Opioidergic mechanisms mediating aggressive behavior in the cat

In the studies presented in this article, we have described the role of opioid peptides in the regulation of feline aggression. In the first study, stimulation via monopolar electrodes elicited affective defense behavior from the ventromedial hypothalamus and midbrain periaqueductal gray (PAG). Afte...

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Veröffentlicht in:Aggressive behavior 1990, Vol.16 (3-4), p.191-206
Hauptverfasser: Shaikh, Majid B., Dalsass, Mario, Siegel, Allan
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Sprache:eng
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Zusammenfassung:In the studies presented in this article, we have described the role of opioid peptides in the regulation of feline aggression. In the first study, stimulation via monopolar electrodes elicited affective defense behavior from the ventromedial hypothalamus and midbrain periaqueductal gray (PAG). After determining response baseline thresholds or latencies, the opioid antagonist naloxone (0.5, 1.0, 4.0, 7.0, and 10.0 mg/kg) was administered systematically. Naloxone significantly reduced the threshold and latency values for this behavior in a dose‐ and time‐dependent manner, but increased response latencies for predatory attack, and had no effect upon PAG‐elicited circling behavior. In the next study, intracerebral microinjections of D‐Ala2‐Met5‐enkephalinamide (DAME) at dose levels of 1.0 and 10.0 μg/0.5 μl were placed into the bed nucleus of stria terminalis (BNST) and nucleus accumbens via cannula electrodes, and the effects of drug infusion upon affective defense elicited from ventromedial hypothalamus were examined. DAME, when microinjected into the BNST and nucleus accumbens at dose levels of 1.0 and 10.0 μg/0.5 μ1, resulted in 100–300% increases in response latencies. Pretreatment with naloxone completely blocked the suppressive effects of DAME. In a separate study, microinjections of DAME (0.25, 0.5, and 1.0 μg/0.5 μ1) into PAG sites from which affective defense was elicited significantly suppressed this behavior. A maximum suppressive effect (87% increase in thresholds) was indicated at the dose level of 1.0 μg/0.5 μ1. Pretreatment with naloxone entirely eliminated the suppressive effects of DAME. In the third study, microinjections of selective agonists and antagonists for mu, delta, and kappa opioid receptor subtypes were placed into the PAG sites from which affective defense was elicited. Morphiceptin (a mu agonist) was highly effective in suppressing this response at a very low dose (0.4 nmol). Pretreatment with beta‐funaltrexamine (B‐FNA), a selective antagonist for mu receptors, completely blocked the suppressive effects of morphiceptin. In addition, a selective delta agonist—[D‐Pen2,D‐Pen5]enkephalin (DPDPE)—also had a suppressive effect upon affective defense behavior, but its effect was of a smaller magnitude relative to that of morphiceptin. Pretreatment with a selective antagonist for delta receptors, ICI 174,864, blocked the suppressive effect of DPDPE. Furthermore, a kappa agonist, U‐50488H, failed to alter this behavior. Collectively, th
ISSN:0096-140X
1098-2337
DOI:10.1002/1098-2337(1990)16:3/4<191::AID-AB2480160306>3.0.CO;2-7