Increase of extracellular acetylcholine level in rat frontal cortex induced by (+)N-allylnormetazocine as measured by brain microdialysis

Matsuno, Kiyoshi; Matsunaga, Keiko; Mita, Shiro

doi:10.1016/0006-8993(92)90096-r

Cited by 48 publications

(24 citation statements)

References 24 publications

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“…First, o ligands are able to selectively stimulate several NMDA responses in vitro and in vivo (Monnet et al, 1990(Monnet et al, , 1991(Monnet et al, , 1992Roman et al, 1991). Then, (+)-SKF-10,047 was shown to increase acetylcholine release from guinea-pig and rat frontal cortex in vivo (Siniscalchi et al, 1987;Matsuno et al, 1992Matsuno et al, , 1993. JO-1784 potentiated the KCl-evoked [3H]acetylcholine release from rat hippocampal slices in vitro and high affinity [3H]choline uptake from mouse hippocampal synaptosomes in vivo .…”

Section: Discussionmentioning

confidence: 97%

Prevention of nimodipine-induced impairment of learning by the selective ? ligand PRE-084

Maurice

Parish

et al. 1995

J. Neural Transmission

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The high selectivity of the phencyclidine derivative PRE-084 for sigma (sigma) sites is demonstrated. We previously reported that this compound is able to markedly attenuate the impairment of learning induced in mice by the non-competitive NMDA antagonist MK-801, and the cholinergic nicotinic antagonist mecamylamine. In this study, we examined the effect of PRE-084 on the impairment of learning induced by acute administration of the calcium channel antagonist nimodipine. Nimodipine (0.3 mg/kg i.p.) impaired the spontaneous alternation behaviour in a Y-maze, decreased the step-down latency (SDL) in a passive avoidance task, and altered place learning and retention in a water-maze paradigm, with no marked effect on the motility observed using an open-field test. Preadministration of PRE-084 resulted in an attenuation of the impairment of alternation, in the 0.3-1 mg/kg s.c. range, in a marked increase in SDL, at 1-3 mg/kg, and improved place learning and retention in the water-maze, at 1 mg/kg. The effects on alternation behaviour and passive avoidance were completely prevented by co-administration of the purported sigma antagonist BMY-14802 (10 mg/kg i.p.), implicating the sigma sites. These results confirm the beneficial effect of the sigma ligand PRE-084 on pharmacological models of learning impairments, and indicate that sigma sites may modulate Ca2+ fluxes through VDCC, which may in turn bear some as yet unknown relationship to the previously described interaction with neurotransmitter systems.

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Section: Discussionmentioning

confidence: 97%

Prevention of nimodipine-induced impairment of learning by the selective ? ligand PRE-084

Maurice

Parish

et al. 1995

J. Neural Transmission

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“…On the other hand, a direct interaction could be evoked. For example, (+)-SKF-10,047 was shown to increase acetylcholine release from guinea-pig cortical slices (30) and from rat frontal cortex in vivo (14,15). JO-1784 potentiated the KCl-evoked [3H]acetylcholine release from rat hippocampal slices in vitro and high affinity [3H]choline uptake from mouse hippocampal synaptosomes in vivo (10).…”

Section: Discussionmentioning

confidence: 99%

“…3). SDL was drastically decreased to 17 s [14][15][16][17][18][19][20][21][22][23][24][25][26][27][28][29][30][31][32][33] (n = 17) with the MK-801 (0.2 mg/kg) treatment, and the preadministration of PRE-084 (0.1-1 mg/kg) prior to MK-801 led to a significant increase in SDL (Fig. 3).…”

Section: Effect Of Pre-084 On the Mk-8ol-induced Impairment Of Learningmentioning

confidence: 99%

PRE-084, a σ selective PCP derivative, attenuates MK-801-induced impairment of learning in mice

Maurice

Parish³

et al. 1994

Pharmacology Biochemistry and Behavior

119

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-084, a aselectivePCPderivative, attenuates MK-8Ol-induced impairment of learning in mice. PHARMACOL BIOCHEM BEHAV 49(4) [859][860][861][862][863][864][865][866][867][868][869] 1994.-We investigated the effect of the tr selective PCP derivative PRE-084 on the impairment of learning induced in mice by the noncompetitive NMDA antagonist MK-801. Learning capacities were evaluated using the spontaneous alternation in a Y-maze test for spatial working memory, the step-down passive avoidance and the elevated plus-maze test for long-term memory. At doses about 1 mg/kg IP, PRE-084 significantly attenuated MK-801 (0.2 mg/kg IP) induced impairment of learning. The dose-response curve was bell-shaped which is typical for cognition enhancers. The effect of PRE-084 was antagonized by BMY-14802 (10 mg/kg IP) and suppressed by a chronic treatment with haloperidol (4 mg/kg/day SC for 7 days). Furthermore, PRE-084 did not affect scopolamine (1 mg/kg SC) induced amnesia but significantly attenuated mecamylamine (10 mg/kg IP) induced amnesia. These results show that a sites mediate a modulation of the NMDA receptor complex-dependent learning processes and may similarly affect the cholinergic nicotinic memory processes. Moreover, the PCP derivative PRE-084, acting selectively at a sites, reverses the amnesia induced by a drug acting at the PCP site. , and dextrometorphan bind with a high affinity and stereoselectivity, and the a2 site, which has lower affinity and is not stereoselective for these ligands. Both 1,3-di-(2-tolyl)guanidine (DTG) and haloperidol are nonselective drugs and bind with a similar high affinity to the two classes of sites (25,34,42). Further, it has been shown that haloperidol, rimcazole, o~-(4-fluorophenyl)-4-(5-fluoro-2-pyrimidinyl)-1-piperazinebutanol (BMY-14802) and N,N-dipropyl-2-(4-methoxy-3-(2-phenylethoxy)phenyl)-ethylamine hydrochloride (NE-100) appear to act as antagonists in several behavioralTo whom request for reprints should be addressed.tests (23,35,36). On the other hand, it is now clear that these sites are different entities from opiate receptors, for which they were initially classified, and from the high affinity phencyclidine (PCP) binding site (26). The PCP site is located inside the ion channel associated with the N-methyl-Daspartate (NMDA) type of glutamate receptor. Drugs, such as PCP, its more selective derivative TCP, or MK-801, bind with high affinity to this site and lead to a noncompetitive antagonism of the NMDA type of glutamatergic neurotransmission (1,18).Although the pharmacological roles of cr sites are not yet well understood, evidences indicate that they may have several biological functions (32,41). Among them, a facilitatory role 859

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“…The effect of SKF 10,047 was stereoselective and it could be reversed by the sigma antagonist haloperidol [75,76]. In later experiments, (+)-SKF 10,047 was shown to also increase extracellular acetylcholine in the hippocampus in a stereoselective fashion and this effect could also be blocked by haloperidol [77].…”

Section: Acetylcholine and Sigma-1 Receptor Functionmentioning

confidence: 99%

The cholinergic system, sigma-1 receptors and cognition

Waarde

Ramakrishnan

Rybczynska

et al. 2011

Behavioural Brain Research

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a b s t r a c tThis article provides an overview of present knowledge regarding the relationship between the cholinergic system and sigma-1 receptors, and discusses potential applications of sigma-1 receptor agonists in the treatment of memory deficits and cognitive disorders. Sigma-1 receptors, initially considered as a subtype of the opioid family, are unique ligand-regulated molecular chaperones in the endoplasmatic reticulum playing a modulatory role in intracellular calcium signaling and in the activity of several neurotransmitter systems, particularly the cholinergic and glutamatergic pathways. Several central nervous system (CNS) drugs show high to moderate affinities for sigma-1 receptors, including acetylcholinesterase inhibitors (donepezil), antipsychotics (haloperidol, rimcazole), selective serotonin reuptake inhibitors (fluvoxamine, sertraline) and monoamine oxidase inhibitors (clorgyline). These compounds can influence cognitive functions both via their primary targets and by activating sigma-1 receptors in the CNS. Sigma-1 agonists show powerful anti-amnesic and neuroprotective effects in a large variety of animal models of cognitive dysfunction involving, among others (i) pharmacologic target blockade (with muscarinic or NMDA receptor antagonists or p-chloroamphetamine); (ii) selective lesioning of cholinergic neurons; (iii) CNS administration of ␤-amyloid peptides; (iv) aging-induced memory loss, both in normal and senescentaccelerated rodents; (v) neurodegeneration induced by toxic compounds (CO, trimethyltin, cocaine), and (vi) prenatal restraint stress.

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Increase of extracellular acetylcholine level in rat frontal cortex induced by (+)N-allylnormetazocine as measured by brain microdialysis

Cited by 48 publications

References 24 publications

Prevention of nimodipine-induced impairment of learning by the selective ? ligand PRE-084

Prevention of nimodipine-induced impairment of learning by the selective ? ligand PRE-084

PRE-084, a σ selective PCP derivative, attenuates MK-801-induced impairment of learning in mice

The cholinergic system, sigma-1 receptors and cognition

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