Time gradient for post-test vulnerability to scopolamine-induced amnesia following the initial acquisition session of a spatial reference memory task in mice

• Published in: Behavioral and neural biology Vol. 60; no. 2; pp. 139 - 151
• Main Authors: Toumane, Abdoulaye, Durkin, Thomas P.
• Format: Journal Article
• Language: English
• Published: New York, NY Elsevier B.V 01.09.1993; Academic Press
• Subjects: Animals; Behavioral psychophysiology; Biological and medical sciences; Cerebral Cortex - drug effects; Cholinergic Fibers - drug effects; Discrimination Learning - drug effects; Dose-Response Relationship, Drug; Fundamental and applied biological sciences. Psychology; Hippocampus - drug effects; Injections, Intraperitoneal; Male; Mental Recall - drug effects; Mice; Mice, Inbred C57BL; N-Methylscopolamine; Neural Pathways - drug effects; Neurotransmission and behavior; Orientation - drug effects; Parasympatholytics - pharmacology; Psychology. Psychoanalysis. Psychiatry; Psychology. Psychophysiology; Scopolamine Derivatives - pharmacology; Scopolamine Hydrobromide - pharmacology; Septal Nuclei - drug effects; Substantia Innominata - drug effects; Reference memory; Memory disorder; Acquisition process; Sensitivity resistance; Muscarinic receptor; Amnesia; Antagonist; Time analysis; Cholinergic pathway; Spatial memory
• ISSN: 0163-1047; 1557-8003
• DOI: 10.1016/0163-1047(93)90243-B

The time course for vulnerability to the amnestic effects of the cholinergic antagonist, scopolamine, during the postacquisition period has been investigated. We have examined the effects of post-test injections of scopolamine (1 mg/kg ip) given at different times from 30 s for up to 6 h following the end of the first acquisition session of a concurrent spatial discrimination (reference memory) protocol in an 8-arm radial maze on subsequent long-term (24 h) retention performance in C57BL/6 mice. Results show that the immediate (30 s) post-test injection of scopolamine—HCl on Day 1 produces marked perturbation (amnesia) of long-term retention as attested to by significant deficits in various indices of spatial discrimination performance gain on Day 2 as compared to control subjects injected either with scopolamine—MBr or saline. The severity of this scopolamine-induced amnesia declines only slightly as a function of the treatment period 30 s—3 h post-test. However, no evidence for amnesia is observed if scopolamine—HCl injections are delayed for 6 h postsession. This important latter observation attests to the absence of any significant proactive effects of scopolamine on the ability of mice to perform the retention test via possible long-term effects on attention, motivation, or locomotor performance. These results thus constitute evidence for the existence of a limited (30 s–3 h) time gradient for vulnerability of the early memory trace to disruption by scopolamine. The present results are dis cussed in relation to our previous direct neurochemical observations describing the differential time courses of intervention of the ascending septohippocampal and nBM—cortical cholinergic pathways in the postlearning period. In particular, the presently observed time window concerning post-test vulnerability to scopolamine-induced amnesia corresponds more closely to the time course of the acute activation of the nBM—cortical cholinergic pathway, induced by testing with the same spatial memory protocol as used in the present study in mice.