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cold turkey withdrawal




In Animal Study, “Cold Turkey” Withdrawal from Drugs Triggers Mental Decline


WASHINGTON; November 3, 2013—Can quitting drugs without treatment trigger a decline in mental health? That appears to be the case in an animal model of morphine addiction. Georgetown University Medical Center researchers say their observations suggest that managing morphine withdrawal could promote a healthier mental state in people.

“Over time, drug-abusing individuals often develop mental disorders,” says Italo Mocchetti, PhD, a professor of neuroscience. “It’s been thought that drug abuse itself contributes to mental decline, but our findings suggest that ‘quitting cold turkey’ can also lead to damage.”

In the study published in the November issue of Brain, Behavior and Immunity and presented at Neuroscience 2013, Mocchetti and his research colleagues treated the animals with morphine, or allowed them to undergo withdrawal by stopping the treatment. Then, they measured pro-inflammatory cytokines, which can promote damage and cell death, and the protein CCL5, which has various protective effects in the brain.

“Interestingly, we found that treating the addicted animals with morphine both increased the protective CCL5 protein while decreasing pro-inflammatory cytokines, suggesting a beneficial effect,” Mocchetti explains. The animals that ween’t treated during withdrawal had the opposite results—decreased CCL5 and increased levels of the damaging cytokines.

“From these findings, it appears that morphine withdrawal may be a causative factor that leads to mental decline, presenting an important avenue for research in how we can better help people who are trying to quit using drugs,” concludes Mocchetti.


CCL5 and cytokine expression in the rat brain: Differential modulation by chronic morphine and morphine withdrawal,” Lee A. Campbella, Valeriya Avdoshinab, Summer Rozzic, Italo Mocchetti. Brain, Behavior and Immunity, Volume 34, November 2013, Pages 130–140.



"Opioids have been shown to influence the immune system and to promote the expression of pro-inflammatory cytokines in the central nervous system. However, recent data have shown that activation of opioid receptors increases the expression and release of the neuroprotective chemokine CCL5 from astrocytes in vitro. To further define the interaction between CCL5 and inflammation in response to opioids, we have examined the effect of chronic morphine and morphine withdrawal on the in vivo expression of CCL5 as well as of pro-inflammatory cytokines interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α). Rats undergoing a chronic morphine paradigm (10 mg/kg increasing to 30 mg/kg, twice a day for 5 days) showed a twofold increase of CCL5 protein and mRNA within the cortex and striatum. No changes were observed in the levels of IL-1β and TNF-α. Naltrexone blocked the effect of morphine. A chronic morphine paradigm with no escalating doses (10 mg/kg, twice a day) did not alter CCL5 levels compared to saline-treated animals. On the contrary, rats undergoing spontaneous morphine withdrawal exhibited lower levels of CCL5 within the cortex as well as increased levels of pro-inflammatory cytokines and Iba-1 positive cells than saline-treated rats. Overall, these data suggest that morphine withdrawal may promote cytokines and other inflammatory responses that have the potential of exacerbating neuronal damage."



Press materials provided by Georgetown University Medical Center Office of Communications.

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