Chronic morphine affects working memory during treatment and withdrawal in rats

Sala, Mariaelvina; Braida, Daniela; Leone, M.P.; Calcaterra, P.; Frattola, D.; Gori, E

doi:10.1097/00008877-199410000-00002

Cited by 47 publications

(14 citation statements)

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“…The observed reduction in 2-AG content in this heterogeneous region could play a role in the complex emotional and motivational state observed during chronic morphine exposure, being the septum and anterior amygdala notoriously linked to the inhibition of anxiety-like responses (Adamec and Young, 2000) and the nucleus accumbens a key region in the reward neural circuitry as well as in drug and food craving and in drug addiction. (6) Finally, the widespread reduced levels of 2-AG found in the brain of morphine-tolerant rats could account for the enhanced susceptibility to neurodegenerative processes observed after chronic morphine exposure (Pearson et al, 1975/76;Coomb et al, 1985;London et al, 1989;Sala et al, 1994). In fact, recently it has been demonstrated that 2-AG exerts a neuroprotective action in rats after brain injury (Panikashvili et al, 2001), and the reduction in its amounts could in part underlie morphine-induced premature aging (Sala et al, 1994).…”

Section: Discussionmentioning

confidence: 99%

“…(6) Finally, the widespread reduced levels of 2-AG found in the brain of morphine-tolerant rats could account for the enhanced susceptibility to neurodegenerative processes observed after chronic morphine exposure (Pearson et al, 1975/76;Coomb et al, 1985;London et al, 1989;Sala et al, 1994). In fact, recently it has been demonstrated that 2-AG exerts a neuroprotective action in rats after brain injury (Panikashvili et al, 2001), and the reduction in its amounts could in part underlie morphine-induced premature aging (Sala et al, 1994). …”

Section: Discussionmentioning

confidence: 99%

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Chronic Morphine Modulates the Contents of the Endocannabinoid, 2-Arachidonoyl Glycerol, in Rat Brain

Viganò

Cascio

Rubino

et al. 2002

Neuropsychopharmacol

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Opioids and cannabinoids are among the most widely consumed drugs of abuse in humans and the phenomena of cross-tolerance or mutual potentiation have been demonstrated between the two drugs. Several authors have suggested that both drugs share common links in their molecular mechanisms of action, although this has been a matter of controversy. Furthermore, no data exist on the possible adaptive changes in the contents of arachidonoylethanolamide (anandamide, AEA) and 2-arachidonoylglycerol (2-AG), the two major endogenous ligands for cannabinoid receptors, in morphine-tolerant rats. In the present work, we investigated the alterations in cannabinoid receptor functionality and endocannabinoid levels in rats chronically treated with morphine (5 mg/kg, s.c., twice a day for 5 days). Autoradiographic-binding studies using [ ]GTPgS binding showed a strong decrease (40%) in receptor/G protein coupling in the limbic area of these animals. Moreover, in the same brain regions we measured, by isotopedilution gas chromatography/mass spectrometry, the contents of AEA and 2-AG. Chronic morphine exposure produced a strong reduction in 2-AG contents without changes in AEA levels in several brain regions (ie striatum, cortex, hippocampus, limbic area, and hypothalamus). These findings clearly demonstrate that prolonged activation of opioid receptors could alter the cannabinoid system, in terms of both receptor functionality and endocannabinoid levels, and suggest the involvement of this system, alone or in combination with other mediators, in the phenomenon of morphine tolerance.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Chronic Morphine Modulates the Contents of the Endocannabinoid, 2-Arachidonoyl Glycerol, in Rat Brain

Viganò

Cascio

Rubino

et al. 2002

Neuropsychopharmacol

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“…Drug addiction is associated with adaptive changes in the neural systems related to learning and memory (Kelley, 2004). Although great advances have been made in the cellular mechanisms of tolerance and dependence to opioids (Bailey and Connor, 2005), little is known about the course of learning and memory deficits after cessation of chronic opiate use in behavioral animal models (Pu et al, 2002;Sala et al, 1994;Spain and Newsom, 1991). In humans, opiate addiction is usually associated with cognitive impairments such as poor impulse control, planning, memory, and decision-making (Chastain et al, 1986;Franken et al, 2000;Grant et al, 2000;Guerra et al, 1987;Lee and Pau, 2002;Strang and Gurling, 1989;Stout and Farrell, 2002).…”

Section: Introductionmentioning

confidence: 99%

Chronic Morphine Selectively Impairs Cued Fear Extinction in Rats: Implications for Anxiety Disorders Associated with Opiate Use

et al. 2007

Neuropsychopharmacol

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Previous studies have shown that opioid transmission plays an important role in learning and memory. However, little is known about the course of opiate-associated learning and memory deficits after cessation of chronic opiate use in a behavioral animal model. In the present study, we examined the effects of chronic morphine on fear extinction, an important preclinical model for behavior therapy of human anxiety disorders. Rats were administrated subcutaneously morphine hydrochloride or saline twice per day for continuous 10 days. Rats received a cued or contextual fear conditioning session 7 days after the last morphine injection. During subsequent days, rats received four cued or contextual extinction sessions (one session per day). Percent freezing was assessed during all phases of training. Chronic morphine did not affect the acquisition of cued fear response or the initial encoding of extinction memory within each session, but produced an impairment in the between-session extinction. However, the same morphine treatment schedule did not affect the acquisition or extinction of contextual fear response. These results suggest that the effects of chronic morphine on memory for fear extinction are complex. Chronic morphine selectively impairs extinction of cued fear response. This deficit in fear extinction may be one of those critical components that contribute to the high prevalence of anxiety disorders in opiate addicts.

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“…In rodents, acute and chronic administration of morphine has been reported to interfere with learning and memory in a variety of tasks including discriminative avoidance paradigms, radial-, Y-and plus-mazes, and the Morris water maze (Spain and Newsom 1991;Sala et al 1994;Li et al 2001;Zheng et al 2002). Although methadone is amongst the opioids most frequently prescribed in the clinic, only a few studies have examined its effects on psychomotor and cognitive performance in the experimental animal.…”

mentioning

confidence: 99%

Chronic methadone treatment and repeated withdrawal impair cognition and increase the expression of apoptosis-related proteins in mouse brain

2007

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Chronic morphine affects working memory during treatment and withdrawal in rats

Cited by 47 publications

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Chronic Morphine Modulates the Contents of the Endocannabinoid, 2-Arachidonoyl Glycerol, in Rat Brain

Chronic Morphine Modulates the Contents of the Endocannabinoid, 2-Arachidonoyl Glycerol, in Rat Brain

Chronic Morphine Selectively Impairs Cued Fear Extinction in Rats: Implications for Anxiety Disorders Associated with Opiate Use

Chronic methadone treatment and repeated withdrawal impair cognition and increase the expression of apoptosis-related proteins in mouse brain

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