Prevention of precipitated withdrawal symptoms by activating central cholinergic systems during a dependence-producing schedule of morphine in rats

Buccafusco, Jerry J.; Zhang, Lu C; Shuster, Laura; Jonnala, Ramamohana R.; Gattu, Mahanandeeshwar

doi:10.1016/s0006-8993(99)02197-6

Cited by 20 publications

(15 citation statements)

References 33 publications

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“…It is well established that acetylcholine is crucially involved in modulation of learning and memory [10]. It has also been shown that the attenuation of central cholinergic activity is involved in the expression of opioid withdrawal symptom [43,44] and impairment of learning and memory [7]. Morphine has been shown to inhibit hippocampal acetylcholine release [45,46].…”

Section: Discussionmentioning

confidence: 99%

Expression changes of hippocampal energy metabolism enzymes contribute to behavioural abnormalities during chronic morphine treatment

Chen

Lü

Gong³

et al. 2007

Cell Res

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Cell Research (2007) 17:689-700. © 2007 IBCB, SIBS, CAS All rights reserved 1001-0602/07 $ 30.00 www.nature.com/cr npg Dependence and impairment of learning and memory are two well-established features caused by abused drugs such as opioids. The hippocampus is an important region associated with both drug dependence and learning and memory. However, the molecular events in hippocampus following exposure to abused drugs such as opioids are not well understood. Here we examined the effect of chronic morphine treatment on hippocampal protein expression by proteomic analyses. We found that chronic exposure of mice to morphine for 10 days produced robust morphine withdrawal jumping and memory impairment, and also resulted in a significant downregulation of hippocampal protein levels of three metabolic enzymes, including Fe-S protein 1 of NADH dehydrogenase, dihydrolipoamide acetyltransferase or E2 component of the pyruvate dehydrogenase complex and lactate dehydrogenase 2. Further real-time quantitative PCR analyses confirmed that the levels of the corresponding mRNAs were also remarkably reduced. Consistent with these findings, lower ATP levels and an impaired ability to convert glucose into ATP were also observed in the hippocampus of chronically treated mice. Opioid antagonist naltrexone administrated concomitantly with morphine significantly suppressed morphine withdrawal jumping and reversed the downregulation of these proteins. Acute exposure to morphine also produced robust morphine withdrawal jumping and significant memory impairment, but failed to decrease the expression of these three proteins. Intrahippocampal injection of d-glucose before morphine administration significantly enhanced ATP levels and suppressed morphine withdrawal jumping and memory impairment in acute morphine-treated but not in chronic morphine-treated mice. Intraperitoneal injection of high dose of d-glucose shows a similar effect on morphine-induced withdrawal jumping as the central treatment. Taken together, our results suggest that reduced expression of the three metabolic enzymes in the hippocampus as a result of chronic morphine treatment contributes to the development of drug-induced symptoms such as morphine withdrawal jumping and memory impairment.

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Section: Discussionmentioning

confidence: 99%

Expression changes of hippocampal energy metabolism enzymes contribute to behavioural abnormalities during chronic morphine treatment

Chen

Lü

Gong³

et al. 2007

Cell Res

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“…Unfortunately, no data on the interactions between endomorphins and the nonopioid systems are available, although dopamine (DA) (El-Kadi and Sharif, 1998;Samini et al, 2000;Tokuyama et al, 2000), NA (Milanes et al, 1998;Fuentealba et al, 2000;Fuertes et al, 2000;Laorden et al, 2000), ACh (Zhang and Buccafusco, 1998;Buccafusco et al, 2000), benzodiazepine (Tejwani et al, 1998), N-methyl-D-aspartate (Popik et al, 1998), imidazoline (Su et al, 2000), Glu (Rockhold et al, 2000), and GABAergic (Sayin et al, 1998) pathways were suggested to play an important role in the development of physical dependence. Nitric oxide (NO) may also be involved in endomorphin-induced dependence, both directly, as systemic injections of NO synthase inhibitors attenuated some signs of naloxone-precipitated withdrawal and hyperactivity of the LC (Pineda et al, 1998), and indirectly, as the i.t.…”

Section: A Biological Effects Of Endomorphinsmentioning

confidence: 99%

The Endomorphin System and Its Evolving Neurophysiological Role

Fichna

Janecka²,

Costentin³

et al. 2007

Pharmacological Reviews

222

171

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“…Naloxone blocked this effect of morphine in the striatum (Green et al, 1976). In addition, cholinergic receptor agonists inhibit the withdrawal signs induced by morphine in animals (Buccafusco et al, 2000;Padmanabha Phillai et al, 1982). For example, the central acting cholinergic receptor agonist, arecoline, suppressed withdrawal body shakes (wet dog shakes) occurred in morphine withdrawal rat (Buccafusco et al, 2000).…”

Section: Introductionmentioning

confidence: 96%

“…In addition, cholinergic receptor agonists inhibit the withdrawal signs induced by morphine in animals (Buccafusco et al, 2000;Padmanabha Phillai et al, 1982). For example, the central acting cholinergic receptor agonist, arecoline, suppressed withdrawal body shakes (wet dog shakes) occurred in morphine withdrawal rat (Buccafusco et al, 2000). It seems that the µ-opioid receptors play an important role in regulating the central cholinergic system.…”

Section: Introductionmentioning

confidence: 99%

Roles of .Mu.-Opioid Receptors in Development of Tolerance to Diisopropylfluorophosphate (Dfp)

Tien

Fan

et al. 2005

J. Toxicol. Sci.

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-Anatomical evidence indicates that cholinergic and opioidergic systems are co-localized and acting on the same neuron. However, the regulatory mechanisms between cholinergic and opioidergic system have not been well characterized. In the present study, the potential involvement of µ-opioid receptors in mediating the changes of toxic signs and muscarinic receptor binding after administration of irreversible anti-acetylcholinesterase diisopropylfluorophosphate (DFP) was investigated. DFP (1 mg/kg/day, subcutaneous injection, s.c.)-induced tremors and chewing movements were monitored during the 28-day treatment period in µ-opioid receptor knockout and wild type mice. Autoradiographic studies of total, M1, and M2 muscarinic receptors were conducted using [ ]-AF-DX384 as ligands, respectively. DFP-induced tremors in both µ-opioid receptor knockout and wild type mice showed tolerance development. However, DFP-induced tremors in µ-opioid receptor knockout mice showed delayed tolerance development than that of DFP-treated wild type controls. DFPinduced chewing movements in both µ-opioid receptor knockout and wild type mice failed to show development of tolerance after four weeks of treatment. M2 muscarinic receptor binding of DFP-treated µ-opioid receptor knockout mice was significantly decreased than that of the DFP-treated wild type controls in the striatum, but not in the cortex and hippocampus. However, there were no significant differences in total and M1 muscarinic receptor binding between DFP-treated µ-opioid receptor knockout and wild type mice in the cortex, striatum and hippocampus. These studies indicate that µ-opioid receptors play an important role through the striatal M2 muscarinic receptors to regulate the development of tolerance to DFP-induced tremors.

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Prevention of precipitated withdrawal symptoms by activating central cholinergic systems during a dependence-producing schedule of morphine in rats

Cited by 20 publications

References 33 publications

Expression changes of hippocampal energy metabolism enzymes contribute to behavioural abnormalities during chronic morphine treatment

Expression changes of hippocampal energy metabolism enzymes contribute to behavioural abnormalities during chronic morphine treatment

The Endomorphin System and Its Evolving Neurophysiological Role

Roles of .Mu.-Opioid Receptors in Development of Tolerance to Diisopropylfluorophosphate (Dfp)

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