Affective Neuroscience: The Foundations of Human and Animal Emotions

By Jaak Panksepp | Go to book overview

"improvement" of the human race by selective breeding or destruction. 50 Nazi and Communist criminals during this century experimented with their own variants of such conceptual monstrosities. We should be aware, however, that the threats posed by biological knowledge can be tempered if we always discriminate between "what is" and "what should be" in discussing the human condition. We can accept the former without ascribing to the "naturalistic fallacy" that biological facts provide any logical mandates for "ought" statements. 51

It will be intriguing to find out how various emotional characteristics of animals are inherited and the extent to which they can be modified by experience. Although emotional traits can be selectively strengthened or weakened by breeding as well as by crossrearing in animal experiments, 52 comparatively little has been done with a direct neural end point, such as selection for the strength of specific neurochemical systems or the sensitivity of a specific neuronal system. One of the few relevant pieces of work is the demonstration that animals can be selected for high and low lateral hypothalamic self-stimulation tendencies. 53 Other recent work has shown that neurochernical profiles of the brain can be inherited in both animals and humans. 54

Such analyses have great potential for advancing our understanding of how the innate operating systems of the mammalian brain control the behavioral proclivities that characterize different temperaments, as well as the emotional disorders and other forms of mental illness that can run in families. 55 Although it is likely that affective proclivities can be inherited, we do not yet understand which genes and what aspect of brain organization are conveying different emotional inclinations. Some appreciation of how things might operate is emerging from ongoing work on various neuropsychiatric disorders in humans.

Recently, there has been great success in revealing the genetic mechanisms of certain disorders such as Huntington's disease, which arises from a specific type of degeneration in ancient brain systems called the basal ganglia (see Chapter 4) and is accompanied by an emotional lability and cognitive disintegration that initially resemble schizophrenia. After an initial phase of mental deterioration, the normal flow of motor activities becomes impaired and individuals begin to exhibit uncontrollable and irregular muscle movements, the spontaneous "dance" of the motor apparatus known as Huntington chorea. The source of this disorder has been tracked to a segment on the end of the long arm of chromosome 4, where the normal nucleotide repeat of CAG (cytosine, adenine, guanine), which in normal individuals never exceeds 34 repeats and usually comes in 11 to 24 repeats, has increased to more than 42 and even up to 100 among individuals afflicted with Huntington's. 56 Indeed, many other psychiatric and neurological disorders may also be due to similarly excessive "trinucleotide repeats" within other genes. 57

The most severe forms of Huntington's disease, with childhood onset, have the largest number of repetitions of the CAG triplet, which codes for glutamate, one of the most powerful and important brain transmittersone that is an essential component of normal emotional, cognitive, and motor responses (see Chapter 6). Excessive generation of glutamate in the brain seems to explain the symptoms of Huntington's disease, and perhaps even the brain damage that eventually develops. It has long been known that high levels of glutamate can be neurotoxic. 58 In the United States, this finding eventually led to an FDA-mandated elimination of monosodium glutamate (MSG) as a taste enhancer in baby foods. In other words, a "good" molecule that normally allows us to behave and think normally becomes a "bad" molecule in excess, destroying a person's normal ability to live in the world.

As we emphasize such issues, we should remember that all brain organ systems, even straightforward sensory ones such as vision, are susceptible to modification at the biological level as a result of early experiences (including intrauterine ones). 59 From this vantage, it will be most interesting to determine whether powerful emotional experiences early in life are able to modify the underlying neural circuits for the life span of an organism. There are now excellent new genetic and anatomical tracing techniques to analyze such questions at the neural level (see Chapter 4).


*3*Suggested Readings

Ekman, P., & Davidson, R. (eds.) ( 1994). Questions about emotions. New York: Oxford Univ. Press.

Gallistel, C. R. ( 1980). The organization of action: A new synthesis. Hillsdale, N.J.: Lawrence Erlbaum.

Konner, M. ( 1982). The tangled wing: Biological constraints over the human spirit. New York: Holt, Rinehart and Winston.

Oaksford, M., & Brown, G. (eds.) ( 1994). Neurodynamics and psychology. New York: Academic Press.

Plomin, R., De J. C. Fries, & McClearn, G. E. ( 1990). Behavioral genetics: A primer (2d ed.). San Francisco: Freeman.

Schulkin, J. (ed.) ( 1993). Hormonally induced changes in mind and brain. San Diego: Academic Press.

Tinbergen, N. ( 1951). The study of instinct. London: Oxford Univ. Press.

Valenstein, E. S. ( 1973). Brain control. New York: Wiley.

Vernon, P. A. (ed.) ( 1994). The neuropsychology of individual differences. New York: Academic Press.

Wright, R. ( 1994). The moral animal. New York: Random House.

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