20 May 2016

It's time to ban experiments on animals!

Excerpt from the book by Asi Kazantseva
"Someone is wrong on the Internet! Scientific research of controversial issues" Published in the newspaper "Troitsky variant" No. 204

It is important to understand that researchers have absolutely no desire to ruin as many innocent animals as possible. Any search for scientific publications on the words animal testing brings mainly materials on how to minimize the need for such research. Any experiments on animals are regulated by strict rules and are limited to ethical commissions.

In addition, working with animals is simply an expensive, time–consuming and time-consuming process; wherever it is possible to do without it, scientists strive to do so. The number of doctoral degrees in biology awarded in the USA has almost doubled over the past 30 years [1], while the number of animals used has not increased.

Rats and mice (as well as fish, amphibians, reptiles and birds) in the USA are not counted with accuracy to the individual, but, according to rough estimates, the total number of vertebrates used in experiments was about 20 million per year in the mid-1980s [2] and about 17 million per year in the mid-2000-x [3]. Much more accurate statistics exist for all mammals besides rats and mice (that is, for hamsters, rabbits, pigs, etc.) – in 1984, a little more than 2 million of these animals were used, and in 2014 exactly 834,453 pieces [4]. These figures seem impressive only until we compare them with the number of animals used for food annually. For example, with 8,666,62,000 chickens eaten in America in 2014 [5].

What are laboratory animals for? The three million mice used in 2013 in the UK are distributed [6] as follows. 59% of animals are involved in obtaining new lines using various methods of genetic modification, 28% move fundamental science, 11.5% are needed for applied medical research. 0.5% of animals are required for veterinary and environmental studies, and the remaining half percent are divided into educational projects and the use of mice for diagnosis (for example, if you have a patient with a suspicion of a particular infectious disease, but standard tests do not detect it yet, you can take some blood from him, try to infect mice and observe their condition).

If I correctly understood the British statistics, then these 59% reflect an intermediate stage of research. These are the animals whose genome has been changed in some way, and now they are crossed with each other to obtain genetically homogeneous lines and check whether the modified genes are now working (or, conversely, have stopped working) exactly as it was intended. When this process is completed, they will begin to participate in basic or applied research. A significant part of such animals is needed to understand the causes of human diseases [7]. Do you have any gene that you know for sure (or assume) that its mutations increase people's risk of developing diabetes, or Alzheimer's disease, or atherosclerosis, or some kind of cancer. You find the corresponding gene in a mouse, disrupt its work, make sure that the resulting animals really get sick more often, and then find out exactly why this happens and what drugs can compensate for the effect.

This approach turns out to be widely used precisely due to the fact that we are relatives with mice and many of our genes are almost identical. But there is another task: the study of those genes that, in the case of humans, on the contrary, differ markedly not only from mice, but even from the genes of chimpanzees. Almost every such gene is naturally suspected of "making us human," and sometimes with the help of genetically modified mice, you can get funny confirmations of this hypothesis.

The most famous – and most important – of such stories began in the late 1980s in one of the primary schools in the city of Brentford (de facto part of London). Elizabeth Auger, who worked there with children who lag behind the school curriculum, drew attention to the fact that several students from the same family demonstrate similar speech disorders. They started talking late, pronounced words unintelligibly (for example, bu instead of blue), did not use sentences longer than two or three words, had difficulty choosing words and often pronounced them inaccurately (for example, they said "glass" or "tea" when they were shown a cup and asked to tell them the name of this object), and also experienced difficulties with the perception of grammatical constructions (for example, they did not feel the difference between the sentences "a horse runs after a girl" and "a girl runs after a horse"). At the same time, the children did not have mental retardation, they coped with mathematics normally, could read and write; the problems were associated with oral speech. Elizabeth and her colleagues at the school contacted the clinical genetics department of the London Children's Hospital. The specialists who worked there compiled the family's pedigree [8].

It turned out that a child can inherit the disease from his parent with a 50% probability, and children in the same family may either have a pronounced problem or be completely absent. This is a classic picture of inheritance of a single dominant allele* and it became a sensation: until then it was assumed, and not unreasonably, that many different genes contribute to the development of speech. There are really a lot of them, but we managed to identify one particularly important one among them. Later it was identified; it was named FOXP2; it was found out that it encodes a transcription factor (a protein that activates the reading of certain genes), important for brain development; that this protein in humans is only two amino acids different from the protein of chimpanzees and that in Neanderthals it was the same as ours; that FOXP2 is involved in many processes related to the development of the brain, but most importantly – it is associated with speech not only in humans, but, apparently, in general in all animals that have sound communication between relatives in one form or another. For example, this applies to songbirds: normally zebra amadines reproduce quite accurately the song they heard in childhood, but when suppressing the work of FOXP2, they emit rather disparate (and all the time different) sounds instead of a single melody [9].

You have already noticed that in most cases, new information about the functions of genes is obtained as follows: they find or create a creature whose gene is broken, and look at what has gone wrong. FOXP2 is no exception: mice have been created for which it is simply turned off. In the event that not a single copy of the gene worked for them (in general, there are two of them: inherited from mom and dad), the animals, in principle, felt very bad, but including the mice, there was completely no ultrasonic squeak, which they normally use to call mom. If one normal copy of the gene was still present, the mice squeaked, but much less than normal [10].

But you can not spoil the genes of mice, but on the contrary, sorry for the anthropocentricity, improve them. Namely, to replace the mouse FOXP2 with a human one and see what kind of beast it turns out to be. Such mice were first created in 2009 [11]. They differed from ordinary mice in a number of structural and functional features of the brain, but in the context of the story about speech, the most interesting observation was due to the fact that the mice taken from the nest really squeaked a little differently, for example, they had longer episodes of complex squeaking (with differences in sound frequencies). However, the scientific community was more interested not in the differences in the squeak, but in the differences in learning ability. In 2014, a large study was published [12] in which mice with human FOXP2 (animals that are made to resemble humans in some way for research purposes, and are called: humanized) and ordinary mice wandered through mazes in search of food.

There are two ways to determine which of the corridors leads to the feeder. First, you can look at external landmarks. "The food will be in the side where the cross is drawn," the mouse could say, if it were sufficiently humanized for this. Secondly, you can memorize your own movements. "Straight and to the right," the mouse would explain. During preliminary tests, the scientists noted that humanized mice learn to use external landmarks faster than ordinary mice. However, the researchers were interested in something else: how quickly an animal can abandon a strategy that has lost its relevance. After scientists had demonstrated to mice for two weeks that in order to search for food, you need to raise your head, look at the wall of the laboratory, see the painted cross and go in this direction, they took and turned the maze 180 degrees. If at the same time they began to put food in another sleeve so that it would be next to the cross again, then ordinary and humanized mice realized equally quickly that they only need to believe the cross, and it doesn't matter that we are now turning left instead of right. But if you still had to turn to the right, and ignore the cross, then the humanized mice switched to the correct behavior much faster.

Why is this important? Because such a learning result shows that mice with human FOXP2 learn their own movements better. As the authors of the same work have shown, the striatum works differently in humanized mice - a part of the brain necessary for the formation of complex and multi–stage motor reactions. This suggests that human FOXP2, among its other functions, may be associated with our complex articulation, the ability to quickly and consistently control the lips, tongue, vocal cords to generate a variety of different sounds. It is clear that further research is required – and there will clearly be no shortage of them…


1. The National Center for Education statistics is a valuable storehouse of data on all aspects of American education. Data about biologists can be found at this link.
2. U. S. Congress, Office of Technology Assessment. Alternatives to Animal Use in Research, Testing, and Education. Washington, DC: U. S. Government Printing Office, OTA-BA-273, February 1986. The document is available at the link.
3. Taylor K. et al. Estimates for worldwide laboratory animal use in 2005 // Alternatives to Laboratory Animals, 2008 July, Vol. 36 (3), 327–342.
4. A graph clearly demonstrating the decline in the number of experimental animals in recent years is available at the link, and the data on which it is based are collected by the Animal and Plant Health Control Service at the US Department of Agriculture (Research Facility Annual Reports tab).
5. The number of animals slaughtered in 2014 according to the US Department of Agriculture: birds on the first link, mammals on the second.
6. Data from the Home Office, the British government's public safety unit. Home office. Annual Statistics of Scientific Procedures on Living Animals. Great Britain, 2013. The publication is available at the link.
7. Bagle T. et al. Transgenic animals and their application in medicine // International Journal of Medical Research & Health Sciences, 2013, Vol. 1, Issue 2, 107–116.
8. Hurst J. et al. An extended family with a dominantly inherited speech disorder // Developmental Medicine & Child Neurology, Apr. 1990, Vol. 32, Id. 4, 352–355.
9. Haesler S. et al. Incomplete and inaccurate vocal imitation after knockdown of FoxP2 in songbird basal ganglia nucleus area X // PLoS Biology, Dec. 2007, Vol. 5 (12), e321.
10. Shu W. et al. Altered ultrasonic vocalization in mice with a disruption in the Foxp2 gene // PNAS, July 2005; Vol. 102 (27), 9643–9648.
11. Enard W. et al. A humanized version of Foxp2 affects cortico-basal ganglia circuits in mice // Cell, May 2009, Vol. 137, Issue 5, 961–971.
12. Schreiweis C. et al. Humanized Foxp2 accelerates learning by enhancing transitions from declarative to procedural performance // PNAS, Sep. 2014, Vol. 111 (39), 14253–14258. 13 Hajar R. Animal testing and medicine // Heart Views.

Portal "Eternal youth" http://vechnayamolodost.ru  20.05.2016

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