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Imaging and analysis of evoked excitatory-postsynaptic-calcium-transients by individual presynaptic-boutons of cultured Aplysia sensorimotor synapse. | LitMetric

AI Article Synopsis

  • - The Aplysia gill withdrawal reflex serves as a crucial model for studying synaptic transmission and the mechanisms behind learning and memory, highlighting the importance of the sensory-motor (SN-MN) synapse.
  • - Recent research suggests that long-term potentiation (LTP) at the Aplysia SN-MN synapse, similar to mammalian synapses, is dependent on increased levels of calcium ions in the postsynaptic neuron.
  • - The study discovered that presynaptic stimulation triggers transient increases in postsynaptic calcium levels, revealing two main mechanisms: calcium influx through specific receptors and through voltage-gated calcium channels, with most presynaptic boutons linked to functional synapses.

Article Abstract

The use of the sensory-motor (SN-MN) synapse of the Aplysia gill withdrawal reflex has contributed immensely to the understanding of synaptic transmission, learning and memory acquisition processes. Whereas the majority of the studies focused on analysis of the presynaptic mechanisms, recent studies indicated that as in mammalian synapses, long term potentiation (LTP) formed by Aplysia SN-MN synapse depends on elevation of the postsynaptic free intracellular calcium concentration ([Ca2+](i)). Consistently, injection of the fast calcium chelator BAPTA to the MN prevents the formation of serotonin-induced LTP. Nevertheless, currently there are no published reports that directly examine and document whether evoked synaptic transmission is associated with transient increase in the postsynaptic [Ca2+](i). In the present study we imaged, for the first time, alterations in the postsynaptic [Ca2+](i) in response to presynaptic stimulation and analyzed the underlying mechanisms. Using live imaging of the postsynaptic [Ca2+](i) while monitoring the EPSP, we found that evoked transmitter release generates excitatory postsynaptic calcium concentration transients (EPSCaTs) by two mechanisms: (a) activation of DNQX-sensitive postsynaptic receptors-gated calcium influx and (b) calcium influx through nitrendipine-sensitive voltage-gated calcium channels (VGCCs). Concomitant confocal imaging of presynaptic boutons and EPSCaTs revealed that approximately 86% of the presynaptic boutons are associated with functional synapses.

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Source
http://dx.doi.org/10.1016/j.ceca.2009.12.015DOI Listing

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