McIntyre et al., 1976; Ounsted, 1969; Serafetinides, 1965). (Further discussion of human studies on aggression and the implications of the results of these studies to our understanding of underlying neural regulatory mechanisms appears later in this chapter). On the basis of these clinical reports, we have proposed that the limbic system functions as a major "modulator" of aggressive behavior. Implicit in this assumption is that the limbic system regulates the tendency for aggressive reactions to occur or be suppressed by its direct or indirect actions upon the hypothalamus or midbrain PAG. Findings relevant to these issues have been described fully in other review articles (Siegel and Edinger, 1981, 1983; Siegel and Brutus, 1990), which provide details as to the methods and the results of various limbic system manipulations. It is clear that limbic structures have a major modulatory action, and these are summarized in Table 1.
Thus, the principal finding of these studies is that the limbic system (including ventral and dorsal hippocampus, septal area, amygdala, and portions of the prefrontal cortex and cingulate gyrus) modulates predatory attack and affective defense behavior (Brutus et al., 1986). The anatomic studies detailing the outputs of the limbic structures indicate that the primary sites of interaction from the limbic system most probably include the medial and lateral hypothalamus with respect to modulation of aggressive reactions. While it is also conceivable that limbic structures may modulate PAG neurons intrinsic to the expression of affective defense and predatory attack, little information is presently available that bears upon this possibility. Further studies along these lines would be helpful in clarifying this issue. We have also shown that limbic seizures may produce enduring modulating effects in the post-ictal period on predatory attack and affective defense behavior (Brutus et al., 1986).
Over the past several decades, a number of studies by various investigators have been directed at examining the possible role of several different putative transmitter systems, such as the monoamines and acetylcholine, in the regulation of affective defense and predatory attack. Unfortunately, much of this work remains incomplete, and a clear-cut understanding of the actions of these transmitters of feline aggression is not yet available. Nevertheless, we have summarized the results of these studies in Table 2.
TABLE 1 Effects of Stimulation of Limbic System Structures on Predatory Attack and Affective Defense Behavior
TABLE 2 Effects of Drugs on Aggressive Behavior in Cats
|
Neurotransmitter System |
Route of Administration |
Effect on Affective Defense |
Effect on Quiet Biting Attack |
Effect on Flight |
Referencea |
||
|
Cholinergic |
|
|
|
|
|
|
|
|
|
Muscarinic |
Systematic |
|
|
|
George et al., 1962 |
|
|
|
|
|
|
|
|
|
Leslie, 1965 |
|
|
|
|
|
|
|
|
Zablocka and Esplin, 1964 |
|
|
|
|
|
|
|
|
Berntson, 1976 |
|
|
|
|
|
|
|
|
Berntson and Leibowitz, 1973 |
|
|
|
|
|
|
|
|
Berntson and Leibowitz, 1973 |
|
|
|
|
|
|
|
|
Katz and Thomas, 1975 |
|
Nicotinic |
Systemic |
|
|
|
Berntson, 1976 |
||
|
Nicotinic |
Intraventricular |
|
|
|
Feldberg and Sherwood, 1954 |
||
|
|
anticholinesterase |
|
|
|
|
|
Feldberg and Fleischhauer, 1962 |
|
|
|
Intracerebral |
|
|
|
|
|
|
|
Acetylcholine |
|
Hypothalamus, |
|
|
|
Allikmets, 1974 |
|
|
|
PAG |
|
|
|
Allikmets, 1974 |
|
|
|
|
|
Hypothalamus |
|
|
|
Meyers, 1964 |
|
|
|
|
Hypothalamus |
|
|
|
Kono, 1984 |
|
|
|
|
Hypothalamus |
|
|
|
Kono, 1984 |
|
|
|
|
Hypothalamus |
|
|
|
Karmos-Varzegi and Karnos, 1977 |
|
|
|
|
Ventral tegmentum |
|
|
Karmos-Varzegi and Karnos, 1977 |
|
|
|
|
|
Hypothalamus |
|
|
|
Desci and Karmos-Varzegi, 1969 |