Adaptation in auditory-nerve fibers: A revised model

Adaptation of firing rates in auditory-nerve fibers appears to reflect two distinct processes. Rapid adaptation occupies the first few milliseconds of response and is superimposed upon short-term adaptation which has a time constant of about 40 ms. The properties of the two processes are reviewed and compared, and a phenomenological model is developed that successfully accounts for them. The model consists of several stages which have been tentatively associated with underlying physiological processes. In the first stage stimulus intensity is transformed by a static nonlinearity, followed by a low-pass filter. The filtered output may correspond to the hair-cell receptor potential. It modulates the release of a substance that possibly represents synaptic transmitter. Adaptation is produced by the depletion of transmitter which is located in three stores in cascade. A global store with fixed concentration controls the steady-state response and replenishes a local store which is responsible for short-term adaptation. The local store seplenishes a rapidly depleted immediate store. Flow between stores is proportional to concentration gradients with the following exceptions. The immediate store is subdivided into independent volumes or sites and there is no flow among sites or back to the local store. A given site becomes activated only when the receptor potential exceeds its particular activation value and the number of activated sites is proportional to the receptor potential. The flow of transmitter from the immediate store is assumed to be proportional to neural firing rate, with some minor modifications described in the text. The properties of the model are determined from the underlying equations and from a computer simulation. The model produces realistic response properties including PST histograms, onset and steady-state rate-intensity functions, incremental and decremental responses, response modulation for amplitude modulated stimuli, and period histograms for low-frequency tones.     

Mechanisms of integrin-mediated calcium signaling in MDCK cells: regulation of adhesion by IP3- and store-independent calcium influx.

Peptides containing Arg-Gly-Asp (RGD) immobilized on beads bind to integrins and trigger biphasic, transient increases in intracellular free Ca2+ ([Ca2+]i) in Madin-Darby canine kidney epithelial cells. The [Ca2+]i increase participates in feedback regulation of integrin-mediated adhesion in these cells. We examined influx pathways and inositol 1,4,5-trisphosphate (IP3)-mediated Ca2+ store release as possible sources of the [Ca2+]i rise. The RGD-induced [Ca2+]i response requires external Ca2+ (threshold approximately 150 microM), and its magnitude is proportional to extracellular calcium. RGD-induced transients were attenuated by Ca2+ channel inhibitors (Ni2+ and carboxy-amidotriazole) or by plasma membrane depolarization, indicating that Ca2+ influx contributes to the response. Loading cells with heparin reduced the size of RGD-induced [Ca2+]i transients, indicating that IP3-mediated release of Ca2+ from stores may also contribute to the RGD response. Depletion of Ca2+ stores with thapsigargin activated Ni(2+)-sensitive Ca2+ influx that might also be expected to occur after IP3-mediated depletion of stored Ca2-. However, RGD elicited a Ni(2+)-sensitive Ca2+ influx even after pretreatment with thapsigargin, indicating that Ca2+ influx is controlled by a mechanism independent of IP3-mediated store depletion. We conclude that RGD-induced [Ca2+]i transients in Madin-Darby canine kidney cells result primarily from the combination of two distinct mechanisms: 1) IP3-mediated release of intracellular stores, and 2) activation of a Ca2+ influx pathway regulated independently of IP3 and Ca2+ store release. Because Ni2+ and carboxy-amidotriazole inhibited adhesion, whereas store depletion with thapsigargin had little effect, we suggest that the Ca2+ influx mechanism is most important for feedback regulation of integrin-mediated adhesion by increased [Ca2+]i.     

Mechanism of store-operated calcium entry

Activation of receptors coupled to the phospholipase C/IP₃ signalling pathway results in a rapid release of calcium from its intracellular stores, eventually leading to depletion of these stores. Calcium store depletion triggers an influx of extracellular calcium across the plasma membrane, a mechanism known as the store-operated calcium entry or capacitative calcium entry. Capacitative calcium current plays a key role in replenishing calcium stores and activating various physiological processes. Despite considerable efforts, very little is known about the molecular nature of the capacitative channel and the signalling pathway that activates it. This review summarizes our current knowledge about store operated calcium entry and suggests possible hypotheses for its mode of activation.     

Impact of short-term rainfall fluctuation on interannual land cover change in sub-Saharan Africa

Aim Interannual land cover change plays a significant role in food security, ecosystem processes, and regional and global climate modelling. Measuring the magnitude and location and understanding the driving factors of interannual land cover change are therefore of utmost importance to improve our understanding and prediction of these impacts and to better differentiate between natural and human causes of land cover change. Despite advances in quantifying the magnitude of land cover change, the interpretation of the observed land cover change in terms of climatic, ecological and anthropogenic processes still remains a complex issue. In this paper, we map land cover change across sub‐Saharan Africa and examine the influences of rainfall fluctuations on interannual change. Location The analysis was applied to sub‐Saharan Africa. Methods Ten‐day rainfall estimates (RFE) obtained from National Oceanic and Atmospheric Administration's (NOAA) Climate Prediction Center (CPC) were used to extract information on inter and intra‐annual rainfall fluctuations. The magnitude of land cover change was quantified based on the multitemporal change vector method measuring year‐to‐year differences in bidirectional reflectance distribution function (BRDF) corrected 16‐day enhanced vegetation index (EVI) data from the Moderate Resolution Imaging Spectro‐radiometer (MODIS). Statistical models were used to estimate the relationship between short‐term rainfall variability and the magnitude of land cover change. The analysis was stratified first by physiognomic vegetation type and second by chorological data on species distribution to gain insights into spatial variations in response to short‐term rainfall fluctuations. Results The magnitude of land cover change was significantly related to rainfall variability at the 5% level. Stratification considerably strengthened the relationship between the magnitude of change and rainfall variability. Explanatory power of the models ranged from R² = 0.22 for the unstratified model to 0.40–0.96 for the individual models stratified by patterns of species distribution. The total variability explained by the combined models including the influence of rainfall and differences in vegetation response ranged from 22% for the model not stratified by vegetation to 76% when stratified by chorological data. Main conclusions Using this methodology, we were able to measure the contribution of natural variation in precipitation to land cover change. Several ecosystems across sub‐Saharan Africa are highly sensitive to short‐term rainfall variability.     

Voltage- and Ca2+-activated potassium channels in Ca2+ store control Ca2+ release

Ca2+ release from Ca2+ stores is a 'quantal' process; it terminates after a rapid release of stored Ca2+. To explain the quantal nature, it has been supposed that a decrease in luminal Ca2+ acts as a 'brake' on store release. However, the mechanism for the attenuation of Ca2+ efflux remains unknown. We show that Ca2+ release is controlled by voltage- and Ca2+-activated potassium channels in the Ca2+ store. The potassium channel was identified as the big or maxi-K (BK)-type, and was activated by positive shifts in luminal potential and luminal Ca2+ increases, as revealed by patch-clamp recordings from an exposed nuclear envelope. The blockage or closure of the store BK channel due to Ca2+ efflux developed lumen-negative potentials, as revealed with an organelle-specific voltage-sensitive dye [DiOC5(3); 3,3'-dipentyloxacarbocyanine iodide], and suppressed Ca2+ release. The store BK channels are reactivated by Ca2+ uptake by Ca2+ pumps regeneratively with K+ entry to allow repetitive Ca2+ release. Indeed, the luminal potential oscillated bistably by approximately 45 mV in amplitude. Our study suggests that Ca2+ efflux-induced store BK channel closures attenuate Ca2+ release with decreases in counter-influx of K+.     

A realistic model of biphasic calcium transients in electrically nonexcitable cells.

In many electrically nonexcitable cells, the release of calcium from internal stores is followed by a much slower phase in which the intracellular calcium concentration decreases gradually to a sustained value higher than the concentration before stimulation. This elevated calcium plateau has been shown to be the result of calcium influx. The model presented in this work describes a system consisting of a cytoplasmic calcium store and a plasma membrane calcium channel, both excitable by a membrane receptor; a fast cytoplasmic calcium buffer; and calcium pumps in both the calcium store and cellular membranes. Inherent difficulties in the numerical evaluation of the model, caused by very large calcium fluxes across the store membrane, were overcome by analytically separating the fast processes of calcium release from the slower processes of calcium cycling across the plasma membrane. This enabled the simulation of realistic biphasic calcium transients similar to those observed experimentally. The model predicted 1) a strong correlation between the rate of calcium cycling across the plasma membrane and the rate of calcium decay; and 2) a dependence on the level of cell excitation of the maximum rise in cytoplasmic calcium concentration, the level of the elevated calcium plateau, and the rate of calcium decay. Using the model, we simulated the washout of agonist from the bathing solution and the depletion of the calcium store by a pharmacological agent (such as thapsigargin) under several experimental conditions.     

毛乌素沙地流动沙丘不同深度土壤渗漏特征

沙地的土壤深漏是沙地水分循环及水量平衡中的重要环节,对这一分量的准确测算,能够增进对沙地降雨的分配、转移及运输过程规律的认识。利用土壤深层水量渗漏测试记录仪(YWB-01),对毛乌素沙地典型的流动沙丘50、100 cm和200 cm的3个层次的土壤渗漏水量进行定点实时监测,定量分析降雨条件下沙地土壤渗漏特征,得出以下结论:(1)在降雨条件下,2016年4—6月3个沙层的渗漏过程都不明显,从7月开始,渗漏过程与降雨过程的一致性随沙层的增加而逐渐减弱;(2)随沙层深度的增加,累计渗漏天数以及连续渗漏天数在增加,累计渗漏水量、最大日渗漏水量逐渐减小,渗漏水量的波动也逐渐减小;渗漏水量10 mm的天数和渗漏水量所占的比例明显减少;(3)对降雨量和各沙层渗漏水量日、周、半月、月累积量之间进行相关分析和线性拟合后发现,越往深处渗漏水量对降雨的响应越弱,月渗漏水量与月降雨量的关系更密切。     

Modelling carbon dynamics in coniferous forest soils in a temperature gradient

Climate change and changes in land use will alter the stores of carbon and turnover of soil organic matter. We have used a theory for carbon cycles in terrestrial ecosystems to analyse changes in soil organic matter turnover in coniferous forests. The central concepts of the theory are a continuously changing substrate quality, a constant decomposer efficiency and a climatically controlled decomposer growth rate. Measurements on litter production and soil carbon stores from field experiments have been used to successfully validate the model predictions. Measured litter production increased with increasing temperature but the response was not identical for forests of different vegetation types which reflect variations in productivity. The temperature response of needle-litter production and decomposition rate were strongest in the most productive forests and weakest for the low productive forests. Initial decay rates of soil C store from steady state showed the same trend in temperature response as decay of a single litter cohort did, but the absolute values are 16% of the decay rates of a single litter cohort. Predicted soil C ranged from 5 to 9 kg C m^–2. There exists a remarkable variation in forest soil C store response to temperature; the magnitude and even the sign depends on productivity as defined by vegetation type. The assumption that, in general, decomposition rates increase more than NPP with temperature, and consequently, soil C stores should decrease in response to a climate warming, seems therefore too simplistic.     

Calcium release in HSY cells conforms to a steady-state mechanism involving regulation of the inositol 1,4,5-trisphosphate receptor Ca2+ channel by luminal [Ca2+]

In many cell types, low concentrations of inositol 1,4,5-trisphosphate (IP3) release only a portion of the intracellular IP3-sensitive Ca2+ store, a phenomenon known as "quantal" Ca2+ release. It has been suggested that this effect is a result of reduced activity of the IP3- dependent Ca2+ channel with decreasing calcium concentration within the IP3-sensitive store ([Ca2+]s). To test this hypothesis, the properties of IP3-dependent Ca2+ release in single saponin-permeabilized HSY cells were studied by monitoring [Ca2+]s using the Ca(2+)-sensitive fluorescent dye mag-fura-2. In permeabilized cells, blockade of the sarco/ER Ca(2+)-ATPase pump in stores partially depleted by IP3 induced further Ca2+ release via an IP3-dependent route, indicating that Ca2+ entry via the sarco/ER Ca(2+)-ATPase pump had been balanced by Ca2+ loss via the IP3-sensitive channel before pump inhibition. IP3- dependent Mn2+ entry, monitored via quenching of luminal mag-fura-2 fluorescence, was readily apparent in filled stores but undetectable in Ca(2+)-depleted stores, indicating markedly reduced IP3-sensitive channel activity in the latter. Also consistent with reduced responsiveness of Ca(2+)-depleted stores to IP3, the initial rate of refilling of these stores was unaffected by the presence of 0.3 microM IP3, a concentration that was clearly effective in eliciting Ca2+ release from filled stores. Analysis of the rate of Ca2+ release at various IP3 concentrations indicated a significant shift of the IP3 dose response toward higher [IP3] with decreasing [Ca2+]s. We conclude that IP3-dependent Ca2+ release in HSY cells is a steady-state process wherein Ca2+ efflux via the IP3 receptor Ca2+ channel is regulated by [Ca2+]s, apparently via changes in the sensitivity of the channel to IP3.     

Store-operated Ca2+ entry uncoupled with ryanodine receptor and junctional membrane complex in heart muscle cells

Store-operated Ca2+ entry (SOCE) is the Ca2+ influx that is activated on depletion of intracellular Ca2+ stores. Although SOCE is found in a variety of cell types, its activation mechanism and molecular identity remain to be clarified. Current experimental results suggest that SOCE channels are activated by direct coupling with Ca2+ release channels on depleted stores. Here we report SOCE in cardiac myocytes, that was prominently sensitive to Zn2+ but resistant to inhibitors for voltage-dependent Ca2+ channels and Na+/Ca2+ exchangers. The SOCE activity may be developmentally regulated, because the SOCE was easily detected during embryonic and neonatal stages but not in mature myocytes from adult hearts. In cardiac myocytes, ryanodine receptor type 2 (RyR-2) is thought to be the sole Ca2+ release channel on the intracellular store, and junctophilin type 2 (JP-2) contributes to formation of the junctional complex between the cell surface and store membranes. Using the knockout mice, we also examined possible involvement of the Ca2+ release channel and junctional membrane complex in cardiac SOCE. Apparently normal SOCE activities were retained in mutant myocytes lacking RyR-2 or JP-2, suggesting that neither the Ca2+ release channel nor junctional membrane complex is involved in activation of cardiac SOCE.     

STIM1L is a new actin-binding splice variant involved in fast repetitive Ca2+ release

Cytosolic Ca(2+) signals encoded by repetitive Ca(2+) releases rely on two processes to refill Ca(2+) stores: Ca(2+) reuptake from the cytosol and activation of a Ca(2+) influx via store-operated Ca(2+) entry (SOCE). However, SOCE activation is a slow process. It is delayed by >30 s after store depletion because stromal interaction molecule 1 (STIM1), the Ca(2+) sensor of the intracellular stores, must form clusters and migrate to the membrane before being able to open Orai1, the plasma membrane Ca(2+) channel. In this paper, we identify a new protein, STIM1L, that colocalizes with Orai1 Ca(2+) channels and interacts with actin to form permanent clusters. This property allowed the immediate activation of SOCE, a characteristic required for generating repetitive Ca(2+) signals with frequencies within seconds such as those frequently observed in excitable cells. STIM1L was expressed in several mammalian tissues, suggesting that many cell types rely on this Ca(2+) sensor for their Ca(2+) homeostasis and intracellular signaling.     

Forest-scale sap flux responses to rainfall in a dryland eucalyptus plantation

Dryland salinity is caused by rising saline water tables, the result of relatively recent landscape-scale clearance of deep-rooted vegetation. One obvious solution to this problem is the reintroduction of deep-rooted vegetation into these landscapes, most likely non-deciduous trees. Ideally, continually-transpiring deep-rooted trees would remove moisture from throughout the soil profile, increasing the capacity of the soil to store water, thus lowering water tables by effectively reducing the number of rainfall events that contribute to groundwater recharge. In this study, we examined how water use by a Eucalyptus sideroxylon A. Cunn. ex Woolls plantation, growing in a salinity-prone landscape, varied in response to rainfall events across four years of sap flux monitoring. Responses of the plantation were observed across multiple seasons, from above average to well below average rainfall. We observed that the plantation forest, while capable of continuous water use during drought, was also quite responsive to rainfall events. During the driest periods, during which shallow soil moisture was reduced to a stable minimum, the forest continued using water at around 1 mm/day. Generally we observed increases in forest water use following only 5 mm of rainfall, in contrast to 20 mm for neighbouring native vegetation. We compared a range of plausible empirical models for describing forest water use responses to rainfall. The best model demonstrated that rainfall size, post-rainfall PET and the interaction between rainfall size and antecedent soil moisture made significant contributions to variation in forest water use across rainfall events. Interestingly, the model showed that all else equal, higher antecedent soil moisture tended to reduce potential increases in forest water use in response to rainfall.     

Coupling Ca2+ store release to Icrac channel activation in B lymphocytes requires the activity of Lyn and Syk kinases

Activation of the B cell receptor complex in B lymphocytes causes Ca(2+) release from intracellular stores, which, in turn, activates ion channels known as Icrac. We investigated the mechanisms that link Ca(2+) store release to channel gating in DT40 B lymphocyte cell lines genetically manipulated to suppress the expression of several tyrosine kinases: Btk, Lyn, Syk, and the Blnk adaptor molecule. The simultaneous but not the independent suppression of Lyn and Syk expression prevents the activation of Icrac without interfering with thapsigargin-sensitive Ca(2+) store release. Icrac activation by Ca(2+) is reversed in mutant cells by the homologous expression of the missing kinases. Pharmacological inhibition of kinase activity by LavendustinA and PP2 cause the same functional deficit as the genetic suppression of enzyme expression. Biochemical assays demonstrate that kinase activity is required as a tonic signal: targets must be phosphorylated to link Ca(2+) store release to Icrac gating. The action of kinases on Icrac activation does not arise from control of the expression level of the stromal interaction molecule 1 and Orai1 proteins.     

容量性钙内流通道的分子代表

细胞内钙库排空产生一种信号,诱导细胞膜上的钙库操纵的钙通道（SOC）开放,使Ca^2 由细胞外进入细胞内,称为容量性钙内流（CCE）,或钙释放激活的钙通道（CRAC）,可能由果蝇一过性受体电位（trp)和trp样（trpl)基因编码,钙库排空和通道开放之间的偶联机制不清,目前主要提出三种机制：（1）弥散信使;（2）蛋白质－蛋白质之间的相互作用;（3）囊泡分泌。本文综述了CCE的分子代表 ,可能机制及电生理表型。     

三峡库区典型茶园土壤水分对不同降雨模式的响应

土壤水分是坡面产流和生物地球化学过程的关键控制因素。降水事件可以通过引起土壤剖面不同深度的土壤水分响应,从而影响流域中的径流路径、产流机制和土壤侵蚀过程等。基于三峡库区典型分布的茶园为对象,通过长期定点、高频的气象和水分数据观测,研究不同降雨模式下茶园不同土层深度(0—10、10—20、20—30、30—40cm)土壤水分的时空变化特征,分析茶园不同深度土壤在雨季的水分动态变化规律和对不同降雨模式的响应特征。结果表明：(1)研究区内的降雨和土壤水分含量均表现出明显的季节性特征。降雨在7月达到最大值,土壤水分含量则在8月达到峰值。表明降雨是影响土壤水分含量变化的重要因子,土壤水分对降雨有着明显的响应过程。(2)在相同降雨条件下,土壤含水量具有明显的垂直梯度变化。随着土层深度的增加,土壤水分对降雨的响应逐渐呈现出滞后现象。表层土壤(0—20cm)对降雨的响应较为迅速且幅度更加明显,深层土壤(30—40cm)水分含量变化相对稳定,并且对降雨的响应时间更加滞缓。随着土层深度的增加,土壤水分含量的变化幅度逐渐趋于平稳。(3)土壤水分含量对不同的降雨模式表现出显著差异。在较大雨强条件下,土壤水分变...     

Synchronous Ca(2+) oscillation emerges from voltage fluctuations of Ca(2+) stores

Synchronous Ca(2+) oscillation occurs in various cell types to regulate cellular functions. However, the mechanism for synchronization of Ca(2+) increases between cells remains unclear. Recently, synchronous oscillatory changes in the membrane potential of internal Ca(2+) stores were recorded using an organelle-specific voltage-sensitive dye [Yamashita et al. (2006) FEBS J273, 3585-3597], and an electrical coupling model of the synchronization of store potentials and Ca(2+) releases has been proposed [Yamashita (2006) FEBS Lett580, 4979-4983]. This model is based on capacitative coupling, by which transient voltage changes can be synchronized, but oscillatory slow potentials cannot be communicated. Another candidate mechanism is synchronization of action potentials and ensuing Ca(2+) influx through voltage-dependent Ca channels. The present study addresses the question of whether Ca(2+) increases are synchronized by action potentials, and how oscillatory store potentials are synchronized across the cells. Electrophysiological and Ca(2+)-sensitive fluorescence measurements in early embryonic chick retina showed that synchronous Ca(2+) oscillation was caused by releases of Ca(2+) from Ca(2+) stores without any evidence of action potentials in retinal neuroepithelial cells or newborn neurons. High-speed fluorescence measurement of store membrane potential surprisingly revealed that the synchronous oscillatory changes in the store potential were periodic repeats of a burst of high-frequency voltage fluctuations. The burst coincided with a Ca(2+) increase. The present study suggests that synchronization of Ca(2+) release is mediated by the high-frequency fluctuation in the store potential. Close apposition of the store membrane and plasma membrane in an epithelial structure would allow capacitative coupling across the cells.     

Is the interspecific variation of body size of land snails correlated with rainfall in Israel and Palestine?

The hypothesis that body size of land snail species increases with aridity in Israel and Palestine because large snails lose relatively less water due to their lower surface to volume ratio has been investigated. Data on rainfall amplitudes of 84 land snail species in Israel and Palestine and on their body sizes were used to test for interspecific correlations between body size and rainfall. Four methods, means of body sizes in rainfall categories, the midpoint method, the across-species method, and a phylogenetically controlled analysis (CAIC) showed that there is no significant correlation between body size of land snail species and their rainfall amplitude in Israel and Palestine. The lack of an interspecific correlation between body size and rainfall amplitude may be the result of conflicting selective forces on body size.     

Is the interspecific variation of body size of land snails correlated with rainfall in Israel and Palestine?

The hypothesis that body size of land snail species increases with aridity in Israel and Palestine because large snails lose relatively less water due to their lower surface to volume ratio has been investigated. Data on rainfall amplitudes of 84 land snail species in Israel and Palestine and on their body sizes were used to test for interspecific correlations between body size and rainfall. Four methods, means of body sizes in rainfall categories, the midpoint method, the across-species method, and a phylogenetically controlled analysis (CAIC) showed that there is no significant correlation between body size of land snail species and their rainfall amplitude in Israel and Palestine. The lack of an interspecific correlation between body size and rainfall amplitude may be the result of conflicting selective forces on body size.