inmunología , Línea Celular Tumoral , Técnicas de Cocultivo , Inmunoglobulina D/genética , Activación de Linfocitos/genética , Proteínas de la Membrana/genética , Proteínas de la Membrana/metabolismo , Ratones , Ratones Endogámicos BALB C , Transducción de Señal/inmunología , Transgenes/genéticaRESUMEN
Organelles in the endocytic pathway interact and communicate through the crucial mechanisms of fusion and fission. However, any specific link between fusion and fission has not yet been determined. To study the endosomal interactions with high spatial and temporal resolution, we enlarged the endosomes by two mechanistically different methods: by expression of the MHC-class-II-associated chaperone invariant chain (Ii; or CD74) or Rab5, both of which increased the fusion rate of early endosomes and resulted in enlarged endosomes. Fast homotypic fusions were studied, and immediately after the fusion a highly active and specific tubule formation and fission was observed. These explosive tubule formations following fusion seemed to be a direct effect of fusion. The tubule formations were dependent on microtubule interactions, and specifically controlled by Kif16b and dynein. Our results show that fusion of endosomes is a rapid process that destabilizes the membrane and instantly induces molecular-motor-driven tubule formation and fission.