| Abstract No.: | B-B2057 |
| Country: | Canada |
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| Title: | BIDIRECTIONAL PLASTICITY OF GLIAL CELLS FOLLOWING LONG-TERM MODIFICATIONS OF SYNAPTIC EFFICACY. |
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| Authors/Affiliations: | 1 Eve-Lyne Bélair*; 1 Joanne Vallée; 1 Richard Robitaille;
1 Université de Montréal, QC, Canada
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| Content: | Strong evidence showing the ability of glial cells to detect and respond to synaptic transmission and, in return, modulate synaptic activity and plasticity, has contributed to the notion of glial cells as active synaptic partners. However, the plasticity of glia themselves in response to changing synaptic activity as never been investigated. Here we used the amphibian neuromuscular junction (NMJ) to study the plasticity of perisynaptic Schwann cell (PSC) activity following long-term modifications of synaptic activity. To induce such modifications, we used two different models that oppositely altered synaptic activity. Chronic in vivo blockade of postsynaptic nicotinic receptors using α-bungarotoxin (α-btx) resulted in an increased quantal release and a decreased resistance to synaptic depression. On the other hand, increasing synaptic activity with chronic in vivo nerve stimulation decreased quantal release and increased resistance to synaptic depression. Nerve-evoked PSC calcium responses largely differ in both models even though the total amount of transmitter released by nerve terminals during a 40 Hz, 30s stimulation was similar. While in stimulated NMJs, nerve-evoked PSC calcium responses were similar to control, in α-btx treated NMJs, they were delayed and smaller in amplitude. This suggests that the neuronal message perceived by PSCs in conditions of elevated synaptic activity, might be altered. However, when isolating purinergic and muscarinic components of PSC calcium responses, we found an increased sensitivity to ATP and a decreased sensitivity to muscarine in stimulated NMJs, suggesting that purinergic and muscarinic receptors might be oppositely regulated in these cells. Conversely, in α-btx treated NMJs, PSC sensitivity remained unaffected, but ATP and muscarine induced calcium responses were prolonged, revealing the regulation of calcium handling in these PSCs. Our results reveal a bidirectional plasticity of PSC calcium responses to neurotransmitter, a fine tuning of calcium response properties and a differential regulation of signaling pathways, suggesting that PSCs adapt to the synapse they are associated with and to the changes these synapses undergo. Thus, similar to neurons, perisynaptic glial cells undergo plastic changes induced by synaptic activity. |
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