The Spemann-Mangold organizer, also known as the Spemann organizer, is a cluster of cells in the developing embryo of an amphibian that induces development of the central nervous system. Hilde Mangold was a PhD candidate who conducted the organizer experiment in 1921 under the direction of her graduate advisor, Hans Spemann, at the University of Freiburg in Freiburg, German. The discovery of the Spemann-Mangold organizer introduced the concept of induction in embryonic development. Now integral to the field of developmental biology, induction is the process by which the identity of certain cells influences the developmental fate of surrounding cells. Spemann received the Nobel Prize in Medicine in 1935 for his work in describing the process of induction in amphibians. The Spemann-Mangold organizer drew the attention of embryologists, and it spurred numerous experiments on the nature of induction in many types of developing embryos.

Maternal consumption of alcohol (ethanol) during pregnancy can inhibit prenatal growth, resulting in fetuses that are small for gestational age. Those prenatal growth deficiencies can have lasting consequences for early childhood development and are often reflected by low weight and stature. Those alcohol-induced pre- and post-natal growth deficiencies ("failure to thrive") are among the abnormal developmental criteria used to identify Fetal Alcohol Syndrome (FAS). FAS is characterized by minor facial abnormalities and deficiencies of the central nervous system as well. A deficiency in prenatal growth is often referred to as an intrauterine growth restriction (IUGR), a general term that refers to stunted fetal growth that may be a result of genetic or environmental factors.

In 1830, a dispute erupted in the halls of lÕAcad mie des Sciences in Paris between the two most prominent anatomists of the nineteenth century. Georges Cuvier and tienne Geoffroy Saint-Hilaire, once friends and colleagues at the Paris Museum, became arch rivals after this historical episode. Like many important disputes in the history of science, this debate echoes several points of contrasts between the two thinkers. The two French Ânaturalists not only disagreed about what sorts of comparisons between vertebrates were acceptable, but also about which principles ought to underlie a rational system of animal taxonomy and guide the study of animal anatomy. Digging deeper into their differences, their particular disagreements over specific issues within zoology and anatomy culminated in the articulation of two competing and divergent philosophical views on the aims and methods of the life sciences. The emergence of these two distinct positions has had a lasting impact in the development of evolutionary and developmental biology. This essay will provide an overview of the conceptual themes of the debate, its implications for the development of the life sciences, and its role in the history of embryology and developmental biology.

The Golgi staining technique, also called the black reaction after the stain's color, was developed in the 1870s and 1880s in Italy to make brain cells (neurons) visible under the microscope. Camillo Golgi developed the technique while working with nervous tissue, which required Golgi to examine cell structure under the microscope. Golgi improved upon existing methods of staining, enabling scientists to view entire neurons for the first time and changing the way people discussed the development and composition of the brain's cells. Into the twenty-fist century, Golgi's staining method continued to inform research on the nervous system, particularly regarding embryonic development.

William Hunter’s Anatomia Uteri Humani Gravidi Tabulis Illustrata (The Anatomy of the Human Gravid Uterus Exhibited in Figures), hereafter called The Human Gravid Uterus, is an anatomical atlas depicting the pregnant form through both engravings and descriptions. William Hunter, an anatomist working in England during the eighteenth century, compiled the work based on observations from his dissections of pregnant women. The collection of thirty-four copper plate illustrations details the anatomy of the pregnant human womb (gravid uterus), and includes depictions of unborn fetuses at various stages of development. Hunter compiled The Human Gravid Uterus to provide an objective anatomical depiction of pregnancy and development at a time when midwifery and obstetrics were becoming prominent fields of medical practice in England.

Maternal consumption of alcohol (ethanol) during pregnancy can result in a continuum of embryonic developmental abnormalities that vary depending on the severity, duration, and frequency of exposure of ethanol during gestation. Alcohol is a teratogen, an environmental agent that impacts the normal development of an embryo or fetus. In addition to dose-related concerns, factors such as maternal genetics and metabolism and the timing of alcohol exposure during prenatal development also impact alcohol-related birth defects.

Prenatal exposure to alcohol (ethanol) can result in a continuum of developmental abnormalities that are highly variable depending on the severity, duration, frequency, and timing of exposure during gestation. Defects of the corpus callosum (CC) have proven to be a reliable indicator of prenatal alcohol exposure as it affects the brain. Structural abnormalities of the CC occur along a continuum, like most alcohol-induced anomalies, whereby more severe prenatal exposure results in a greater expression of the abnormal trait. A variety of cognitive deficiencies are associated with defects of the fetal CC, the morphology of which can vary greatly between individuals and can be observed through neuroimaging over a broad transect of life stages.

A variety of developmental defects occur as a result of prenatal exposure to alcohol (ethanol) in utero. In humans, those defects are collectively classified as Fetal Alcohol Spectrum Disorders, with Fetal Alcohol Syndrome (FAS) representing the more severe defects. FAS is defined by pre- and post-natal growth retardation, minor facial abnormalities, and deficiencies in the central nervous system (CNS). In addition to those defects, prenatal exposure to alcohol impacts cardiogenesis, the developmental stage of heart formation.

Prenatal exposure to alcohol (ethanol) in human and animal models results in a range of alcohol-induced developmental defects. In humans, those collective birth defects are called Fetal Alcohol Spectrum Disorders, with the most severe manifestation being Fetal Alcohol Syndrome (FAS). FAS is defined by pre- and post-natal growth retardation, minor facial abnormalities, and deficiencies in the central nervous system (CNS). The basal ganglia, one of the central nervous system components, are affected by exposure to ethanol during development. When exposed to alcohol in utero, the basal ganglia decrease in size resulting in poor motor coordination and defects in executive functioning.

Prenatal exposure to alcohol (ethanol) results in a continuum of physical, neurological, behavioral, and learning defects collectively grouped under the heading fetal alcohol spectrum disorders (FASD). Fetal alcohol syndrome (FAS) is the most severe combination of these defects under this heading, and is characterized by pre- and postnatal growth deficiencies, facial abnormalities, and defects of the central nervous system (CNS). The developing brain is particularly vulnerable to the toxicity of ethanol, given the broad time frame of susceptibility from neurulation, when the neural tube is formed, all the way through to birth. The cerebellum is an area of the brain particularly vulnerable to prenatal ethanol exposure. Mechanisms proposed for this drastic reduction in brain cells include apoptosis, oxidative stress, and damage to the radial glia stem cell progenitor pool. Physical dexterity, coordination, and visuospatial processing are all affected by these stressors, and eyeblink classical conditioning tests have proven that ethanol-induced damage goes beyond motor coordination by permanently impacting learning and memory.