Effects of concurrent manipulations of nicotinic and muscarinic receptors on spatial and passive avoidance learning

Riekkinen, Paavo; Sirviö, Jouni; Aaltonen, Minna

doi:10.1016/0091-3057(90)90004-2

Cited by 85 publications

(20 citation statements)

References 18 publications

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“…However, scopolamine did not impair spatial memory in the water maze. This result is consistent with previous reports that post-training or pre-retention testing injections of scopolamine had no effect on performance in the water maze (31,32). While the cause of the discrepancy regarding reference memory in the 8-arm radial maze and water maze in scopolamine-treated rats remains unclear, the two mazes are different with regard to motivation.…”

Section: Discussionsupporting

confidence: 82%

Characteristics of Learning and Memory Impairment Induced by ⊿9-Tetrahydrocannabinol in Rats

Mishima

Egashira

Hirosawa

et al. 2001

Japanese Journal of Pharmacology

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ABSTRACT-We investigated the characteristics of D 9 -tetrahydrocannabinol (THC)-induced impairment of learning and memory using an 8-arm radial maze task, a water maze, a visual discrimination task with 2 figures and a passive avoidance test in rats. THC (6 mg /kg, i.p.) impaired spatial memory in the standard task of the 8-arm radial maze. THC (4 -6 mg /kg, i.p.) selectively impaired working memory in a reference and working memory task of the 8-arm radial maze. Even at a dose of 10 mg /kg, THC did not impair spatial memory in the water maze. In addition, THC at a dose of 6 mg /kg, which had inhibitory effects in the 8-arm radial maze, did not affect performance in the visual discrimination task. These results indicate that at low doses (2 -6 mg/kg), THC may not produce visual function abnormalities. THC impaired retrieval (6 mg /kg, i.p.) as well as acquisition (10 mg /kg, i.p.) in the passive avoidance test. The consolidation process was also impaired by i.c.v. injection (100 m g), but not i.p. injection (6 -10 mg /kg) of THC. These results suggest that THC-induced impairment of spatial memory is based on the selective impairment of working memory through its effects on acquisition and retrieval processes.

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Section: Discussionsupporting

confidence: 82%

Characteristics of Learning and Memory Impairment Induced by ⊿9-Tetrahydrocannabinol in Rats

Mishima

Egashira

Hirosawa

et al. 2001

Japanese Journal of Pharmacology

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“…Unfortunately, the lack of a scopolamine-alone test condition in that experiment prevented the determination of whether the effect was attributable to scopolamine alone or the combined condition of scopolamine ϩ mecamylamine. Our results, consistent with animal studies in which the co-administration of mecamylamine and scopolamine increased memory impairment (Levin et al 1989(Levin et al , 1990Riekkinen et al 1990; Cozzolino . 1994), suggest that at least episodic memory may be more impaired with the drug combination than with either drug alone.…”

Section: Discussionsupporting

confidence: 82%

Combined Nicotinic and Muscarinic Blockade in Elderly Normal Volunteers: Cognitive, Behavioral, and Physiologic Responses

Little

Johnson

Minichiello

et al. 1998

Neuropsychopharmacology

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Establishing a pharmacologic model of the memory deficits of Alzheimer's disease could be an important tool in understanding how memory fails. We examined the combined effects of the muscarinic antagonist scopolamine and the nicotinic antagonist mecamylamine in eight normal elderly volunteers (age 61.9 Ϯ 8.3 yrs, SD). Each received four separate drug challenges (scopolamine (0.4 mg IV), mecamylamine (0.2 mg/kg up to 15 mg PO), mecamylamine ϩ scopolamine, and placebo). There was a trend toward increased impairment in explicit memoryGiven the limited animal models of Alzheimer's disease (AD) and other cognitive disorders, pharmacologic modeling of memory deficits in humans has been proposed as an approach that can be used to probe the neurochemistry of memory (Sunderland et al. 1986). Because there is abundant evidence that the cholinergic system is of special importance in AD (Davies and Verth 1978;Bowen et al. 1983;Coyle et al. 1983;Mash et al. 1985;Shimohama et al. 1986;Whitehouse and Au 1986;D'Amato et al. 1987;Zubenko et al. 1988), many cognitive dysfunction modeling studies have focused on this system (Beatty et al. 1986;Sunderland et al. 1987;Broks et al. 1988;Dunne 1990;Flicker et al. 1990;Sunderland et al. 1990;Molchan et al. 1992). An earlier report of a potential noninvasive test for AD using the cholinergic antagonist tropicamide (Scinto et al. 1994) and the ongoing clinical use of the anticholinesterase inhibitors tacrine and donepezil (Davis et al. 1992;Farlow et al. 1992;Knapp et al. 1994;Rogers et al. 1996) for the treatment of AD further highlight the importance of cholinergic neurons in AD.Modeling studies involving the cholinergic system in humans have focused principally on the muscarinic system, but the nicotinic system is also important in cognition and AD Newhouse et al. 1992;Newhouse et al. 1994 Nordberg et al. 1990;Perry et al. 1990;Nordberg et al. 1992;Kellar et al. 1987;Flynn and Mash 1986). Hence, we became interested in the combined effects of these two systems, specifically employing scopolamine as a centrally active muscarinic antagonist and mecamylamine as a nicotinic antagonist.To our knowledge, mecamylamine and scopolamine have only been combined in one previous human study (Gitelman and Prohovnik 1992), which showed with 133 ⌾ e inhalation methods that the nicotinic antagonist mecamylamine decreased perfusion in parietotemporal cortex, while the addiction of scopolamine reduced blood flow in frontal cortex. Because central blood flow in parietal and temporal cortex are known to be affected by AD (Haxby et al. 1988;Prohovnik et al. 1988;Friedland et al. 1989;Kumar et al. 1991), the blood flow pattern induced by scopolamine and mecamylamine together may more closely model AD than scopolamine alone. Because cognitive testing was limited, behavioral measurements were absent, and there was no placebo or scopolamine-alone condition in the Gitelman and Prohovnik study, speculations about the cognitive modeling of this combination were limited. Hence, the current study was initiated in n...

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“…1990b). Riekkinen et al (1990) have found that combined nicotinic and muscarinic blockade caused more pronounced performance deficits in passive avoidance and water maze tasks.…”

Section: Nicotinic-muscarinie Interactionsmentioning

confidence: 98%

Nicotinic systems and cognitive function

1992

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Nicotinic acetylcholine receptors have been found to be important for maintaining optimal performance on a variety of cognitive tasks. In humans, nicotine-induced improvement of rapid information processing is particularly well documented. In experimental animals nicotine has been found to improve learning and memory on a variety of tasks, while the nicotinic antagonist mecamylamine has been found to impair memory performance. Nicotine has been found to be effective in attenuating memory deficits resulting from lesions of the septohippocampal pathway or aging in experimental animals. Nicotinic receptors are decreased in the cortex of patients with Alzheimer's disease. Preliminary studies have found that some aspects of the cognitive deficit in Alzheimer's disease can be attenuated by nicotine. Nicotine may prove to be useful therapeutic treatment for this and other types of dementia.

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Effects of concurrent manipulations of nicotinic and muscarinic receptors on spatial and passive avoidance learning

Cited by 85 publications

References 18 publications

Characteristics of Learning and Memory Impairment Induced by ⊿9-Tetrahydrocannabinol in Rats

Characteristics of Learning and Memory Impairment Induced by ⊿9-Tetrahydrocannabinol in Rats

Combined Nicotinic and Muscarinic Blockade in Elderly Normal Volunteers: Cognitive, Behavioral, and Physiologic Responses

Nicotinic systems and cognitive function

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