Aggression during morphine withdrawal: Effects of method of withdrawal, fighting experience, and social role

Kantak, Kathleen M.; Miczek, Klaus A.

doi:10.1007/bf00174059

Cited by 30 publications

(8 citation statements)

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“…A more detailed analysis of the social confrontations promises to reveal whether aggression during withdrawal is reactive and defensive or proactive and offensive. As is the case with opiate and benzodiazepine withdrawal-induced aggression, we speculate that EtOH withdrawal-induced aggression is also reactive in nature (Gianutsos and Lal 1978, Kantak and Miczek 1986; Krŝiak et al 1998). …”

Section: Discussionmentioning

confidence: 64%

Aggression and increased glutamate in the mPFC during withdrawal from intermittent alcohol in outbred mice

et al. 2015

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Rationale Disrupted social behavior, including occasional aggressive outbursts, is characteristic of withdrawal from long-term alcohol (EtOH) use. Heavy EtOH use and exaggerated responses during withdrawal may be treated using glutamatergic N-methyl-D-aspartate receptor (NMDAR) antagonists. Objectives The current experiments explore aggression and medial prefrontal cortex (mPFC) glutamate as consequences of withdrawal from intermittent access to EtOH, and changes in aggression and mPFC glutamate caused by NMDAR antagonists memantine and ketamine. Methods Swiss male mice underwent withdrawal following 1-8 weeks of intermittent access to 20% EtOH. Aggressive and non-aggressive behaviors with a conspecific were measured 6-8 h into EtOH withdrawal after memantine or ketamine (0-30 mg/kg, i.p.) administration. In separate mice, extracellular mPFC glutamate after memantine was measured during withdrawal using in vivo microdialysis. Results At 6-8 h withdrawal from EtOH, mice exhibited more convulsions and aggression, and decreased social contact compared to age-matched water controls. Memantine, but not ketamine, increased withdrawal aggression at the 5 mg/kg dose in mice with a history of 8 weeks EtOH but not 1 or 4 weeks of EtOH or in water drinkers. Tonic mPFC glutamate was higher during withdrawal after 8 weeks EtOH compared to 1 week EtOH or 8 weeks water. Five mg/kg memantine increased glutamate in 8 week EtOH mice, but also in 1 week EtOH and water drinkers. Conclusions These studies reveal aggressive behavior as a novel symptom of EtOH withdrawal in outbred mice and confirm a role of NMDARs during withdrawal aggression and for disrupted social behavior.

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Section: Discussionmentioning

confidence: 64%

Aggression and increased glutamate in the mPFC during withdrawal from intermittent alcohol in outbred mice

et al. 2015

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“…A quarter of study participants expressed concern about overdose victims becoming aggressive after being revived with THN, which was associated with lower access to and administration of THN. An aggressive response post-revival may be the result of an overdose victim going into withdrawal or being disoriented [22,26]. The principles of trauma-informed care suggest that responders should supportively and clearly provide information about the status of the situation to the overdose victim after they have been revived [27].…”

Section: Discussionmentioning

confidence: 99%

More than just availability: Who has access and who administers take-home naloxone in Baltimore, MD

et al. 2019

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BackgroundFatal opioid overdose is a pressing public health concern in the United States. Addressing barriers and augmenting facilitators to take-home naloxone (THN) access and administration could expand program reach in preventing fatal overdoses.MethodsTHN access (i.e., being prescribed or receiving THN) was assessed in a Baltimore, Maryland-based sample of 577 people who use opioids (PWUO) and had a history of injecting drugs. A sub-analysis examined correlates of THN administration among those with THN access and who witnessed an overdose (N = 345). Logistic generalized estimating equations with robust standard errors were used to identify facilitators and barriers to accessing and using THN.ResultsThe majority of PWUO (66%) reported THN access. In the multivariable model, decreased THN access was associated with the fear that a person may become aggressive after being revived with THN (aOR: 0.55, 95% CI: 0.35–0.85), police threaten people at an overdose event (aOR: 0.68, 95% CI: 0.36–1.00), and insufficient overdose training (aOR: 0.43, 95% CI: 0.28–0.68). Enrollment in medication-assisted treatment, personally experiencing an overdose, and graduating from high school were associated with higher access. About half (49%) of PWUO with THN access and who had witnessed an overdose reported having administered THN. THN use was positively associated with “often” or “always” carrying THN (aOR: 3.47, 95% CI: 1.99–6.06), witnessing more overdoses (aOR:5.18, 95% CI: 2.22–12.07), experiencing recent homelessness, and injecting in the past year. THN use was reduced among participants who did not feel that they had sufficient overdose training (aOR: 0.56, 95% CI: 0.32–0.96).ConclusionTHN programs must bolster confidence in administering THN and address barriers to use, such as fear of a THN recipient becoming aggressive. Normative change around carrying THN is an important component in an overdose prevention strategy.

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“…For example, an opioid antagonist can be used to precipitate withdrawal in the case of opiate dependency (Espejo et al, 1994, Koob et al, 1992. In rats, opiate withdrawal causes severe somatic signs (Martin et al, 1963, Way et al, 1969, decreases in body temperature (Ary et al, 1976), aggression (Kantak and Miczek, 1986), and anxiety (Schulteis et al, 1998), as well as a motivational syndrome characterized by dysphoria and depression (De Shippenberg, 2002, Koob andLe Moal, 1997).…”

Section: B "Withdrawal": Anxiety and Behavioral Depression Inducedmentioning

confidence: 99%

Evidence for sugar addiction: Behavioral and neurochemical effects of intermittent, excessive sugar intake

Avena

Rada

Hoebel

2008

Neuroscience & Biobehavioral Reviews

1,117

914

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[Avena, N.M., Rada, P., Hoebel B.G., 2007. Evidence for sugar addiction: Behavioral and neurochemical effects of intermittent, excessive sugar intake. Neuroscience and Biobehavioral Reviews XX(X), XXX-XXX]. The experimental question is whether or not sugar can be a substance of abuse and lead to a natural form of addiction. "Food addiction" seems plausible because brain pathways that evolved to respond to natural rewards are also activated by addictive drugs. Sugar is noteworthy as a substance that releases opioids and dopamine and thus might be expected to have addictive potential. This review summarizes evidence of sugar dependence in an animal model. Four components of addiction are analyzed. "Bingeing," "withdrawal," "craving" and "cross-sensitization" are each given operational definitions and demonstrated behaviorally with sugar bingeing as the reinforcer. These behaviors are then related to neurochemical changes in the brain that also occur with addictive drugs. Neural adaptations include changes in dopamine and opioid receptor binding, enkephalin mRNA expression and dopamine and acetylcholine release in the nucleus accumbens. The evidence supports the hypothesis that under certain circumstances rats can become sugar dependent. This may translate to some human conditions as suggested by the literature on eating disorders and obesity.

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Aggression during morphine withdrawal: Effects of method of withdrawal, fighting experience, and social role

Cited by 30 publications

References 20 publications

Aggression and increased glutamate in the mPFC during withdrawal from intermittent alcohol in outbred mice

Aggression and increased glutamate in the mPFC during withdrawal from intermittent alcohol in outbred mice

More than just availability: Who has access and who administers take-home naloxone in Baltimore, MD

Evidence for sugar addiction: Behavioral and neurochemical effects of intermittent, excessive sugar intake

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