- Email: [email protected]
The physiology of motivation by Eliot Stellar
Brain Research Bulletin, Vol. 50, Nos. 5/6, pp. 451– 452, 1999 Copyright © 1999 Elsevier Science Inc. Printed in the USA. All rights reserved 0361-9230/99/$–see front matter
PII S0361-9230(99)00129-X
The Physiology of Motivation by Eliot Stellar Philip Winn* School of Psychology, University of St Andrews, Fife, Scotland [Received 30 April 1999; Accepted 8 May 1999] relate specific psychological functions to specific pieces of tissue. Stellar’s work no longer occupies the place it once did— modern techniques have led to rejection of the idea of drive centres [4,7]— but in its time, his theory was little short of perfect. I chose this as a high point in twentieth century neuroscience not because it is right, but for two other reasons: first, because of the profound impact it had on the study of brain mechanisms of motivation. A search through behavioural neuroscience journals from the mid-1950s to the mid-1970s reveals article after article concerned with motivated behaviour, all working within Eliot Stellar’s theoretical compass. Second, retrospective consideration of The Physiology of Motivation serves to illustrate what a change has occurred in the way we conceive of the relationships between brain and behaviour. Stellar’s theory represents a high point for what was in essence the phrenological conception of the nervous system—the belief that specific psychological functions can be tagged to specific brain structures. Such a view will no longer do. Theories about parallel distributed processes, neural networks and novel theoretical approaches to neural architectures [3,5] are producing changes in the way we approach relationships between brain systems and psychology. It should not be forgotten though, that the best stimulus to theoretical development is the existence of a theory against which observations can be gauged. For 25 years, Eliot Stellar’s The Physiology of Motivation was the best account of the relationship between brain systems and motivated behaviour and, even as the theory broke down, provided the impetus to develop fresh approaches: a genuinely magisterial conception.
In the 1940s and early 1950s it was clear that specific stimuli were associated with individual motivated behaviours. But while, for example, a relationship between levels of glucose and eating was known [1], it was also apparent that specific stimuli were not, in and of themselves, sufficient to produce motivated behaviour. Motivation, as a construct in its own right, was growing in importance for learning theorists and physiological psychologists, to the extent that Morgan [2] suggested various factors governing motivated behaviour could combine to produce a “central motive state” which, on achieving a particular level, would trigger production of appropriate behaviour. What Eliot Stellar provided in The Physiology of Motivation was a neural basis for this central motive state [6]. His claim was that “the amount of motivated behavior is a direct function of the amount of activity in certain excitatory centers of the hypothalamus” (p. 6), these excitatory centres being governed by inhibitory hypothalamic centres, sensory stimuli, the internal environment and cortical and thalamic centres. Stellar stressed that a variety of stimuli, both conditioned and unconditioned, were processed by the hypothalamus and that no one stimulus was indispensable to the production of motivated behaviour. He also recognized that, because of the variety of factors involved, and different responses required, no part of the brain could have absolute control over motivated behaviour, though he nevertheless gave a central role to the hypothalamus: the “ . . . interaction of factors occurs in the hypothalamus and takes the form of the ‘addition’ of all excitatory influences and the ‘subtraction’ of all inhibitory influences” (p. 14). Stellar’s conception came to be expressed in terms of reciprocally acting drive centres—an excitatory centre to start behaviour and an inhibitory one to stop it—and nowhere was this better expressed than in the control of feeding. Bilateral electrolytic lesions of the ventromedial hypothalamic area produced a syndrome involving overeating and body weight gain, while similar lesions of the lateral hypothalamic area produced the opposite—a syndrome involving body weight loss and aphagia. These were excitatory and inhibitory centres made real, and huge efforts were expended over the next 20 years to characterize them. The Physiology of Motivation had extraordinarily wide appeal. It accounted for a growing body of literature regarding the effects of discrete hypothalamic lesions on motivated behaviours and made predictions as to what one might expect to find. It was compatible with physiological concepts of homeostasis and psychological theories of motivation, and it followed a long tradition of thinking in neuroscience that sought to
REFERENCES 1. Mayer, J.; Vitale, J. J.; Bates, M. W. Mechanism of the regulation of food intake. Nature 167:562–563; 1951. 2. Morgan, C. T. Physiological psychology, 1st ed. New York: McGrawHill; 1943. 3. Prescott, T. J.; Redgrave, P.; Gurney, K. Layered control architectures in robots and vertebrates. Adaptive Behav. 7:99 –127; 1999. 4. Risold, P. Y.; Thompson, R. H.; Swanson, L. W. The structural orga-
* Address for correspondence: Dr. Philip Winn, School of Psychology, University of St Andrews, St Andrews, Fife KY16 9JU, Scotland. Fax: ⫹44 1334 463042; E-mail: [email protected]
451
452 nization of connections between hypothalamus and cerebral cortex. Brain Res. Rev. 24:197–254; 1997. 5. Spitzer, M. The mind within the net. Cambridge, MA: The MIT Press; 1999.
WINN 6. Stellar, E. M. The physiology of motivation. Psychol. Rev. 154:5–22; 1954. 7. Winn, P. The lateral hypothalamus and motivated behavior: An old syndrome reassessed and a new perspective gained. Curr. Dir. Psychol. Sci. 4:182–187; 1995.
PII S0361-9230(99)00129-X
The Physiology of Motivation by Eliot Stellar Philip Winn* School of Psychology, University of St Andrews, Fife, Scotland [Received 30 April 1999; Accepted 8 May 1999] relate specific psychological functions to specific pieces of tissue. Stellar’s work no longer occupies the place it once did— modern techniques have led to rejection of the idea of drive centres [4,7]— but in its time, his theory was little short of perfect. I chose this as a high point in twentieth century neuroscience not because it is right, but for two other reasons: first, because of the profound impact it had on the study of brain mechanisms of motivation. A search through behavioural neuroscience journals from the mid-1950s to the mid-1970s reveals article after article concerned with motivated behaviour, all working within Eliot Stellar’s theoretical compass. Second, retrospective consideration of The Physiology of Motivation serves to illustrate what a change has occurred in the way we conceive of the relationships between brain and behaviour. Stellar’s theory represents a high point for what was in essence the phrenological conception of the nervous system—the belief that specific psychological functions can be tagged to specific brain structures. Such a view will no longer do. Theories about parallel distributed processes, neural networks and novel theoretical approaches to neural architectures [3,5] are producing changes in the way we approach relationships between brain systems and psychology. It should not be forgotten though, that the best stimulus to theoretical development is the existence of a theory against which observations can be gauged. For 25 years, Eliot Stellar’s The Physiology of Motivation was the best account of the relationship between brain systems and motivated behaviour and, even as the theory broke down, provided the impetus to develop fresh approaches: a genuinely magisterial conception.
In the 1940s and early 1950s it was clear that specific stimuli were associated with individual motivated behaviours. But while, for example, a relationship between levels of glucose and eating was known [1], it was also apparent that specific stimuli were not, in and of themselves, sufficient to produce motivated behaviour. Motivation, as a construct in its own right, was growing in importance for learning theorists and physiological psychologists, to the extent that Morgan [2] suggested various factors governing motivated behaviour could combine to produce a “central motive state” which, on achieving a particular level, would trigger production of appropriate behaviour. What Eliot Stellar provided in The Physiology of Motivation was a neural basis for this central motive state [6]. His claim was that “the amount of motivated behavior is a direct function of the amount of activity in certain excitatory centers of the hypothalamus” (p. 6), these excitatory centres being governed by inhibitory hypothalamic centres, sensory stimuli, the internal environment and cortical and thalamic centres. Stellar stressed that a variety of stimuli, both conditioned and unconditioned, were processed by the hypothalamus and that no one stimulus was indispensable to the production of motivated behaviour. He also recognized that, because of the variety of factors involved, and different responses required, no part of the brain could have absolute control over motivated behaviour, though he nevertheless gave a central role to the hypothalamus: the “ . . . interaction of factors occurs in the hypothalamus and takes the form of the ‘addition’ of all excitatory influences and the ‘subtraction’ of all inhibitory influences” (p. 14). Stellar’s conception came to be expressed in terms of reciprocally acting drive centres—an excitatory centre to start behaviour and an inhibitory one to stop it—and nowhere was this better expressed than in the control of feeding. Bilateral electrolytic lesions of the ventromedial hypothalamic area produced a syndrome involving overeating and body weight gain, while similar lesions of the lateral hypothalamic area produced the opposite—a syndrome involving body weight loss and aphagia. These were excitatory and inhibitory centres made real, and huge efforts were expended over the next 20 years to characterize them. The Physiology of Motivation had extraordinarily wide appeal. It accounted for a growing body of literature regarding the effects of discrete hypothalamic lesions on motivated behaviours and made predictions as to what one might expect to find. It was compatible with physiological concepts of homeostasis and psychological theories of motivation, and it followed a long tradition of thinking in neuroscience that sought to
REFERENCES 1. Mayer, J.; Vitale, J. J.; Bates, M. W. Mechanism of the regulation of food intake. Nature 167:562–563; 1951. 2. Morgan, C. T. Physiological psychology, 1st ed. New York: McGrawHill; 1943. 3. Prescott, T. J.; Redgrave, P.; Gurney, K. Layered control architectures in robots and vertebrates. Adaptive Behav. 7:99 –127; 1999. 4. Risold, P. Y.; Thompson, R. H.; Swanson, L. W. The structural orga-
* Address for correspondence: Dr. Philip Winn, School of Psychology, University of St Andrews, St Andrews, Fife KY16 9JU, Scotland. Fax: ⫹44 1334 463042; E-mail: [email protected]
451
452 nization of connections between hypothalamus and cerebral cortex. Brain Res. Rev. 24:197–254; 1997. 5. Spitzer, M. The mind within the net. Cambridge, MA: The MIT Press; 1999.
WINN 6. Stellar, E. M. The physiology of motivation. Psychol. Rev. 154:5–22; 1954. 7. Winn, P. The lateral hypothalamus and motivated behavior: An old syndrome reassessed and a new perspective gained. Curr. Dir. Psychol. Sci. 4:182–187; 1995.