Differential effects of NK1 receptors in the midbrain periaqueductal gray upon defensive rage and predatory attack in the cat.

This study utilized anatomical and behavioral-pharmacological methods to determine the role of NK(1)-Substance P receptors in the midbrain periaqueductal gray (PAG) in defensive rage behavior in cats. For behavioral pharmacological experiments, monopolar stimulating electrodes were implanted in the medial hypothalamus for elicitation of defensive rage behavior and cannula-electrodes were implanted in the PAG for microinjections of receptor compounds. Microinjections of the NMDA antagonist, AP-7 (2 nmol), into the dorsal PAG blocked defensive rage elicited by medial hypothalamic stimulation, thus establishing the PAG as a synaptic region that receives hypothalamic inputs linked to defensive rage behavior.

Lead exposure potentiates predatory attack behavior in the cat.

Epidemiologic studies have demonstrated that environmental lead exposure is associated with aggressive behavior in children; however, numerous confounding variables limit the ability of these studies to establish a causal relationship. The study of aggressive behavior using a validated animal model was used to test the hypothesis that there is a causal relationship between lead exposure and aggression in the absence of confounding variables. We studied the effects of lead exposure on a feline model of aggression: predatory (quiet biting) attack of an anesthetized rat.

NK1 receptors in the medial hypothalamus potentiate defensive rage behavior elicited from the midbrain periaqueductal gray of the cat.

Defensive rage in the cat occurs naturally in response to a threat and is also elicited by electrical or chemical stimulation over the rostro-caudal extent of the medial hypothalamus and dorsolateral aspect of the periaqueductal gray (PAG). This behavior is mediated over a descending projection from the hypothalamus to the midbrain PAG. The underlying hypothesis for the present study was that medial hypothalamic defensive rage neurons are excited in two ways: by NK(1) receptors and by an ascending input from the PAG.