Scopolamine (3 mg/kg IP) given before an acquisition trial, reduced the retention of a one-trial passive avoidance "step through" response in mice. A single administration of cholinergic agonists such as oxotremorine, BM-5, or arecoline, antagonized this amnesic effect of scopolamine. A significant
Attenuation of scopolamine-induced amnesia in mice
β Scribed by William S. Stone; Carolyn E. Croul; Paul E. Gold
- Publisher
- Springer
- Year
- 1988
- Tongue
- English
- Weight
- 413 KB
- Volume
- 96
- Category
- Article
- ISSN
- 0033-3158
No coin nor oath required. For personal study only.
β¦ Synopsis
Numerous studies suggest that age-related declines in memory storage are related to impairment of central cholinergic systems. Scopolamine, a muscarinic cholinergic antagonist, has been used with young humans and other animal species as a model of the cognitive impairment that often accompanies normal and pathological aging. The present study examined whether amnesia induced by scopolamine could be counteracted in mice by arecoline, a cholinergic agonist, or by other drugs, epinephrine or glucose, which have been found to enhance memory in aged rodents and humans. Young mice were administered scopolamine (3 mg/kg, IP) or saline prior to training on an inhibitory avoidance apparatus. Immediately after training, animals received injections of epinephrine (0.01, 0.05, 0.1, and 0.2 mg/kg), glucose (10, 100, and 250 mg/kg), arecoline (0.5, 1, 2, 5, 10, and 20 mg/kg), or saline. The results indicate that pre-training scopolamine reliably impaired retention assessed in test trials 48 h after training. This impairment was not attenuated by any post-training dose of arecoline; however, immediate post-training injections of both epinephrine (at 0.05 mg/kg) and glucose (at 100 mg/kg) significantly reduced the amnesia. Neither of these drugs was effective if injections were delayed by 1 h after training. These results support the value of scopolamine as a model of age-related memory impairments, but suggest further that these memory deficits may be particularly susceptible to attenuation with non-cholinergic treatments.
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