Inhibitory avoidance memory deficit induced by scopolamine: Interaction of cholinergic and glutamatergic systems in the ventral tegmental area

Mahmoodi, Gelavij; Ahmadi, Shamseddin; Pourmotabbed, Ali; Oryan, Shahrbanoo; Zarrindast, Mohammad Reza

doi:10.1016/j.nlm.2010.04.004

Cited by 27 publications

(16 citation statements)

References 63 publications

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“…However, animal studies have shown that inhibitory avoidance memory consolidation can be repressed by co-administration of muscarinic and NMDA antagonists to the ventral tegmentum, at doses that were ineffective when used alone (Mahmoodi et al, 2010), indicating a synergistic interaction. Thus, it is possible that the disturbances in central function seen in schizophrenia could be underpinned by a loss of synaptic plasticity due to suppression of both glutamatergic and cholinergic signaling.…”

Section: Interactions With Intrinsic Neurotransmittersmentioning

confidence: 99%

Cholinergic connectivity: it's implications for psychiatric disorders

Scarr

Gibbons

Neo

et al. 2013

Front. Cell. Neurosci.

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Acetylcholine has been implicated in both the pathophysiology and treatment of a number of psychiatric disorders, with most of the data related to its role and therapeutic potential focusing on schizophrenia. However, there is little thought given to the consequences of the documented changes in the cholinergic system and how they may affect the functioning of the brain. This review looks at the cholinergic system and its interactions with the intrinsic neurotransmitters glutamate and gamma-amino butyric acid as well as those with the projection neurotransmitters most implicated in the pathophysiologies of psychiatric disorders; dopamine and serotonin. In addition, with the recent focus on the role of factors normally associated with inflammation in the pathophysiologies of psychiatric disorders, links between the cholinergic system and these factors will also be examined. These interfaces are put into context, primarily for schizophrenia, by looking at the changes in each of these systems in the disorder and exploring, theoretically, whether the changes are interconnected with those seen in the cholinergic system. Thus, this review will provide a comprehensive overview of the connectivity between the cholinergic system and some of the major areas of research into the pathophysiologies of psychiatric disorders, resulting in a critical appraisal of the potential outcomes of a dysregulated central cholinergic system.

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Section: Interactions With Intrinsic Neurotransmittersmentioning

confidence: 99%

Cholinergic connectivity: it's implications for psychiatric disorders

Scarr

Gibbons

Neo

et al. 2013

Front. Cell. Neurosci.

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show abstract

“…Recent studies confirmed significant deficits when sub-threshold doses were co-administered intracerebrally. Specifically, injections in the medial septum or CA1 [9] or the ventral tegmental area [10] induced amnesia in inhibitory avoidance. Secondly, systemic pre-learning infusions of d-cycloserine (DCS), a NMDAR partial agonist at the glycine modulatory site that enhances memory processes [11], [12], [13], [14], [15], attenuated SCOP-induced deficits in the acquisition of spatial tasks [16], [17], [18], [19].…”

Section: Introductionmentioning

confidence: 99%

D-cycloserine in Prelimbic Cortex Reverses Scopolamine-Induced Deficits in Olfactory Memory in Rats

et al. 2013

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A significant interaction between N-methyl-D-aspartate (NMDA) and muscarinic receptors has been suggested in the modulation of learning and memory processes. The present study further investigates this issue and explores whether d-cycloserine (DCS), a partial agonist at the glycine binding site of the NMDA receptors that has been regarded as a cognitive enhancer, would reverse scopolamine (SCOP)-induced amnesia in two olfactory learning tasks when administered into the prelimbic cortex (PLC). Thus, in experiment 1, DCS (10 µg/site) was infused prior to acquisition of odor discrimination (ODT) and social transmission of food preference (STFP), which have been previously characterized as paradigms sensitive to PLC muscarinic blockade. Immediately after learning such tasks, SCOP was injected (20 µg/site) and the effects of both drugs (alone and combined) were tested in 24-h retention tests. To assess whether DCS effects may depend on the difficulty of the task, in the STFP the rats expressed their food preference either in a standard two-choice test (experiment 1) or a more challenging three-choice test (experiment 2). The results showed that bilateral intra-PLC infusions of SCOP markedly disrupted the ODT and STFP memory tests. Additionally, infusions of DCS alone into the PLC enhanced ODT but not STFP retention. However, the DCS treatment reversed SCOP-induced memory deficits in both tasks, and this effect seemed more apparent in ODT and 3-choice STFP. Such results support the interaction between the glutamatergic and the cholinergic systems in the PLC in such a way that positive modulation of the NMDA receptor/channel, through activation of the glycine binding site, may compensate dysfunction of muscarinic neurotransmission involved in stimulus-reward and relational learning tasks.

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“…Co-administration of inefficient doses of scopolamine and MK-801 into the ventral tegmental area impaired inhibitory avoidance in rats [64]. Interestingly, recent data have shown that acute inhibition of NMDA receptors with MEM significantly elevated the hippocampal ACh level; this effect was not associ-ated with learning improvement [65].…”

Section: Discussionmentioning

confidence: 94%

Combined treatment with pantothenic acid derivatives and memantine alleviates scopolamine-induced amnesia in rats: The involvement of the thiol redox state and coenzyme A

et al. 2016

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Free-radical-mediated processes are involved in a variety of physiological events, while oxidative stress and related redox deregulation are implicated in various pathological events. Tripeptide glutathione plays an important role in the antioxidant defense of the brain, particularly in the maintenance of the optimal redox state in neurons and glial cells. We studied the combined effects of pantothenic acid derivatives, pantothenol and calcium pantothenate, and memantine, which is a glutamate receptor antagonist that is widely used for the treatment of dementia, on amnesia induced by scopolamine in rats. Scopolamine induced amnesia in rats; however, unexpectedly, this effect was even more expressed in the memantine-pretreated animals. Memory impairments were less manifested in the rats that were pretreated with memantine in combination with panthenol or calcium pantothenate. The detrimental scopolamine effect on memory was accompanied by significant depletions of glutathione and coenzyme A in the brain. While memantine recovered the glutathione status to some extent, it nevertheless further aggravated the scopolamine influence on coenzyme A levels. An alleviation of scopolamine-induced memory impairments that was observed after combined pretreatment with memantine and panthenol or calcium pantothenate was accompanied by a normalization of coenzyme A levels, while the effects on glutathione redox did not correlate with the behavioral data.

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Inhibitory avoidance memory deficit induced by scopolamine: Interaction of cholinergic and glutamatergic systems in the ventral tegmental area

Cited by 27 publications

References 63 publications

Cholinergic connectivity: it's implications for psychiatric disorders

Cholinergic connectivity: it's implications for psychiatric disorders

D-cycloserine in Prelimbic Cortex Reverses Scopolamine-Induced Deficits in Olfactory Memory in Rats

Combined treatment with pantothenic acid derivatives and memantine alleviates scopolamine-induced amnesia in rats: The involvement of the thiol redox state and coenzyme A

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