The cortical actin network is a mesh of filaments distributed beneath the plasmalemma that dynamically reacts in response to stimuli.This dynamic network of cortical filaments,together with motor myosin partners,adjus...The cortical actin network is a mesh of filaments distributed beneath the plasmalemma that dynamically reacts in response to stimuli.This dynamic network of cortical filaments,together with motor myosin partners,adjusts the plasmalemma tension,organizes membrane protein microdomains,remodels the cell surface and drives vesicle motion in order to fine-tune exocytosis,endocytosis and recycling of secretory vesicles.In this review,we discuss how these mechanisms work in secretory cells.展开更多
The hypothesis of the calcium paradox has its origin in experiments done in neurogenically stimulated rat and mouse vas deferentia. Some old studies reported that reduction of Ca2+ entry by mild concentrations of ver...The hypothesis of the calcium paradox has its origin in experiments done in neurogenically stimulated rat and mouse vas deferentia. Some old studies reported that reduction of Ca2+ entry by mild concentrations of verapamil, diltiazem or nifedipine elicited the surprising augmentation of vas deferens contractions. Recent reports have also found that nifedipine caused a paradoxical augmentation of the exocytotic release of catecholamine elicited by paired depolarising pulses in voltage-clamped bovine chromaffin cells. Because these drugs are blocking the L-subtype of VACCs (voltage-activated calcium channels), augmented contraction and exocytosis was an unexpected outcome. Recent experiments in neurogenically-stimulated rat vas deferens have found a more drastic potentiation of contractions with the association of verapamil and cAMP-enhancer compounds. Thus, the interaction between the signalling pathways mediated by Ca2+ and cAMP could explain those unexpected findings and the so-called calcium paradox.展开更多
Fishes exert stress response in a various ways depending on the type of the stressor.The stress responses are activated through a cascade mechanism stimulated by the stressor which involves the hypothalamus-hypophysea...Fishes exert stress response in a various ways depending on the type of the stressor.The stress responses are activated through a cascade mechanism stimulated by the stressor which involves the hypothalamus-hypophyseal-interrenal(HHI)axis,catecholamines(CA),and gonadotropins.Adaptive stress responses may positively impact the fish survival and reproduction,while continuous or prolonged stress causes adverse effects on the fish reproduction.Corticotropin-releasing factor and adrenocorticotropic hormone are the principal hormones responsible for producing corticosteroids through the HHI axis.Cortisol acts differentially on the stress response as it helps at the early developmental stage;conversely,it impairs the gonadal function.CA have a critical role in maintaining body homeostasis and intermediary metabolism,and they also have a predominant role in reproductive function.Besides hormones,few genetic and epigenetic factors have been identified to understand the molecular responses to stress however,genome-wide associated studies will be initiated to investigate a complete picture of the stress mechanism.Further,recent evidence suggests a growing concern in determining the correlation between the stress hormone level and its associated gene function.Hence,this review highlights the regulation of stress responses in different axes,genetic and epigenetic factors related to stress,and the integration of recent technologies and novel hypotheses to unravel the stress response mechanism in fish reproduction.展开更多
Background Airway symptoms in asthma are related to decrease of epinephrine secretion, which may be ascribed to elevated nerve growth factor (NGF) in the organism. The aim of this study was to monitor the neuroendoc...Background Airway symptoms in asthma are related to decrease of epinephrine secretion, which may be ascribed to elevated nerve growth factor (NGF) in the organism. The aim of this study was to monitor the neuroendocrine alteration in the adrenal medulla of asthmatic rats. Methods Sixteen rats were randomly divided into two groups (n=-8), control group and asthma group, and the asthmatic rats were sensitized and challenged with ovalbumin (OVA). The levels of NGF, epinephrine and norepinephrine in serum were detected by enzyme linked immunosorbent assay (ELISA), the NGF expression in adrenal medulla was detected by immunohistochemistry, and the changes in the ultrastructure of the adrenal medulla was observed by electron microscopy. Results The NGF expression was increased in asthmatic rats compared with control rats. Compared with control rats, the results indicated that the epinephrine level was decreased in asthmatic rats, but no significant difference was found in norepinephrine levels. We found more ganglion cells in the adrenal medulla of asthmatic rats than in control rats, with NGF immunostaining mainly located in these ganglion cells. Electron microscopic images showed the density of chromaffin granula decreased and there was shrunken nucleolemma in the adrenal medullary cells of asthmatic rats. Conclusion The innervation of the adrenal medulla is changed in asthmatic rats, and it may contribute to the epinephrine decrease in asthma.展开更多
基金This work was supported by the Grants PICT 2764-2016,PICT 02849-2018 and PICT 02041-2019 from the Agencia Nacional de Promoción de la Investigación,el Desarrollo Tecnológico y la Innovación(Argentina)ICN09_022 from ICM-ANID(Chile).
文摘The cortical actin network is a mesh of filaments distributed beneath the plasmalemma that dynamically reacts in response to stimuli.This dynamic network of cortical filaments,together with motor myosin partners,adjusts the plasmalemma tension,organizes membrane protein microdomains,remodels the cell surface and drives vesicle motion in order to fine-tune exocytosis,endocytosis and recycling of secretory vesicles.In this review,we discuss how these mechanisms work in secretory cells.
文摘The hypothesis of the calcium paradox has its origin in experiments done in neurogenically stimulated rat and mouse vas deferentia. Some old studies reported that reduction of Ca2+ entry by mild concentrations of verapamil, diltiazem or nifedipine elicited the surprising augmentation of vas deferens contractions. Recent reports have also found that nifedipine caused a paradoxical augmentation of the exocytotic release of catecholamine elicited by paired depolarising pulses in voltage-clamped bovine chromaffin cells. Because these drugs are blocking the L-subtype of VACCs (voltage-activated calcium channels), augmented contraction and exocytosis was an unexpected outcome. Recent experiments in neurogenically-stimulated rat vas deferens have found a more drastic potentiation of contractions with the association of verapamil and cAMP-enhancer compounds. Thus, the interaction between the signalling pathways mediated by Ca2+ and cAMP could explain those unexpected findings and the so-called calcium paradox.
文摘Fishes exert stress response in a various ways depending on the type of the stressor.The stress responses are activated through a cascade mechanism stimulated by the stressor which involves the hypothalamus-hypophyseal-interrenal(HHI)axis,catecholamines(CA),and gonadotropins.Adaptive stress responses may positively impact the fish survival and reproduction,while continuous or prolonged stress causes adverse effects on the fish reproduction.Corticotropin-releasing factor and adrenocorticotropic hormone are the principal hormones responsible for producing corticosteroids through the HHI axis.Cortisol acts differentially on the stress response as it helps at the early developmental stage;conversely,it impairs the gonadal function.CA have a critical role in maintaining body homeostasis and intermediary metabolism,and they also have a predominant role in reproductive function.Besides hormones,few genetic and epigenetic factors have been identified to understand the molecular responses to stress however,genome-wide associated studies will be initiated to investigate a complete picture of the stress mechanism.Further,recent evidence suggests a growing concern in determining the correlation between the stress hormone level and its associated gene function.Hence,this review highlights the regulation of stress responses in different axes,genetic and epigenetic factors related to stress,and the integration of recent technologies and novel hypotheses to unravel the stress response mechanism in fish reproduction.
基金This work was supported by grants from the National Natural Science Foundation of China (No. 30570802, No. 30800502 and No. 30801505).
文摘Background Airway symptoms in asthma are related to decrease of epinephrine secretion, which may be ascribed to elevated nerve growth factor (NGF) in the organism. The aim of this study was to monitor the neuroendocrine alteration in the adrenal medulla of asthmatic rats. Methods Sixteen rats were randomly divided into two groups (n=-8), control group and asthma group, and the asthmatic rats were sensitized and challenged with ovalbumin (OVA). The levels of NGF, epinephrine and norepinephrine in serum were detected by enzyme linked immunosorbent assay (ELISA), the NGF expression in adrenal medulla was detected by immunohistochemistry, and the changes in the ultrastructure of the adrenal medulla was observed by electron microscopy. Results The NGF expression was increased in asthmatic rats compared with control rats. Compared with control rats, the results indicated that the epinephrine level was decreased in asthmatic rats, but no significant difference was found in norepinephrine levels. We found more ganglion cells in the adrenal medulla of asthmatic rats than in control rats, with NGF immunostaining mainly located in these ganglion cells. Electron microscopic images showed the density of chromaffin granula decreased and there was shrunken nucleolemma in the adrenal medullary cells of asthmatic rats. Conclusion The innervation of the adrenal medulla is changed in asthmatic rats, and it may contribute to the epinephrine decrease in asthma.