| Abstract No.: | C-G3191 |
| Country: | Canada |
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| Title: | DISRUPTING MOLECULES INVOLVED IN SYNAPSE FORMATION PREVENTS MEMORY CONSOLIDATION IN OPERANTLY CONDITIONED LYMNAEA STAGNALIS. |
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| Authors/Affiliations: | 1 Anthony Senzel*; 1 Zhong-Ping Feng;
1 University of Toronto, ON, Canada;
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| Content: | The ability to learn a new behaviour or to learn to avoid a potentially harmful situation is a trait inherent in all species, from flies to humans. While increasing evidence contributing to our understanding of the molecular mechanisms involved in memory formation progresses, questions still remain regarding what is happening at the level of the synapse during these processes. In this study, we asked whether new synapses are required for the acquisition/consolidation of a new memory. To address this question, we disrupted the function of specific molecules involved in synaptogenesis both pre- and post-synaptically, and subsequently tested for long-term memory (LTM) following operant conditioning, using the well-established adverse operant conditioning model of aerial respiration in Lymnaea stagnalis (Lukowiak et al., J Exp Biol, 1996). Briefly, when L. stagnalis is placed into a hypoxic environment they significantly increase aerial respiratory behaviour. 24 hours following a pre-train screening period, the snails were conditioned during two 45 minute sessions separated by one hour by applying an aversive tactile stimulus to the pneumostome contingent upon each opening. LTM was established by examining the snails 24 hours following training, with control groups showing significant decreases in total breathing time and number of pneumostome openings. Injections of the putative calcium sensor synaptotagmin I (syt I) C2A loop 3 peptide -a dominant negative peptide recently shown by our laboratory to prevent presynaptic structure formation (Gardzinski et al., J Physiol, 2007)- given at 15-45 minutes and 1.5-2 hours post-training prevented the formation of memory, as shown by no significant changes in the total breathing time and number of pneumostome openings when compared to pre-train results. In contrast, a control peptide showed no disruptions in memory formation, similar to the control group. To confirm this finding, we treated the animals with double stranded RNA (dsRNA) specific to the tumor suppressor gene encoding the transcription factor menin (MEN1), which is required for postsynaptic formation (Van Kesteren et al., J Neurosci, 2003). We found that effective knockdown of MEN1 by MEN1 dsRNA injections (not the control dsRNA) given prior to training resulted in deficits in memory formation of the snails. Taken together, our results demonstrate that disruptions of pre- and post-synaptic molecules involved in synapse formation lead to snails unable to form LTM, demonstrating a necessary involvement of synaptogenesis during memory consolidation. |
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