Glucose and physostigmine effects on morphine- and amphetamine-induced increases in locomotor activity in mice

Stone, William S.; Rudd, Rebecca J.; Gold, Paul E.

doi:10.1016/0163-1047(90)91338-c

Cited by 27 publications

(29 citation statements)

References 30 publications

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“…While these suggestions remain to be investigated, the fact that physostigmine reversed scopolamine-but not amphetamine-induced LI disruption sets this compound apart from APDs, which reverse both deficits. The latter is inconsistent with the report that physostigmine acted like 'dopaminergic' APDs, and in particular, blocked amphetamine-induced stereotypy (Karan et al, 2000), but is in line with Stone et al's (1990) finding of low susceptibility of amphetamine-induced hyperactivity to physostigmine, because here we used a low, activity-producing dose of amphetamine. To the best of our knowledge, this is the first demonstration of distinct effects of physostigmine on scopolamine-and amphetamine-induced behavioral deficits produced in the same behavioral phenomenon.…”

Section: Discussioncontrasting

confidence: 57%

Scopolamine Induces Disruption of Latent Inhibition which is Prevented by Antipsychotic Drugs and an Acetylcholinesterase Inhibitor

Barak

Weiner

2006

Neuropsychopharmacol

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The fact that muscarinic antagonists may evoke a psychotic state ('antimuscarinic psychosis'), along with findings of cholinergic alterations in schizophrenia, have kindled an interest in the involvement of the cholinergic system in this disorder. Latent inhibition (LI) is a crossspecies phenomenon manifested as a poorer conditioning of a stimulus seen when the stage of conditioning is preceded by a stage of repeated nonreinforced pre-exposure to that stimulus, and is considered to index the capacity to ignore irrelevant stimuli. Amphetamine-induced LI disruption and its reversal by antipsychotic drugs (APDs) is a well-established model of positive symptoms of schizophrenia. Here, we tested whether the muscarinic antagonist scopolamine would disrupt LI and whether such disruption would be reversed by APDs and by the acetylcholinesterase inhibitor physostigmine. The results showed that scopolamine at doses of 0.15 and 0.5 mg/kg disrupted LI, and that this effect was due to the action of the drug in the pre-exposure stage, suggesting a role of muscarinic transmission in attentional processes underlying LI. Both the typical and the atypical APDs, haloperidol and clozapine, reversed scopolamine-induced LI disruption when given in conditioning or in both stages, but not in pre-exposure, indicating that the mechanism of antipsychotic action in this model is independent of the mechanism of action of the propsychotic drug. Scopolamine-induced LI disruption was reversed by physostigmine (0.05 and 0.15 mg/kg), which was ineffective in reversing amphetamine-induced LI disruption, pointing to distinct mechanisms underlying LI disruption by these two propsychotic drugs. The latter was further supported by the finding that unlike amphetamine, the LI-disrupting doses of scopolamine did not affect activity levels. We propose scopolamine-induced LI disruption as a model of cholinergic-related positive symptoms in schizophrenia. Neuropsychopharmacology (2007) 32, 989-999.

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Section: Discussioncontrasting

confidence: 57%

Scopolamine Induces Disruption of Latent Inhibition which is Prevented by Antipsychotic Drugs and an Acetylcholinesterase Inhibitor

Barak

Weiner

2006

Neuropsychopharmacol

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“…In previous studies, glucose attenuated increases in locomotor activity produced by scopolamine or morphine (Stone et al 1987(Stone et al , 1988a(Stone et al , 1990b). The present experiment tested possible naloxone attenuation of hyperactivity after scopolamine, as well as morphine, administration.…”

Section: Experiments 2: Naloxone Attenuation Of Scopolamineinduced Hypmentioning

confidence: 94%

“…Recent findings that glucose attenuates morphine-induced increases in locomotor activity (Stone et al 1990b) and impairments of spontaneous alternation performance (Stone et al 1991) suggest that opiate mechanisms may contribute to glucose effects on brain function, perhaps serving as an intermediate step between circulating glucose levels and cholinergic functions. Consistent with this possibility, opiate agonists inhibit cholinergic activity in several brain regions (Lamour and Epelbaum 1988).…”

mentioning

confidence: 98%

Naloxone modulates the behavioral effects of cholinergic agonists and antagonists

et al. 1991

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Peripheral glucose administration enhances memory in rodents and humans. Recent findings suggest that glucose may affect behavior, in part, by augmenting central cholinergic functions and by attenuating central opiate functions. The present experiments examined interactions between an opiate antagonist, naloxone, and cholinergic agents to determine whether the effects would parallel those found with glucose. Three behavioral measures were assessed: tremors, hyperactivity, and spontaneous alternation. Naloxone (1 mg/kg) significantly augmented tremors elicited by physostigmine (0.3 mg/kg). Naloxone (1 mg/kg) also attenuated increases in locomotor activity and impairments in spontaneous alternation performance elicited by scopolamine (1 and 3 mg/kg for activity and alternation measures, respectively). Thus, across three diverse measures, naloxone produced effects similar to those previously reported for glucose. These findings are consistent with the hypothesis that release of cholinergic activity from opiate inhibition may contribute to glucose effects on behavior.

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“…It has also been reported that systemic or intrahippocampal injection of glucose or its metabolite pyruvate attenuates acute morphine-induced memory impairment and increment of locomotor activity [6,[22][23][24][25]. In addition, glucose has also been shown to suppress acute morphine withdrawal signs in rodents and in guinea-pig ileum [26][27][28].…”

Section: Introductionmentioning

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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Glucose and physostigmine effects on morphine- and amphetamine-induced increases in locomotor activity in mice

Cited by 27 publications

References 30 publications

Scopolamine Induces Disruption of Latent Inhibition which is Prevented by Antipsychotic Drugs and an Acetylcholinesterase Inhibitor

Scopolamine Induces Disruption of Latent Inhibition which is Prevented by Antipsychotic Drugs and an Acetylcholinesterase Inhibitor

Naloxone modulates the behavioral effects of cholinergic agonists and antagonists

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

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