Swimming improves the emotional memory deficit by scopolamine via mu opioid receptors

Abstract

AimsThe 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 methodsBilateral guide cannulae were implanted to allow intra-CA1 microinjections. Key findingsData showed that mice with 10 and 20days of swimming, only acquired the emotional memory, while 30days of swimming exercise improved it. On the other hand, pretest intra-CA1 injection of scopolamine at the doses of 2 and 3 but not 1μg/mouse reduced the emotional memory. Our results demonstrated that 20days 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 3μg/mouse. Moreover, once daily injection of the subthreshold doses of morphine (2.5 and 5mg/kg, i.p.) during the last 7days of the 20day-swimming intervention, improved the emotional memory deficit induced by scopolamine (3μg/mouse) and this effect could be blocked by the subthreshold doses of naloxone (0.2 and 0.4mg/kg). It was noted that all previous interventions did not alter the anxiety-like behaviors. SignificanceSwimming 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.