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The central nervous system (CNS) plays a vital role in regulating energy balance and metabolism. Over the last 50 years, studies in animal models have allowed us to identify critical CNS regions involved in these processes and even crucial cell populations. Now, techniques for genetically and anatomically targeted manipulation of specific neural populations using light (optogenetic), ligands (chemogenetic), or magnetic fields (radiogenetic/magnetogenetic) allow detailed investigation of circuits involved in metabolic regulation. In this review, we provide a brief overview of recent studies using light- and magnetic field-regulated neural activity to investigate the neural circuits contributing to metabolic control.

The central nervous system relies on a continual supply of glucose, and must be able to detect glucose levels and regulate peripheral organ functions to ensure that its energy requirements are met. Specialized glucose-sensing neurons, first described half a century ago, use glucose as a signal and modulate their firing rates as glucose levels change. Glucose-excited neurons are activated by increasing glucose concentrations, while glucose-inhibited neurons increase their firing rate as glucose concentrations fall and decrease their firing rate as glucose concentrations rise. Glucose-sensing neurons are present in multiple brain regions and are highly expressed in hypothalamic regions, where they are involved in functions related to glucose homeostasis. However, the roles of glucose-sensing neurons in healthy and disease states remain poorly understood. Technologies that can rapidly and reversibly activate or inhibit defined neural populations provide invaluable tools to investigate how specific neural populations regulate metabolism and other physiological roles. Optogenetics has high temporal and spatial resolutions, requires implants for neural stimulation, and is suitable for modulating local neural populations. Chemogenetics, which requires injection of a synthetic ligand, can target both local and widespread populations. Radio- and magnetogenetics offer rapid neural activation in localized or widespread neural populations without the need for implants or injections. These tools will allow us to better understand glucose-sensing neurons and their metabolism-regulating circuits.

Radiotherapy is involved in many curative treatments of cancer; millions of survivors live with the consequences of treatment, and toxicity in a minority limits the radiation doses that can be safely prescribed to the majority. Radiogenomics is the whole genome application of radiogenetics, which studies the influence of genetic variation on radiation response. Work in the area focuses on uncovering the underlying genetic causes of individual variation in sensitivity to radiation, which is important for effective, safe treatment. In this review, we highlight recent advances in radiotherapy and discuss results from four genome-wide studies of radiotoxicity.

It is shown that the assumption of a cumulative action of many independent random events as the primary cause of induction of a mutation fits the experimental data at least equally as well as the single event hypothesis. The theory is illustrated on the existing data of X-ray induced lethals in the X-chromosome ofDrosophila. Possible shortcomings of the single event theory in connection with these experimental data and alternative ways of its modification are indicated.

SINCE the fundamental work in radiogenetics by H. J. Muller2 it has been shown consistently by all experimenters that short wave radiation possesses a mutation-producing effect. This was demonstrated in the case of ultra-violet light by Altenburg (1934); for Grenz rays by Timofeeff-Ressowsky and Zimmer (1935), Wilhelmi, and Timofeeff-Ressowsky (1931); for x-rays of different degrees of hardness by Muller (1928, 1930, and 1934), Oliver (1932 and 1934), and Timofeeff-Ressowsky (1931, 1934, and 1937); for radium rays and alpha rays by Zimmer and Timofeeff-Ressowsky (1936); for beta and cathode rays by Hanson and Heys (1929) and Timofeeff (1931 and 1934), and for gamma rays by Hanson and Heys (1929), Pickhan (1935), and Timofeeff-Ressowsky (1937). Extensive research with beta rays was carried out by Zimmer, Griffith, and Timofeeff-Ressowsky, in 1937. All these authors came to the conclusion that all types of radiations which they used produced mutations, and that the rate of mutation thereby produced is in di...