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Article

Developmental Time Course of SNAP-25 Isoforms Regulate Hippocampal Long-Term Synaptic Plasticity and Hippocampus-Dependent Learning

1
Department of Cell Biology & Anatomy, New York Medical College, Valhalla, NY 10595, USA
2
Department of Neuroscience, Karolinska Institutet, 171 77 Stockholm, Sweden
*
Authors to whom correspondence should be addressed.
These authors contributed equally to this study.
Int. J. Mol. Sci. 2020, 21(4), 1448; https://doi.org/10.3390/ijms21041448
Received: 31 December 2019 / Revised: 12 February 2020 / Accepted: 18 February 2020 / Published: 20 February 2020
SNAP-25 is essential to activity-dependent vesicle fusion and neurotransmitter release in the nervous system. During early development and adulthood, SNAP-25 appears to have differential influences on short- and long-term synaptic plasticity. The involvement of SNAP-25 in these processes may be different at hippocampal and neocortical synapses because of the presence of two different splice variants, which are developmentally regulated. We show here that the isoform SNAP-25a, which is expressed first developmentally in rodent brain, contributes to developmental regulation of the expression of both long-term depression (LTD) and long-term potentiation (LTP) at Schaffer collateral-CA1 synapses in the hippocampus. In one month old mice lacking the developmentally later expressed isoform SNAP-25b, Schaffer collateral-CA1 synapses showed faster release kinetics, decreased LTP and enhanced LTD. By four months of age, SNAP-25b-deficient mice appeared to have compensated for the lack of the adult SNAP-25b isoform, now exhibiting larger LTP and no differences in LTD compared to wild type mice. Interestingly, learning a hippocampus-dependent task reversed the reductions in LTP, but not LTD, seen at one month of age. In four month old adult mice, learning prevented the compensatory up-regulation of LTD that we observed prior to training. These findings support the hypothesis that SNAP-25b promotes stronger LTP and weakens LTD at Schaffer collateral-CA1 synapses in young mice, and suggest that compensatory mechanisms can reverse alterations in synaptic plasticity associated with a lack of SNAP-25b, once mice reach adulthood. View Full-Text
Keywords: SNARE proteins; long-term potentiation; long-term depression; learning and memory; cognition; Schaffer collateral-CA1 synapses SNARE proteins; long-term potentiation; long-term depression; learning and memory; cognition; Schaffer collateral-CA1 synapses
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MDPI and ACS Style

Gopaul, K.R.; Irfan, M.; Miry, O.; Vose, L.R.; Moghadam, A.; Subah, G.; Hökfelt, T.; Bark, C.; Stanton, P.K. Developmental Time Course of SNAP-25 Isoforms Regulate Hippocampal Long-Term Synaptic Plasticity and Hippocampus-Dependent Learning. Int. J. Mol. Sci. 2020, 21, 1448. https://doi.org/10.3390/ijms21041448

AMA Style

Gopaul KR, Irfan M, Miry O, Vose LR, Moghadam A, Subah G, Hökfelt T, Bark C, Stanton PK. Developmental Time Course of SNAP-25 Isoforms Regulate Hippocampal Long-Term Synaptic Plasticity and Hippocampus-Dependent Learning. International Journal of Molecular Sciences. 2020; 21(4):1448. https://doi.org/10.3390/ijms21041448

Chicago/Turabian Style

Gopaul, Katisha R., Muhammad Irfan, Omid Miry, Linnea R. Vose, Alexander Moghadam, Galadu Subah, Tomas Hökfelt, Christina Bark, and Patric K. Stanton. 2020. "Developmental Time Course of SNAP-25 Isoforms Regulate Hippocampal Long-Term Synaptic Plasticity and Hippocampus-Dependent Learning" International Journal of Molecular Sciences 21, no. 4: 1448. https://doi.org/10.3390/ijms21041448

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