Developmental plasticity

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

Changes in plasticity across the lifespan: cause of disease and target for intervention.

Abstract: We conceptualize brain plasticity as an intrinsic property of the nervous system enabling rapid adaptation in response to changes in an organism's internal and external environment. In prenatal and early postnatal development, plasticity allows for the formation of organized nervous system circuitry and the establishment of functional networks. As the individual is exposed to various sensory stimuli in the environment, brain plasticity allows for functional and structural adaptation and underlies learning and memory. We argue that the mechanisms of plasticity change over the lifespan with different slopes of change in different individuals. These changes play a key role in the clinical phenotype of neurodevelopmental disorders like autism and schizophrenia and neurodegenerative disorders such as Alzheimer's disease. Altered plasticity not only can trigger maladaptive cascades and can be the cause of deficits and disability but also offers opportunities for novel therapeutic interventions. In this chapter, we discuss the importance of brain plasticity across the lifespan and how neuroplasticity-based therapies offer promise for disorders with otherwise limited effective treatment.

Hitting a moving target: Basic mechanisms of recovery from acquired developmental brain injury.

Abstract: Acquired brain injuries represent a major cause of disability in the pediatric population. Understanding responses to developmental acquired brain injuries requires knowledge of the neurobiology of normal development, age-at-injury effects and experience-dependent neuroplasticity. In the developing brain, full recovery cannot be considered as a return to the premorbid baseline, since ongoing maturation means that cerebral functioning in normal individuals will continue to advance. Thus, the recovering immature brain has to ‘hit a moving target’ to achieve full functional recovery, defined as parity with age-matched uninjured peers. This review will discuss the consequences of developmental injuries such as focal lesions, diffuse hypoxia and traumatic brain injury (TBI). Underlying cellular and physiological mechanisms relevant to age-at-injury effects will be described in considerable detail, including but not limited to alterations in neurotransmission, connectivity/network functioning, the extracellular matrix, response to oxidative stress and changes in cerebral metabolism. Finally, mechanisms of experience-dependent plasticity will be reviewed in conjunction with their effects on neural repair and recovery.

Developmental plasticity and acclimation both contribute to adaptive responses to alternating seasons of plenty and of stress in Bicyclus butterflies

Abstract: Plasticity is a crucial component of the life cycle of invertebrates that live as active adults throughout wet and dry seasons in the tropics. Such plasticity is seen in the numerous species of Bicyclus butterfl ies in Africa which exhibit seasonal polyphenism with sequential generations of adults with one or other of two alternative phenotypes. These differ not only in wing pattern but in many other traits. This divergence across a broad complex of traits is associated with survival and reproduction either in a wet season that is favourable in terms of resources, or mainly in a dry season that is more stressful. This phenomenon has led us to examine the bases of the developmental plasticity in a model species, B. anynana, and also the evolution of key adult life history traits, including starvation resistance and longevity. We now understand something about the processes that generate variation in the phenotype, and also about the ecological context of responses to environmental stress. The responses clearly involve a mix of developmental plasticity as cued by different environments in pre-adult development, and the acclimation of life history traits in adults to their prevailing environment.

Short-term ionic plasticity at GABAergic synapses

Abstract: Fast synaptic inhibition in the brain is mediated by the pre-synaptic release of the neurotransmitter γ-Aminobutyric acid (GABA)and the post-synaptic activation of GABA-sensitive ionotropic receptors. As with excitatory synapses, it is being increasinly appreciated that a variety of plastic processes occur at inhibitory synapses, which operate over a range of timescales. Here we examine a form of activity-dependent plasticity that is somewhat unique to GABAergic transmission. This involves short-lasting changes to the ionic driving force for the post-synaptic receptors, a process referred to as short-term ionic plasticity. These changes are directly related to the history of activity at inhibitory synapses and are influenced by a variety of factors including the location of the synapse and the post-synaptic cell's ion regulation mechanisms. We explore the processes underlying this form of plasticity, when and where it can occur, and how it is likely to impact network activity.