Among the methods valuable for assessing spatial learning and memory impairments in rodents, the Barnes maze (BM) task deserves special attention. It is based on the assumption that the animal placed into the aversive environment should learn and remember the location of an escape box located below the surface of the platform. Different phases of the task allow to measure spatial learning, memory retrieval, and cognitive flexibility. Herein, we summarize current knowledge about the BM procedure, its variations and critical parameters measured in the task. We highlight confounding factors which should be taken into account when conducting BM task, discussing briefly its advantages and disadvantages. We then propose an extended version of the BM protocol which allows to measure different aspects of spatial learning and memory in rodents. We believe that this review will help to standardize the BM methodology across the laboratories and eventually make the results comparable.

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Central cholinergic dysfunction contributes to acute spatial memory deficits produced by ethanol administration. Donepezil and rivastigmine elevate acetylcholine levels in the synaptic cleft through the inhibition of cholinesterases—enzymes involved in acetylcholine degradation. The aim of our study was to reveal whether donepezil (acetylcholinesterase inhibitor) and rivastigmine (also butyrylcholinesterase inhibitor) attenuate spatial memory impairment as induced by acute ethanol administration in the Barnes maze task (primary latency and number of errors in finding the escape box) in rats. Additionally, we compared the influence of these drugs on ethanol-disturbed memory. In the first experiment, the dose of ethanol (1.75 g/kg, i.p.) was selected that impaired spatial memory, but did not induce motor impairment. Next, we studied the influence of donepezil (1 and 3 mg/kg, i.p.), as well as rivastigmine (0.5 and 1 mg/kg, i.p.), given either before the probe trial or the reversal learning on ethanol-induced memory impairment. Our study demonstrated that these drugs, when given before the probe trial, were equally effective in attenuating ethanol-induced impairment in both test situations, whereas rivastigmine, at both doses (0.5 and 1 mg/kg, i.p.), and donepezil only at a higher dose (3 mg/kg, i.p.) given prior the reversal learning, attenuated the ethanol-induced impairment in cognitive flexibility. Thus, rivastigmine appears to exert more beneficial effect than donepezil in reversing ethanol-induced cognitive impairments—probably due to its wider spectrum of activity. In conclusion, the ethanol-induced spatial memory impairment may be attenuated by pharmacological manipulation of central cholinergic neurotransmission.

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