Brain Mechanisms for Offense, Defense, and Submission
Defense: Motivating stimuli Page 5

Title/Abstract page

Pages 1 - 2

Defense: motivational mechanism
Page 3

Defense: motivating stimuli
Pages 4 - 5

Defense: motor patterning mechanism
Page 6

Defense: releasing & directing stimuli
Page 7

Pages 8 - 9 - 10

Pages 11 - 12

Primitive mammals & primates
Page 13

Pages 14 - 15 - 16

Figure 1: Defense
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Figure 2: Submission
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Figure 3: Interaction
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Figure 4: Offense
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Figure 5: Composite
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Open Peer Commentary
Pages 22-49

Author's Response:
motivational systems

Pages 50 - 51 - 52

Author's Response:
alternative analyses

Page 53

Author's Response:
specific questions

Pages 54 - 55 - 56

Author's Response:

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References A-E
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References F-M
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References N-Z
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(section continued from previous page)

The neural pathways for visual, auditory, tactile and painful motivating stimuli for defense are shown converging upon the central gray in Figure 1. Since the output pathways from the defense motivational mechanism to motor patterning mechanisms for defense are primarily descending ones, this illustrates why defense is not abolished after removal of the forebrain.

There is at least one major forebrain pathway that activates defense. Lesions of this pathway do not abolish defense, presumably because other motivating stimuli activate pathways that ascend to the defense motivational mechanism through the hindbrain and midbrain. Electrical stimulation of this pathway elicits coordinated defense patterns in the cat (Hess & Brugger 1943; Hunsperger 1956; and many other authors) and rat (Panksepp 1971). The pathway extends from the amygdala to the lateral preoptic area by way of ventral efferent fibers (Milton & Zbrozyna 1963) to the perifornical hypothalamus and then back to the midbrain central gray. The directionality of this pathway has been established by combined stimulation and lesion experiments (Fernandez de Molina & Hunsperger 1962; Hunsperger 1956). Thus, stimulation effects from the amygdala depend upon an intact hypothalamus and central gray, but not vice versa, and stimulation effects from the hypothalamus depend upon an intact midbrain central gray.

Details of the forebrain pathway activating defense have been revealed in experiments using brain stimulation. To some extent defense patterns are a function of the releasing and directing stimuli present during stimulation; thus if no attackable object is present, the stimulated cat may flee, but if a stuffed cat is present, then striking or biting may occur (Brown et al. 1969a). There may also be differences in motor patterns as a function of the locus of stimulation. Affective defense from the perifornical hypothalamus is obtained from a core region surrounded by an area from which fleeing responses are obtained (Hunsperger 1956). Similarly, in the amygdala there are two adjacent regions for affective defense and for fleeing (Ursin & Kaada 1960). As will be discussed later, this may reflect an interaction between defense and submission systems.

The functional significance of the forebrain defense pathway is not known. Bilateral destruction of the perifornical region of the hypotha1amus in the cat does not impair affective defense against an attacking dog (Hunsperger 1956). There are other types of motivating stimuli for defense, however, that have not been tested in animals with forebrain lesions. In particular, pheromones and stimuli associated with neophobia might be expected to involve forebrain pathways. And while defense, as will be noted later, is inhibited by familiar animal odors, it may be facilitated by unfamiliar ones.

One particular surgical effect may be related to destruction of input pathways to the defense-motivational mechanism. Lesions of the far lateral midbrain at the level of its junction with the diencephalon in cats produce a syndrome in which defense behavior is greatly depressed. The cat fails to respond defensively to another attacking cat or dog; it has a high threshold for defense to painful tactile stimulation (Sprague et al. 1961) and does not show the hyperdefensiveness normally seen after lesions of the ventromedial hypothalamus (Kaelber et al. 1965; Glusman et al. 1961), The effect is apparently not due to interruption of medial lemniscal afferents to the thalamus and cortex, since lesions of the thalamic relay nuclei do not produce such an effect (Glusman et al. 1961). Instead, it may be due to interruption of afferents to the central gray from ascending tactile and pain pathways (Sprague et al. 1961) and from visual afferents as well, since lesions that abolish visually-motivated defense always involve undercutting the connections from the pretectum and superior colliculus to the central gray (Sprague et al l961).

(End of section)

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