RESUMO
This study statistically assesses the relationship between the planktic foraminiferal long-term diversity pattern (~170 Ma to Recent) and four major paleobiological diversification models: (i) the 'Red Queen' (Van Valen, 1973; Raup et al., 1973), (ii) the turnover-pulse (Vrba, 1985; Brett and Baird, 1995), (iii) the diversity-equilibrium (Sepkoski, 1978; Rosenzweig, 1995), and (iv) the 'complicated logistic growth' (Alroy, 2010a). Our results suggest that the long-term standing diversity pattern and the interplay between origination and extinction rates displayed by this group do not correspond to the first three models, but can be more readily explained by the fourth scenario. Consequently, these patterns are likely controlled by a combination of planktic foraminiferal interspecific competition as well as various environmental changes such as marine global temperatures that could impacted the niches within the upper mixed layer within the oceans. Moreover, as other global long-term patterns have been interpreted as reflecting 'complicated logistic growth', this study further suggests that the interplay between abiotic and biotic factors are fundamental elements influencing the evolutionary processes over the extensive history of the biota.
Este estudio evalúa estadísticamente la relación entre el patrón de diversidad global de los foraminíferos planctónicos en el largo plazo (~170 Ma al Reciente) y los cuatro modelos de diversificación propuestos desde la rama de la paleobiología: (i) "Reina Roja" (Van Valen, 1973; Raup et al., 1973), (ii) remplazo pausado (Vrba, 1985; Brett y Baird, 1995), (iii) diversidad en equilibrio (Sepkoski, 1978; Rosenzweig, 1995), y (iv) el "crecimiento logístico complicado" (Alroy, 2010a). Nuestros resultados sugieren que la forma de este patrón global de diversidad y la inter-relación entre las tasas de extinción y originación de este grupo no corresponden con los primeros tres modelos anteriormente citados. Sin embargo, estos pueden ser explicados bajo el cuarto escenario. Consecuentemente, las dinámicas de diversidad (i.e. patrón de diversidad y tasas de extinción y originación) de este grupo posiblemente son controladas por la combinación de la competencia interespecífica de los foraminíferos planctónicos y varios cambios ambientales tales como temperaturas globales marinas que pudieron impactar el número de nichos dentro de la capa superior de los océanos. Además, otros patrones globales de diversidad en el largo plazo han sido interpretados como el reflejo del modelo de crecimiento logístico complicado, lo que sugiere que la relación entre factores abióticos y bióticos tiene un carácter fundamental en los procesos evolutivos que han sucedido a lo largo de la historia de la vida.
RESUMO
Both intracellular pH (pHi) and synaptic cleft pH change during neuronal activity yet little is known about how these pH shifts might affect synaptic transmission by influencing vesicle fusion. To address this we imaged pH- and Ca(2+) -sensitive fluorescent indicators (HPTS, Oregon green) in boutons at neuromuscular junctions. Electrical stimulation of motor nerves evoked presynaptic Ca(2+) i rises and pHi falls (â¼0.1 pH units) followed by recovery of both Ca(2+) i and pHi. The plasma-membrane calcium ATPase (PMCA) inhibitor, 5(6)-carboxyeosin diacetate, slowed both the calcium recovery and the acidification. To investigate a possible calcium-independent role for the pHi shifts in modulating vesicle fusion we recorded post-synaptic miniature end-plate potential (mEPP) and current (mEPC) frequency in Ca(2+) -free solution. Acidification by propionate superfusion, NH(4)(+) withdrawal, or the inhibition of acid extrusion on the Na(+)/H(+) exchanger (NHE) induced a rise in miniature frequency. Furthermore, the inhibition of acid extrusion enhanced the rise induced by propionate addition and NH(4)(+) removal. In the presence of NH(4)(+), 10 out of 23 cells showed, after a delay, one or more rises in miniature frequency. These findings suggest that Ca(2+) -dependent pHi shifts, caused by the PMCA and regulated by NHE, may stimulate vesicle release. Furthermore, in the presence of membrane permeant buffers, exocytosed acid or its equivalents may enhance release through positive feedback. This hitherto neglected pH signalling, and the potential feedback role of vesicular acid, could explain some important neuronal excitability changes associated with altered pH and its buffering.