Scopolamine- and morphine-induced impairments of spontaneous alternation performance in mice: Reversal with glucose and with cholinergic and adrenergic agonists.

Abstract

Administration of epinephrine and glucose, as well as drugs that influence cholinergic and opiate systems, can enhance or impair memory. The present experiments examined the possibility that peripheral glucose administration might reverse scopolamine- and morphine-induced impairments in a spontaneous alternation task. Mice received all drug administrations 30 min before testing. Scopolamine-induced (3 mg/kg) deficits in alternation performance were reversed by glucose (100 and 250 mg/kg), amphetamine (1 mg/kg), epinephrine, physostigmine, and oxotremorine (each 0.1 mg/kg). Morphine (10 mg/kg) also impaired spontaneous alternation performance, and glucose (100 and 300 mg/kg) reversed this impairment as well. These findings are consistent with the view that central cholinergic systems, possibly under inhibitory opiate regulation, may contribute to glucose and epinephrine effects on memory storage.

Cognitive Enhancing Properties and Tolerability of Cholinergic Agents in Mice: A Comparative Study of Nicotine, Donepezil, and SIB-1553A, a Subtype-Selective Ligand for Nicotinic Acetylcholine Receptors

“…As previously reported (Stone et al, 1991;Ragozzino et al, 1994;Hiramatsu and Inoue, 2000), scopolamine severely impaired spontaneous alternation in young mice. SIB-1553A was able to reverse this working memory deficit in a dose-dependent manner, and to a similar degree as nicotine.…”

Age-related changes in memory and in acetylcholine functions in the hippocampus in the Ts65Dn mouse, a model of Down syndrome

“…On Week 2, the same mice received physostigmine hemisulfate (50 μg/kg, IP) 10 min prior to another spontaneous alternation test. The dose was selected on the basis of pilot data together with past results (Stone et al, 1991). The sequence was then repeated in Weeks 3 and 4.…”

“…This view is supported by evidence from other studies showing that acetylcholinesterase inhibitors enhance memory in aged rats and mice (e.g., Rispoli et al, 2006;Flood et al, 1993;Normile and Altman, 1992;Riekkinen et al, 1991), and that such drugs can be effective in memory-impaired aged rats but not in young rats (Ohta et al, 1991;Castellano et al, 1989). Similarly, acetylcholinesterase inhibitors are particularly effective in enhancing memory in rats and mice with compromised cholinergic functions and with other memoryimpairing pharmacological manipulations (Chang and Gold, 2004;Degroot and Parent, 2000;Ukai et al, 1995;Walker and Gold, 1992;Beracochea et al, 1992;Stone et al, 1991;Murray and Fibiger, 1986). Acetylcholinesterase inhibitors are also effective enhancers of memory in several rodent models of Alzheimer's Disease (Maurice et al, 1996;Dong et al, 2005;Popovi et al, 1997;Santucci et al, 1991).…”

“…The acetylcholinesterase inhibitor, physostigmine, was selected as the drug with which to enhance memory because of past findings indicating that the drug enhances memory in aging and other conditions (e.g., Rispoli et al, 2006;Flood et al, 1993;Normile and Altman, 1992;Riekkinen et al, 1991;Ohta et al, 1991;Castellano et al, 1989;Chang and Gold, 2004;Degroot and Parent, 2000;Ukai et al, 1995;Walker and Gold, 1992;Beracochea et al, 1992;Stone et al, 1991;Murray and Fibiger, 1986;Maurice et la., 1996;Dong et al, 2005;Popovi et al, 1997;Santucci et al, 1991). In addition, physostigmine was selected because it is an indirect agonist that requires at least some remaining release of ACh in order to exert its pharmacological actions.…”

Effects of N-Nitro-L-Arginine on Isolated Rabbit Afferent Arterioles

“…There has been substantial evidence showing that the memory deficits produced by scopolamine are reinstated by cholinomimetic drugs such as oxotremorine, physostig mine and tacrine (5,6). Recent studies, however, indicate that some adrenergic drugs can attenuate the scopolamine deficits.…”