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Gap junctions and memory: An investigation using a single trial discrimination avoidance task for the neonate chick
Authors:L.J. Verwey  T.M. Edwards
Affiliation:1. School of Psychology, Psychiatry and Psychological Medicine, Monash University, 3800 Victoria, Australia;2. Tabor Victoria, P.O. Box 2223, Ringwood North, 3134 Victoria, Australia;1. Department of Neurosurgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, PR China;2. Institute of Clinical Medicine, Zhengzhou University, Zhengzhou 450001, PR China;3. Department of Bioengineering, Zhengzhou University, Zhengzhou 450001, PR China;4. Department of Radiotherapy, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, PR China;1. Laboratory of Behavioral Neurobiology, Department of Physiology, Faculty of Sciences, Universidad de Valparaíso, Valparaíso, Chile;2. Centro Interdisciplinario de Neurociencia de Valparaíso, Universidad de Valparaíso, Valparaíso, Chile
Abstract:Gap junctions are important to how the brain functions but are relatively under-investigated with respect to their contribution towards behaviour. In the present study a single trial discrimination avoidance task was used to investigate the effect of the gap junction inhibitor 18-α-glycyrrhetinic acid (αGA) on retention. Past studies within our research group have implied a potential role for gap junctions during the short-term memory (STM) stage which decays by 15 min post-training. A retention function study comparing 10 μM αGA and vehicle given immediately post-training demonstrated a significant main effect for drug with retention loss at all times of test (10–180 min post-training). Given that the most common gap junction in the brain is that forming the astrocytic network it is reasonable to conclude that αGA was acting upon these. To confirm this finding and interpretation two additional investigations were undertaken using endothelin-1 (ET-1) and ET-1 + tolbutamide. Importantly, a retention function study using 10 nM ET-1 replicated the retention loss observed for αGA. In order to confirm that ET-1 was acting on astrocytic gap junctions the amnestic action of ET-1 was effectively challenged with increasing concentrations of tolbutamide. The present findings suggest that astrocytic gap junctions are important for memory processing.
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