Autism: A “Critical Period” Disorder?

Cortical circuits in the brain are refined by experience during critical periods early in postnatal life. Critical periods are regulated by the balance of excitatory and inhibitory (E/I) neurotransmission in the brain during development. There is now increasing evidence of E/I imbalance in autism, a complex genetic neurodevelopmental disorder diagnosed by abnormal socialization, impaired communication, and repetitive behaviors or restricted interests. The underlying cause is still largely unknown and there is no fully effective treatment or cure. We propose that alteration of the expression and/or timing of critical period circuit refinement in primary sensory brain areas may significantly contribute to autistic phenotypes, including cognitive and behavioral impairments. Dissection of the cellular and molecular mechanisms governing well-established critical periods represents a powerful tool to identify new potential therapeutic targets to restore normal plasticity and function in affected neuronal circuits

Critical period plasticity and sensory function in a neuroligin-3 model of autism

Extensive experience-dependent refinement of cortical circuits is restricted to critical periods of plasticity early in life. The timing of these critical periods is tightly regulated by the relative levels of excitatory and inhibitory (E/I) neurotransmission during development. Genetic disruption of synaptic proteins that normally maintain E/I balance can result in severe behavioral dysfunction in neurodevelopmental disorders like autism, but the mechanisms are unclear. We propose that abnormal critical periods of sensory circuit refinement could represent a key link between E/I imbalance and the cognitive and behavioral problems in autism

Glial regulation of critical period plasticity

Animal behavior, from simple to complex, is dependent on the faithful wiring of neurons into functional neural circuits. Neural circuits undergo dramatic experience-dependent remodeling during brief developmental windows called critical periods. Environmental experience during critical periods of plasticity produces sustained changes to circuit function and behavior. Precocious critical period closure is linked to autism spectrum disorders, whereas extended synaptic remodeling is thought to underlie circuit dysfunction in schizophrenia. Thus, resolving the mechanisms that instruct critical period timing is important to our understanding of neurodevelopmental disorders. Control of critical period timing is modulated by neuron-intrinsic cues, yet recent data suggest that some determinants are derived from neighboring glial cells (astrocytes, microglia, and oligodendrocytes). As glia make up 50% of the human brain, understanding how these diverse cells communicate with neurons and with each other to sculpt neural plasticity, especially during specialized critical periods, is essential to our fundamental understanding of circuit development and maintenance

2015 Soybean Production in Southeast Kansas

Crop performance and yield varies as a function of the growing environment and soil properties within the field. Optimal soybean planting in southeast Kansas usually occurs from mid-May to mid-June for full-season or late-June to early-July for doublecropped soybean. Planting is timed to capture fall rains and cooler temperatures during critical periods of bean development and yield formation and avoid mid-summer heat and drought. Changing planting configuration (row spacing and plant population), timing of planting, and cultivar selection are methods of optimizing soybean production for different growing environments

Behavioral Changes in Adult C57BL/6J Mice following Prenatal Exposure to Ethanol.

Fetal Alcohol Syndrome (FAS) labels children with physical, mental and behavioral deficits exposed to alcohol in utero. Current research indicates that timing of alcohol exposure of the embryo/fetus is a critical determinant of the behavioral deficits associated with FAS. This study represents a model for binge drinking, in which C57BL mouse embryos were exposed to alcohol during 2 separate critical periods of brain development, gestational day (GD) 7 or 8. As adults, the offspring were tested to determine if loco-motor activity and emotional reaction to a novel environment had been affected. Significant differences due to treatment and sex were noted for both the number of urinations (p=.005 and .001, respectively) and fecal boli (p=.011 and .001, respectively). These results suggest that the quantity of alcohol exposure in utero on the developing brain as in this binge-drinking model is critical in terms of adverse effects on behavioral outcome for the offspring

The Physiological Basis of Geographic Variation in Rates of Embryonic Development within a Widespread Lizard Species

The duration of embryonic development (e.g., egg incubation period) is a critical life‐history variable because it affects both the amount of time that an embryo is exposed to conditions within the nest and the seasonal timing of hatching. Variation in incubation periods among oviparous reptiles might result from variation in either the amount of embryogenesis completed before laying or the subsequent developmental rates of embryos. Selection on incubation duration could change either of those traits. We examined embryonic development of fence lizards (Sceloporus undulatus) from three populations (Indiana, Mississippi, and Florida) that occur at different latitudes and therefore experience different temperatures and season lengths. These data reveal countergradient variation: at identical temperatures in the laboratory, incubation periods were shorter for lizards from cooler areas. This variation was not related to stage at oviposition; eggs of all populations were laid at similar developmental stages. Instead, embryonic development proceeded more rapidly in cooler‐climate populations, compensating for the delayed development caused by lower incubation temperatures in the field. The accelerated development appears to occur via an increase in heart mass (and, thus, stroke volume) in one population and an increase in heart rate in the other. Hence, superficially similar adaptations of embryonic developmental rate to local conditions may be generated by dissimilar proximate mechanisms

The role of fetal, infant, and childhood nutrition in the timing of sexual maturation

Puberty is a crucial developmental stage in the life span, necessary to achieve reproductive and somatic maturity. Timing of puberty is modulated by and responds to central neurotransmitters, hormones, and environmental factors leading to hypothalamic-pituitary-gonadal axis maturation. The connection between hormones and nutrition during critical periods of growth, like fetal life or infancy, is fundamental for metabolic adaptation response and pubertal development control and prediction. Since birth weight is an important indicator of growth estimation during fetal life, restricted prenatal growth, such as intrauterine growth restriction (IUGR) and small for gestational age (SGA), may impact endocrine system, affecting pubertal development. Successively, lactation along with early life optimal nutrition during infancy and childhood may be important in order to set up timing of sexual maturation and provide successful reproduction at a later time. Sexual maturation and healthy growth are also influenced by nutrition requirements and diet composition. Early nutritional surveillance and monitoring of pubertal development is recommended in all children, particularly in those at risk, such as the ones born SGA and/or IUGR, as well as in the case of sudden weight gain during infancy. Adequate macro and micronutrient intake is essential for healthy growth and sexual maturity

Gut microbiota: A potential regulator of neurodevelopment

During childhood, our brain is exposed to a variety of environmental inputs that can sculpt synaptic connections and neuronal circuits, with subsequent influence on behavior and learning processes. Critical periods of neurodevelopment are windows of opportunity in which the neuronal circuits are extremely plastic and can be easily subjected to remodeling in response to experience. However, the brain is also more susceptible to aberrant stimuli that might lead to altered developmental trajectories. Intriguingly, postnatal brain development is paralleled by the maturation of the gut microbiota: the ecosystem of symbionts populating our gastro-intestinal tract. Recent discoveries have started to unveil an unexpected link between the gut microbiome and neurophysiological processes. Indeed, the commensal bacteria seem to be able to influence host behavioral outcome and neurochemistry through mechanisms which remain poorly understood. Remarkably, the efficacy of the gut flora action appears to be dependent on the timing during postnatal life at which the host gut microbes' signals reaches the brain, suggesting the fascinating possibility of critical periods for this microbiota-driven shaping of host neuronal functions and behavior. Therefore, to understand the importance of the intestinal ecosystem's impact on neuronal circuits functions and plasticity during development and the discovery of the involved molecular mechanisms, will pave the way to identify new and, hopefully, powerful microbiota-based therapeutic interventions for the treatment of neurodevelopmental and psychiatric diseases

Lead, Manganese, and Methylmercury as Risk Factors for Neurobehavioral Impairment in Advanced Age

Contamination of the environment by metals is recognized as a threat to health. One of their targets is the brain, and the adverse functional effects they induce are reflected by neurobehavioral assessments. Lead, manganese, and methylmercury are the metal contaminants linked most comprehensively to such disorders. Because many of these adverse effects can appear later in life, clues to the role of metals as risk factors for neurodegenerative disorders should be sought in the exposure histories of aging populations. A review of the available literature offers evidence that all three metals can produce, in advanced age, manifestations of neurobehavioral dysfunction associated with neurodegenerative disease. Among the critical unresolved questions is timing; that is, during which periods of the lifespan, including early development, do environmental exposures lay the foundations for their ultimate effects

How Much Do Weeds Impact Crop Yields?

The primary purpose for controlling weeds in field crops is to prevent or reduce yield losses associated with competition between weeds and the crop. Competition occurs when plants seek the same resource (light, water, etc.) that is available in limited supplies. The interaction between crops and weeds is complicated and impacted by many factors, including characteristics of the weed species, weed populations, timing of weed emergence, characteristics of the crop variety/hybrid, crop population and row spacing, and the environment. This complexity limits our ability to predict yield losses early in the growing season, therefore hindering the development of economic thresholds for weed. This paper will discuss two important factors influencing competition: 1) relative competitiveness of different weeds, and 2) the critical periods of competition. More information on this topic is available in ISU Extension bulletin IPM-35, CropWeed Interactions