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Opioidergic mechanisms mediating aggressive behavior in the cat
Author(s) -
Shaikh Majid B.,
Dalsass Mario,
Siegel Allan
Publication year - 1990
Publication title -
aggressive behavior
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.223
H-Index - 92
eISSN - 1098-2337
pISSN - 0096-140X
DOI - 10.1002/1098-2337(1990)16:3/4<191::aid-ab2480160306>3.0.co;2-7
Subject(s) - microinjections , stria terminalis , periaqueductal gray , nucleus accumbens , (+) naloxone , escape response , endocrinology , medicine , ventromedial nucleus of the hypothalamus , hypothalamus , stimulation , lateral hypothalamus , opioidergic , chemistry , antagonist , microinjection , midbrain , psychology , neuroscience , central nervous system , receptor
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‐Ala 2 ‐Met 5 ‐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‐Pen 2 ,D‐Pen 5 ]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, these studies demonstrate that the opioid peptide system acts as a selective and potent modulator of the affective defense system in the cat. Our findings further suggest that opioid peptides suppress affective defense behavior by acting at synaptic regions within the limbic midbrain which are critical for the expression or modulation of this form of aggressive behavior.