Hormone-Brain Interactions and Their Influence on Agonistic Behavior
Conclusion Page 10


Title & Introduction
Page 1

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Offense, Defense & Patrol/Marking
Page 2

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Neural Circuitry & Motivational Mechanisms
Page 3

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How Circulating Hormones May Affect Behavior
Page 4

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Androgens
Page 5

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Estrogens
Page 6

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Pregnancy and Lactation
Page 7

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ACTH, etc.
Page 8

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Reproductive States
Page 9

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Conclusion
Page 10

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References
Page 11

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Figure 1
Page 12


CONCLUSION

Most of the effects of hormones on agonistic behavior in muroid rodents can be accounted for in terms of their actions on the six hypothetical neural mechanisms illustrated in Figure 1. They are the motivational mechanisms of patrol/marking and offense, the consociate modulator, and three sets of sensory analyzers tuned to pheromones that depend for their secretion on gonadal hormones. Although these mechanisms are still hypothetical, there are some data that suggest what may be their anatomical substrates. The uptake of corticosteroids and progestins in the region of the ventromedial hypothalamus is consistent with the suggestion that neurons of that nucleus are involved in the hypothetical consociate modulator. And the uptake of the gonadal hormones in the preoptic region of the hypothalamus is consistent with the suggestion that neurons in that region are involved in the motivational mechanism of patrol/ marking and sensory analyzers for motivating stimuli of patrol/marking and offense.

The picture of hormonal action presented in Figure 1 is still very hypothetical. It depends on a neural organization of agonistic behavior consisting of four motivational systems and distinctions between components of motivational systems that have been hypothesized only recently and that have not yet received the hard tests of experimentation (Adams, 1979a). It also depends on data concerning the effects of hormones on agonistic behavior, which are still incomplete. For example, data on the effects of progestin on agonistic behavior of females has been obtained only in the past few years and is only preliminary. Similarly, the data on prolactin are still highly controversial and the data on the effects of estrogen on female offense are sketchy. No doubt, new experiments will force a revision of our knowledge of how hormones affect behavior.

Even if the picture presented here is correct in its basic outlines, it will no doubt turn out to be an oversimplification. We can expect that hormones act at more than six points in the motivational systems of agonistic behavior. For example, there are effects of hormones on peripheral receptive fields, mediated perhaps by the sympathetic nervous system (Bereiter, Stanford, & Barker, 1980). And we can expect that hormones besides those illustrated have effects on agonistic behavior. For example, there are reports that vasopressin (Leshner & Roche, 1977) and alpha-melanocyte stimulating hormone (Nowell, Thody, & Woodley, 1980) may have effects on submission and patrol/marking, respectively.

The picture is also oversimplified because the neural mechanisms of agonistic behavior operate within a larger framework of behaviors that are influenced by and play a role in establishing and maintaining the reproductive states of the individual. Not only agonistic behaviors but also sexual and parental behaviors are involved in these reproductive states and need to be considered because they may interact with agonistic behaviors.

Like all such theoretical formulations, the present one is intended to pose hypotheses and stimulate the design of critical experiments. Even if the picture presented here turns out to be incorrect, it will be useful if it leads to the generation of critical data that can be used to draw a new picture of the mechanisms of agonistic behavior that corresponds even more closely to its anatomical basis.

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