Developmental plasticity

About: Developmental plasticity is a research topic. Over the lifetime, 1721 publications have been published within this topic receiving 103438 citations.

Parasitism, developmental plasticity and bilateral asymmetry of wing feathers in alpine swift, Apus melba, nestlings

Abstract: The hypothesis that developmental instability is a cost of developmental plasticity is explored using the alpine swift (Apus melba) as a model organism. In a previous study, experimentally parasitized nestlings showed a reduced wing growth rate in the first half of the rearing period when parasites were abundant (i.e. peak infestation) and an accelerated growth rate (i.e. compensatory growth) in the second half when parasites decreased in number. This suggests that alpine swifts are able to adjust growth rate in relation to variation in parasite loads. Because developmental plasticity may entail fitness costs, the energy required to sustain compensatory growth may be invested at the expense of developmental stability, potentially resulting in larger deviations from symmetry in paired, bilateral traits (i.e. fluctuating asymmetry, FA). This hypothesis predicts higher FA in parasitized than deparasitized nestlings because of compensatory growth, and hence individuals sustaining the highest level of compensatory growth rate should exhibit the highest FA levels. Another non-mutually exclusive hypothesis argues that parasites directly cause FA by diverting energy required by host for maintenance and growth, and predicts that individuals suffering the most from parasitism during peak infestation should exhibit the highest FA levels. The present study shows that wing feathers of experimentally parasitized nestlings were more asymmetrical than those of experimentally deparasitized ones 50 days after hatching. Furthermore, in parasitized individuals FA was negatively correlated with wing growth rate during the period of peak infestation but not during the period of compensatory growth. These findings suggest that developmental homeostasis is more sensitive to parasites than to compensatory growth.

Salinity-induced heterokairy in an upper-estuarine population of the snail Radix balthica (Mollusca: Pulmonata)

Abstract: Climate change is predicted to increase sea level and cause saline intrusion of coastal freshwaters. This will have consequences for freshwater organisms inhabiting such areas; devel- opmental phenotypic plasticity may facilitate the persistence of freshwater species under such scenarios of increased salinity. Here we investigated developmental plasticity under different salin- ity treatments (S = 2, 5, 7 and 9, with artificial pond water (APW) and deionised water (S = 0) as con- trols) in embryos from an upper-estuarine population of the gastropod Radix balthica. We focused on plasticity in the timing of developmental events (heterokairy) at different salinities, including the time of onset (relative and absolute) of 10 developmental events and duration of 4 developmental stages; we also assessed whether salinity affected hatchling morphology and embryonic cardiac activity. There were significant differences in the absolute time of onset of several events with increased salinity, including a delayed first heartbeat in S5 and S7 compared with APW and in the relative time of onset of eye spot formation, first heartbeat and foot attachment between treatments. Stage duration also varied between salinity treatments: the hippo developmental stage lasted signif- icantly longer in S7 compared with APW and development overall was prolonged in S7, with embryos in S9 not developing past the trochophore stage. Salinity also affected both shell size and shell shape of hatchlings. Hence salinity influences the time of onset (absolute and relative) of devel- opmental events and duration of several developmental stages and the morphology of hatchling snails, although the mechanistic basis and fitness implications are, as yet, unknown.

S-nitrosation and neuronal plasticity

Abstract: Nitric oxide (NO) has long been recognized as a multifaceted participant in brain physiology. Despite the knowledge that was gathered over many years regarding the contribution of NO to neuronal plasticity, for example the ability of the brain to change in response to new stimuli, only in recent years have we begun to understand how NO acts on the molecular and cellular level to orchestrate such important phenomena as synaptic plasticity (modification of the strength of existing synapses) or the formation of new synapses (synaptogenesis) and new neurons (neurogenesis). Post-translational modification of proteins by NO derivatives or reactive nitrogen species is a non-classical mechanism for signalling by NO. S-nitrosation is a reversible post-translational modification of thiol groups (mainly on cysteines) that may result in a change of function of the modified protein. S-nitrosation of key target proteins has emerged as a main regulatory mechanism by which NO can influence several levels of brain plasticity, which are reviewed in this work. Understanding how S-nitrosation contributes to neural plasticity can help us to better understand the physiology of these processes, and to better address pathological changes in plasticity that are involved in the pathophysiology of several neurological diseases. Linked Articles This article is part of a themed section on Pharmacology of the Gasotransmitters. To view the other articles in this section visit http://dx.doi.org/10.1111/bph.2015.172.issue-6

Experience-dependent plasticity in hypocretin/orexin neurones: re-setting arousal threshold.

Abstract: The neuropeptide hypocretin is synthesized exclusively in the lateral hypothalamus and participates in many brain functions critical for animal survival, particularly in the promotion and maintenance of arousal in animals - a core process in animal behaviours. Consistent with its arousal-promoting role in animals, the neurones synthesizing hypocretin receive extensive innervations encoding physiological, psychological and environmental cues and send final outputs to key arousal-promoting brain areas. The activity in hypocretin neurones fluctuates and correlates with the behavioural state of animals and intensive activity has been detected in hypocretin neurones during wakefulness, foraging for food and craving for addictive drugs. Therefore, it is likely that hypocretin neurones undergo experience-dependent changes resulting from intensive activations by stimuli encoding changes in the internal and external environments. This review summarizes the most recent evidence supporting experience-dependent plasticity in hypocretin neurones. Current data suggest that nutritional and behavioural factors lead to synaptic plasticity and re-organization of synaptic architecture in hypocretin neurones. This may be the substrate of enhanced levels of arousal resulting from behavioural changes in animals and may help to explain the mechanisms underlying the changes in arousal levels induced by physiological, psychological and environmental factors.