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| Paper IPM / Cognitive / 13851 |
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| Abstract: | |||||||||||||
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Aims:The aim of the present study was to investigate the effect of swimming exercise on elevated plus-maze (EPM)-associated memory deficit induced by intra-CA1 injection of scopolamine (a muscarinic acetylcholine receptor antagonist used to model Alzheimer's disease in rodents) in male mice. In addition, involvement of the mu opioid receptors in this phenomenon was investigated.
MAIN METHODS:
Bilateral guide cannulae were implanted to allow intra-CA1 microinjections.
KEY FINDINGS:
Data showed that mice with 10 and 20 days of swimming, only acquired the emotional memory, while 30 days of swimming exercise improved it. On the other hand, pretest intra-CA1 injection of scopolamine at the doses of 2 and 3 but not 1 μg/mouse reduced the emotional memory. Our results demonstrated that 20 days of swimming by itself and without any drug injection restored the emotional memory deficit induced by intra-CA1 injection of scopolamine, only at the dose of 2 but not 3 μg/mouse. Moreover, once daily injection of the subthreshold doses of morphine (2.5 and 5 mg/kg, i.p.) during the last 7 days of the 20 day-swimming intervention, improved the emotional memory deficit induced by scopolamine (3 μg/mouse) and this effect could be blocked by the subthreshold doses of naloxone (0.2 and 0.4 mg/kg). It was noted that all previous interventions did not alter the anxiety-like behaviors.
SIGNIFICANCE:
Swimming improved the emotional memory by itself and restored the emotional memory deficit induced by the intra-CA1 injection of scopolamine. Mu opioid receptor-dependent mechanism(s) is(are) suggested to play a role in this phenomenon.
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