Brain Mechanisms for Offense, Defense, and Submission
Author's Response:
Specific questions concerning offense, defense, and submission
Page 56

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
Page 58

References F-M
Page 59

References N-Z
Page 60


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(Section continued from previous page)

The role of the cingulate and frontal cortex in aggressive behavior is much more complicated that I indicate in the target article. Although cingulate lesions have been reported to enhance defense in laboratory cats (Koridze and Oniani 1972), Ursin found no changes in defense following cingulate lesions in wild cats. Eichelman points out that cingulate lesions in the rat can decrease the frequency of shock-induced fighting, although in neither of the studies that he quotes were the effects statistically significant (Blanchard and Blanchard 1968; Eichelman 1971). Also, electrical stimulation of the cingulate cortex in the rat does not affect defense and submission in the same way as does septal stimulation (see Albert). A report that cingulate lesions in monkeys can decrease defense, which I quote in the target article (Glees, Cole, Whitty, and Cairns 1950) was not replicated by a later study (Pribram and Fulton 1954). The role of the frontal cortex in aggression is also more difficult to assess than I have indicated. Although the data from frontal lesions in the rat and monkey could be interpreted to mean that the frontal cortex normally inhibits the consociate modulator, Ursin points out that he and Divac showed several years ago that there were no effects of frontal cortex lesions upon the defensiveness of wild cats. About all that one can conclude at this time is that these structures are somehow involved in the defense and submission motivational systems.

My terminology for offense, defense, and submission is questioned, or, at least, not accepted by a number of commentators. The Blanchards and Ursin prefer the term "attack" as a synonym for "offense." I use the term "offense" partly in deference to the traditional use of the term by Grant and Mackintosh (1963). In addition, I do not like the term "attack" in this context because it implies that defense cannot include attack and, as Eichelman points out in his commentary, defensive attacks may inflict severe physical damage. Panksepp would use the terms "rage" and "fear" rather than offense and defense. The term "rage" implies 1ack of control and extreme violence, whereas offense behavior, as l understand it, can occur in a wide range of intensities and can be quite well directed and controlled. The term "fear" does not imply action as much as does "defense." And since 1 think that the motivational systems are primarily programs for action, I think that the latter is a more appropriate term.

Semantic differences also arise in Waldbillig's commentary. He suggests that Baxter (1967) meant offense rather than defense when he said "attack." I disagree, since, as I mention above, I consider that practically all of the aggressive behavior reported from brain manipulations in cats is defense, not offense. Waldbillig also considers that I have been misled by the use of the term "fear" by Roberts (1962) when I call the behavior of cats during dorsomedial thalamic stimulation a form of submission. In the words of Roberts, "In the crouching response, the animal crouched 1ow; looked around its environment, and engaged in occasional locomotor activity which was maintained close to the floor at all times with absence of any climbing upward. If given the opportunity, the animal would run over to a dark corner or a box and crouch as if hiding." Roberts further notes that the crouching and lack of climbing upward distinguishes this response from the behavior induced by hypothalamic stimulation. The crouching and fleeing that Roberts reports, and the absence of striking or lunge-and-bite attack, fit generally with the hypothesis that these lesions enhance submission rather than defense. I have based .my analysis upon the motor patterns described in this case; not upon Roberts' use of the word "fear," which is what Waldbillig suggests. My model cannot, however, explain why following one type of stimulation the cat flees into dark corners and following the other it flees by climbing.

There is another behavior called "submission" that, in my opinion, is totally different from the one described here. It is characterized by Laborit as "the memory of the inescapability of punishment. ..or impossibility of coping with a situation." I do not think that it necessarily represents activation of the submission motivational system. Instead, I conceive of it as an artificial laboratory problem that arises when an animal is given motivating stimuli for submission and defense, such as pain, but is not given any releasing stimuli so that it can produce an appropriate motor pattern in response. It is not given releasing stimuli from a conspecific which would release defensive upright posture, lunge-and-bite attack, full submissive posture, and so on. And it is not given releasing stimuli for escape. Under such a circumstance, which would rarely arise under natural conditions, the animal is left to express the only motor patterns that do not require releasing stimuli, freezing and vocalization.

The consociate modulator is crucial to my distinction between defense and submission. Therefore, it is particularly important to clarify that just because I give the consociate modulator an anatomical locus, I do not make the inference that it is completely hard-wired, as Miczek attributes to me. Instead, as I point out as the third item in the list of learning effects on aggression, the forebrain inputs to the consociate modulator are developed as a function of experiences that may be considered as a form of imprinting. The data supplied by Karli in his commentary support my contention that structures that project to the ventromedial hypothalamus should play a critical role in these imprinting effects. As Karli points out, lesions of the amygdala or stria terminalis interfere with the inhibition of attack upon a familiar consociate (in this case, a rat against a mouse with whom it has become familiar), and the effects of septal lesions depend upon whether or not such familiarity has developed prior to placement of the lesion.

Frustration or extinction-induced aggression is mentioned by several commentators (Eichelman, Andrew, and Panksepp) as if I had not discussed it. I intended to say that I consider these types of aggression as aspects of competitive fighting, which is a type of offense. I use the term "competitive fighting" in deference to its historical usage by Fredericson (1950), rather than using the term "frustration," which is rather anthropomorphic, or the term "extinction-induced aggression," which is restricted in application to artificial laboratory techniques.

(End of section)

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