Abstract
Background: Habituation is the simplest form of non-associative learning and has been found to be impaired in neurodegenerative disorders including Alzheimer’s disease. Habituation of acoustic startle reflex is the reduction of the response to consecutive acoustic stimuli. Habituation measured after a training of short-term inter-trial intervals (ITIs) can be thought of as a form of sensory working memory. Cannabinoids are compounds, which act on cannabinoid receptors in a similar way as Cannabis sativa. Cannabinioid (CB1) receptors are in high density in the areas of the brain required for higher cognitive functioning such as hippocampus, where they are believed to be involved in learning and memory. However, the role of CB1 receptors in non-associative memory in mice remains unclear. The purpose of the present study was to determine the effects of the CB1 agonist, CP55940, and the antagonist, SR14716A, on the habituation of startle reflex in C57BL/6J mice. Methods: Forty naive male C57BL/6J mice were used in this study. Ninety-six trials of 115 dB acoustics stimuli with 2 second inter-trial intervals (ITIs) were delivered to the mice using Med-associates startle apparatus. Mice were treated with a cannabinoid agonist and antagonist in a fully-balanced design and tested in the apparatus. Habituation and the acoustic startle response (ASR) were measured. Results: CP 55940 decreased habituation as well as the initial acoustic startle response (ASR). SR141716A reversed the effect of CP55940 on these measures. SR141716A had no significant effects on its own on habituation. Surprisingly, SR141716A decreased ASR in a similar way as CP55940. Conclusions: The present study shows that cannabinoid CB1 receptors do play an important role in the working memory model/ASR habituation as the effects produced by CP55940 were attenuated by SR141716A.
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