Brain Mechanisms for Offense, Defense, and Submission
Defense: Motivational mechanism Page 3

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
Page 17

Figure 2: Submission
Page 18

Figure 3: Interaction
Page 19

Figure 4: Offense
Page 20

Figure 5: Composite
Page 21

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:

Page 57

References A-E
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References F-M
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References N-Z
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Page 61

The defense motivational mechanism. There are neurons in the midbrain central gray and adjacent tegmentum that meet the criteria for the hypothetical motivational mechanism for defense in the rat. A lesion that totally destroys this region produces a syndrome in rats that includes the loss of all motor defense patterns in response to all motivating stimuli that have been tested. Defensive upright posture and boxing, escape, and vocalization are all abolished in response to footshock, and freezing is abolished in the open-field test situation (Edwards & Adams 1974). Vocalization is abolished in response to restraint and dorsal tactile stimulation (Chaurand et at 1972), and biting and escape as well as vocalization are abolished in response to these motivating stimuli (observation of animals described in Edwards & Adams 1974). Escape in response to footshock (Halpern 1968; Liebman et al. 1970) or loud noise (Lyon 1964) is also abolished by central gray lesions in the rat.

Electrical stimulation of the central gray and adjacent midbrain in the rat produces escape behavior, biting, and vocalization (Wolfle et al 1971; Waldbillig 1975), although it has not been reported to produce the upright posture. Neurons in this region are specifically active during shock-elicited defense (Pond et al. 1977).

Data from the cat are similar to those from the rat. In the cat, lesions of the midbrain central gray abolish defense motor patterns including vocalization, threat postures, attack, and defense in response to various types of motivating stimuli (Kelly et al. 1946; Hunsperger 1956; Skultety 1963). Electrical stimulation (Hunsperger 1956; Skultety 1963; Adams 1968) and chemical stimulation (Baxter 1968) of this region in the cat produce escape and "affective defense," which includes defense postures, vocalization, striking, and biting. There are neurons in this region in the cat that are active if and only if the animal is engaged in affective defense (Adams 1968).

There are even data from the distantly-related chicken that suggest that the same brain region may contain a defense motivational mechanism (DeLanerolle & Andrew 1974). Midbrain central gray lesions in the chicken abolish or depress defense vocalizations, defensive pecking, and freezing in a novel environment (Andrew & DeLanerolle 1974), while electrical stimulation of the region produces escape and defense vocalization (Andrew 1973).

There are two instances of contradictory data from the cat that require discussion. Lesions of the midbrain central gray fail to abolish the aggressive behavior of the "thalamic cat" (Carli et al. 1963), and such lesions only temporarily interrupt the aggressive behavior following lesions of the ventromedial hypothalamus (Glusman 1974). There are two possible explanations consistent with the hypothetical role of the central gray as the defense motivational mechanism. First, it is possible that the observed behavior was offense rather than defense. Second, it is possible, at least in the latter case, that the lesions did not destroy the entire defense motivational mechanism but left some tissue remaining that became supersensitive to remaining inputs.

There is some evidence that following extensive hypothalamic lesions the behavior that is seen may be offense rather than defense. In the rat, lesions of the posterior portion of the ventromedial nucleus lead to offense rather than defense (Olivier 1977), while lesions of the anterior part of the nucleus lead to defense. I have noticed offense behaviors following similar lesions that destroyed both lateral and medial hypothalamus at the level of the ventromedial nucleus (in animals studied by Adams 1971). These rats displayed offensive sideways posture and bite-and-kick attacks when tested in a shock box - an effect I have never seen in normal animals. Upon examination of the histology it was observed that the offense had been exhibited only by animals with sparing of the posterior hypothalamus.

In order to abolish defense, lesions of the midbrain central gray must be complete. The entire rostral-caudal extent of the central gray must be destroyed, as well as part of the tegmentum adjacent to the lateral borders of the central gray. Partial lesions cause increased defense rather than diminishing it (Edwards & Adams 1974). This suggests that there may be some inhibitory processes in the circuitry of the defense system within the central gray which can be released by partial lesions. Although the midbrain central gray is often considered to be separate from the tegmentum that lies lateral to it, this separation may be artificial and due simply to the intrusion of tectofugal and posterior commissure fibers, which swing down and surround the central gray region. Both anatomical (Mehler 1969) and physiological (Ruth & Rosenfeld 1977) data suggest that the separation is artificial, and that the central gray and adjacent tegmentum on its lateral borders should be considered a single functional anatomical unit. The entire rostral-caudal extent of the central gray is also critical for defense. Lesions that destroy only the rostral end, only the caudal end, or both rostral and caudal ends, leaving the central zone intact, do not produce complete deficits (see Figure 6 in Edwards & Adams 1974). Similar data have been reported in the cat (Skultety 1963): lesions that destroyed more than 80% of the central gray abolished defense; lesions that destroyed between 50% and 80% blocked defense for several weeks only; and lesions with less than 50% destruction did not reduce defense.

Consistent with the notion of the role of the midbrain central gray as the defense motivational mechanism, this area appears to be the major locus of the effects of morphine on defense Jacquet & Lajtha 1973; Yaksh et al. 1976; Dostrovsky & Deakin 1977).

The defense motivational system is illustrated in Figure 1. At the center of the system are two hypothetical pools of neurons in the midbrain central gray, one of which corresponds to the defense motivational mechanism, as described above. It is shown as receiving its input from a second set of neurons in the central gray, which receive the motivating inputs for both defense and submission. This distinction between two pools of neurons in the central gray is hypothesized in order to account for the ability of an animal to switch from defense to submission, as explained in the following section on the submission motivational system. Motivating inputs converge upon the central gray, as shown, and outputs diverge from the central gray to activate the various motor patterning mechanisms of defense.

(end of section)

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