Social conflict analgesia: Studies on naloxone antagonism and morphine cross-tolerance in male DBA/2 mice

Rodgers, R.J.; Randall, J.I.

doi:10.1016/0091-3057(85)90087-5

Cited by 70 publications

(24 citation statements)

References 18 publications

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“…It may be that the CFW strain of mice does not perceive being defeated as being so intensely "stressful" compared to inbred strains. Previous work showing long-term tolerance after social defeat was done in B6AF 1 (Miczek et al 1982) and DBA/2 (Rodgers and Randall 1985) mice [i.e., inbred strains that are less aggressive and possibly more anxious (Parmigiani et al 1999)], thereby, possibly showing a more robust stress response. Parallel to the long-lasting analgesic effects in B6AF 1 and DBA/2 mice, enduring sensitization after defeat may be observed in these mice, comparable to what is seen in Long-Evans rats .…”

Section: Discussionmentioning

confidence: 99%

Social defeat stress, sensitization, and intravenous cocaine self-administration in mice

Yap

Miczek

2007

Psychopharmacology

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These data extend the evidence from rats to mice for the process of sensitization leading to more cocaine taking. Contrary to what is seen in rats, increased levels of cocaine self-administration were seen only in the amphetamine-pretreated mice and not after repeated defeat stress, suggesting that the sensitized response to defeat stress may not be as robust as it is in rats in this particular strain of mice.

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Section: Discussionmentioning

confidence: 99%

Social defeat stress, sensitization, and intravenous cocaine self-administration in mice

Yap

Miczek

2007

Psychopharmacology

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“…Endogenous opioid systems, particularly those involving m-opioid receptors, mediate many aspects of defensive and submissive behaviors in rodents (Miczek et al, 1982;Rodgers and Randall, 1985). Midbrain opioid mechanisms participate in the regulation of affective and ultrasonic vocalization, which are components of submissive responses during social defeat stress (Herman and Panksepp, 1981;Vivian and Miczek, 1999).…”

Section: Introductionmentioning

confidence: 99%

Prolonged Effects of Repeated Social Defeat Stress on mRNA Expression and Function of μ-Opioid Receptors in the Ventral Tegmental Area of Rats

Nikulina

Miczek

Hammer

2005

Neuropsychopharmacol

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Social defeat stress alters the activity of mesocorticolimbic dopamine projections from the ventral tegmental area (VTA), a process that has been implicated in the development of sensitization and drug-seeking behavior. We showed previously that acute brief social defeat stress increased short-term expression of m-opioid receptor mRNA in the VTA. The present study assessed the presence and functional significance of m-opioid receptor mRNA expression 1 week after the last episode of social defeat stress. Social defeat stress was induced in intruder rats during short confrontations with an aggressive resident rat, and subsequent exposures behind a protective screen once a day for 5 days. Regional m-receptor mRNA levels were assessed by in situ hybridization histochemistry, and the amount of mRNA labeling was measured in the VTA and the substantia nigra (SN). Expression of m-opioid receptor mRNA was significantly higher in defeated rats relative to handled control animals in the VTA, but not in the SN. In an additional group of rats, bilateral local intra-VTA injection of the selective m-opioid receptor agonist DAMGO (1.0 mg per side) was performed 7-10 days after the last defeat stress or handling control procedure. Baseline motor activity did not differ between control and stressed rats. Intra-VTA DAMGO significantly increased locomotor activity in stressed rats compared to handled control rats. These results suggest that repeated social stress upregulates VTA m-opioid receptors and can produce locomotor activation via stimulation of these receptors. This locomotor effect is probably the consequence of enhanced disinhibition of mesolimbic dopamine neurons.

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“…It has been well established that stressful stimuli can produce inhibition of pain sensitivity. Opioid mediation of analgesia produced by noxious stimuli has been shown by cross-tolerance to morphine (Miczek et al 1982(Miczek et al , 1986Rodgers and Randall 1985;Marek et al 1988) and antagonism by naloxone and naltrexone (Siegfried et al 1975;Tesky et al 1984). Additionally, defeat-induced analgesia results in the activation of central opioid peptides (Miczek and Thompson 1984).…”

Section: Discussionmentioning

confidence: 95%

Aggression modulates genetic influences on morphine analgesia as assessed using a classical mendelian cross analysis

et al. 1993

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Pharmacogenetic techniques allow for the examination of genetic and environmental factors underlying phenotypes associated with drug response. Initial studies of mice bred at Jackson Laboratories (JAX) indicated that C57BL/6J mice were more sensitive to morphine-induced analgesia, as measured by latency to paw lick, than SJL/J mice. A classical Mendelian cross breeding program was initiated in which F1, F2 and backcross generations were derived from C57BL/6J and SJL/J breeding pairs purchased from JAX to examine the genetic factors underlying morphine analgesia. Genetic analysis indicated significant dominance or heterosis for a reduced drug response. The F1 generation was less sensitive to morphine-induced analgesia than either parental strain. Mathematical analysis of the generation means revealed that a simple dominance model with no epistatic interaction between genes best described the data. Environmental factors also affected sensitivity to morphine analgesia, in that C57BL and SJL mice raised in our facility did not differ in latency to paw lick. SJL mice from JAX exhibit a high degree of aggression, while SJL mice raised in our facilities show little or no aggression. The levels of aggression among groups of SJL mice were characterized and found to correlate with sensitivity to morphine analgesia. Mice exposed to increasingly greater levels of aggression were the least sensitive to morphine. Thus, the changes observed in sensitivity to morphine-induced analgesia appear to be related to the degree of aggression to which these mice are exposed, possibly resulting from the stress and/or prolonged exposure to painful stimuli associated with aggressive encounters.

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Social conflict analgesia: Studies on naloxone antagonism and morphine cross-tolerance in male DBA/2 mice

Cited by 70 publications

References 18 publications

Social defeat stress, sensitization, and intravenous cocaine self-administration in mice

Social defeat stress, sensitization, and intravenous cocaine self-administration in mice

Prolonged Effects of Repeated Social Defeat Stress on mRNA Expression and Function of μ-Opioid Receptors in the Ventral Tegmental Area of Rats

Aggression modulates genetic influences on morphine analgesia as assessed using a classical mendelian cross analysis

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