Developmental plasticity

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

Developmental and visual input-dependent regulation of the CB1 cannabinoid receptor in the mouse visual cortex.

Abstract: The mammalian visual system exhibits significant experience-induced plasticity in the early postnatal period. While physiological studies have revealed the contribution of the CB1 cannabinoid receptor (CB1) to developmental plasticity in the primary visual cortex (V1), it remains unknown whether the expression and localization of CB1 is regulated during development or by visual experience. To explore a possible role of the endocannabinoid system in visual cortical plasticity, we examined the expression of CB1 in the visual cortex of mice. We found intense CB1 immunoreactivity in layers II/III and VI. CB1 mainly localized at vesicular GABA transporter-positive inhibitory nerve terminals. The amount of CB1 protein increased throughout development, and the specific laminar pattern of CB1 appeared at P20 and remained until adulthood. Dark rearing from birth to P30 decreased the amount of CB1 protein in V1 and altered the synaptic localization of CB1 in the deep layer. Dark rearing until P50, however, did not influence the expression of CB1. Brief monocular deprivation for 2 days upregulated the localization of CB1 at inhibitory nerve terminals in the deep layer. Taken together, the expression and the localization of CB1 are developmentally regulated, and both parameters are influenced by visual experience.

Structural plasticity can produce metaplasticity.

Abstract: Background: Synaptic plasticity underlies many aspect of learning memory and development. The properties of synaptic plasticity can change as a function of previous plasticity and previous activation of synapses, a phenomenon called metaplasticity. Synaptic plasticity not only changes the functional connectivity between neurons but in some cases produces a structural change in synaptic spines; a change thought to form a basis for this observed plasticity. Here we examine to what extent structural plasticity of spines can be a cause for metaplasticity. This study is motivated by the observation that structural changes in spines are likely to affect the calcium dynamics in spines. Since calcium dynamics determine the sign and magnitude of synaptic plasticity, it is likely that structural plasticity will alter the properties of synaptic plasticity. Methodology/Principal Findings: In this study we address the question how spine geometry and alterations of N-methyl-Daspartic acid (NMDA) receptors conductance may affect plasticity. Based on a simplified model of the spine in combination with a calcium-dependent plasticity rule, we demonstrated that after the induction phase of plasticity a shift of the long term potentiation (LTP) or long term depression (LTD) threshold takes place. This induces a refractory period for further LTP induction and promotes depotentiation as observed experimentally. That resembles the BCM metaplasticity rule but specific for the individual synapse. In the second phase, alteration of the NMDA response may bring the synapse to a state such that further synaptic weight alterations are feasible. We show that if the enhancement of the NMDA response is proportional to the area of the post synaptic density (PSD) the plasticity curves most likely return to the initial state. Conclusions/Significance: Using simulations of calcium dynamics in synaptic spines, coupled with a biophysically motivated calcium-dependent plasticity rule, we find under what conditions structural plasticity can form the basis of synapse specific metaplasticity.

Fitness costs may explain the post-colonisation erosion of phenotypic plasticity.

Abstract: Many organisms can adjust their phenotypes to match local environmental conditions via shifts in developmental trajectories, rather than relying on changes in gene frequencies wrought by natural selection. Adaptive developmental plasticity confers obvious benefits in terms of rapid response and higher mean fitness, so why is it not more common? Plausibly, adaptive plasticity also confers a cost; reshaping the phenotype takes time and energy, so that canalised control of trait values enhances fitness if the optimal phenotype remains the same from one generation to the next. Although this idea is central to interpreting the fitness consequences of adaptive plasticity, empirical data on costs of plasticity are scarce. In Australian tiger snakes, larger relative head size enhances maximal ingestible prey size on islands containing large prey. The trait arises via adaptive plasticity in snake populations on newly colonised islands but becomes genetically canalised on islands where snakes have been present for much longer periods. We experimentally manipulated relative head size in captive neonatal snakes to quantify the costs of adaptive plasticity. Although small-headed snakes were able to increase their head sizes when offered large prey, the delay in doing so, and their inability to consume large prey at the outset, significantly reduced their growth rates relative to conspecifics with larger heads at the beginning of the experiment. This study describes a proximate cause to the post-colonisation erosion of developmental plasticity recorded in tiger snake populations.

Adaptive maternal behavioral plasticity and developmental programming mitigate the transgenerational effects of temperature in dung beetles

Abstract: 1 –––––––––––––––––––––––––––––––––––––––– © 2018 The Authors. Oikos © 2018 Nordic Society Oikos This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. Subject Editor: Morgan Kelly Editor-in-Chief: Dries Bonte Accepted 12 March 2018 00: 1–11, 2018 doi: 10.1111/oik.05215 doi: 10.1111/oik.05215 00 1–11