Developmental plasticity

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

TNF-Mediated Homeostatic Synaptic Plasticity: From in vitro to in vivo Models.

Abstract: Since it was first described almost 30 years ago, homeostatic synaptic plasticity (HSP) has been hypothesized to play a key role in maintaining neuronal circuit function in both developing and adult animals. While well characterized in vitro, determining the in vivo roles of this form of plasticity remains challenging. Since the discovery that the pro-inflammatory cytokine tumor necrosis factor-α (TNF-α) mediates some forms of HSP, it has been possible to probe some of the in vivo contribution of TNF-mediated HSP. Work from our lab and others has found roles for TNF-HSP in a variety of functions, including the developmental plasticity of sensory systems, models of drug addiction, and the response to psychiatric drugs.

Sleep and developmental plasticity not just for kids.

Abstract: In a variety of mammalian species, sleep amounts are highest during developmental periods of rapid brain development and synaptic plasticity than at any other time in life [Frank, M. G. & Heller, H. C. (1997a). Development of REM and slow wave sleep in the rat. American Journal of Physiology, 272, R1792-R1799; Jouvet-Mounier, D., Astic, L., & Lacote, D. (1970). Ontogenesis of the states of sleep in rat, cat and guinea pig during the first postnatal month. Developmental Psychobiology, 2, 216-239; Roffwarg, H. P., Muzio, J. N., & Dement, W. C. (1966). Ontogenetic development of the human sleep-dream cycle. Science, 604-619]. Many of the mechanisms governing developmental plasticity also mediate plasticity in the adult brain. Therefore, studying the role of sleep in developmental plasticity may provide insights more generally into sleep function across the lifespan. In this chapter, I review the evidence that supports a critical role for sleep in developmental brain plasticity. I begin with an overview of past studies that support a role for sleep in general brain maturation. This is followed by more recent findings in the developing visual cortex that more specifically address a possible role for sleep in cortical plasticity.

Synaptic and molecular mechanisms regulating plasticity during early learning.

Abstract: Many behaviors are learned most easily during a discrete developmental period, and it is generally agreed that these "sensitive periods" for learning reflect the developmental regulation of molecular or synaptic properties that underlie experience-dependent changes in neural organization and function. Avian song learning provides one example of such temporally restricted learning, and several features of this behavior and its underlying neural circuitry make it a powerful model for studying how early experience sculpts neural and behavioral organization. Here we describe evidence that within the basal ganglia-thalamocortical loop implicated in vocal learning, song acquisition engages N-methyl-d-aspartate receptors (NMDARs), as well as signal transduction cascades strongly implicated in other instances of learning. Furthermore, NMDAR phenotype changes in parallel with developmental and seasonal periods for vocal plasticity. We also review recent studies in the avian song system that challenge the popular notion that sensitive periods for learning reflect developmental changes in the NMDAR that alter thresholds for synaptic plasticity.

Prenatal programming of postnatal plasticity revisited-And extended.

Abstract: Two sets of evidence reviewed herein, one indicating that prenatal stress is associated with elevated behavioral and physiological dysregulation and the other that such phenotypic functioning is itself associated with heightened susceptibility to positive and negative environmental influences postnatally, raises the intriguing hypothesis first advanced by Pluess and Belsky (2011) that prenatal stress fosters, promotes, or "programs" postnatal developmental plasticity. Here we review further evidence consistent with this proposition, including new experimental research systematically manipulating both prenatal stress and postnatal rearing. Collectively this work would seem to explain why prenatal stress has so consistently been linked to problematic development: stresses encountered prenatally are likely to continue postnatally, thereby adversely affecting the development of children programmed (by prenatal stress) to be especially susceptible to environmental effects. Less investigated are the potential benefits prenatal stress may promote, due to increased plasticity, when the postnatal environment proves to be favorable. Future directions of research pertaining to potential mechanisms instantiating postnatal plasticity and moderators of such prenatal-programming effects are outlined.