Currin, C. B.¹, Swart, P. C.¹, Dimatelis, J.J.¹, Russell, V.V.¹
¹ Dept Human Biology, University of Cape Town, Cape Town, South Africa
Based on Honours thesis:
Foetal alcohol spectrum disorders (FASD) exhibit deficits in hyperactivity, learning and memory. While many factors play a role, the mechanism of ethanol’s toxic effects are still not fully elucidated.
An animal model of FAS was used to test whether a phosphodiesterase inhibitor, vinpocetine, can ameliorate alcohol-induced impairment. Male Sprague-Dawley rats (n=39) were bred and treated at postnatal days (P) 4 – 9 with ethanol or saline. At P25, the rats underwent the Open Field (OF) test, Novel Object test (NOT) and then Morris Water Maze (MWM) test over the succeeding 5 days after subsequent treatment with vinpocetine or DMSO. At P31, prefrontal cortex (PFC) and dorsal hippocampus (DH) were dissected. Synaptophysin and MKP-1 protein levels were measured in these brain areas using Western Blotting.
Early alcohol exposure did not significantly affect hyperactivity in the OF but did increase anxiety as measured in the NOT and thygmotaxic index of the MWM, which was exacerbated by vinpocetine. Ethanol-exposed rats had impaired short-term memory when compared to controls as measured in the MWM, which was restored by vinpocetine treatment. Synaptophysin levels in the PFC and MKP-1 levels in the DH were elevated in vinpocetine treated ethanol rats compared to ethanol-exposed and control groups.
Our results show that ethanol interferes with short-term memory in rats by unknown mechanisms and vinpocetine improves short-term memory by increasing synaptophysin levels in the PFC. Vinpocetine treatment might be stressful since it caused increased MKP-1 levels in the DH which may inevitably affect other aspects of memory.