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Published in

Society for Neuroscience, Journal of Neuroscience, 39(30), p. 13016-13020, 2010

DOI: 10.1523/jneurosci.1659-10.2010

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GABAergic synaptic scaling in embryonic motoneurons is mediated by a shift in the chloride reversal potential

This paper is made freely available by the publisher.
This paper is made freely available by the publisher.

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Abstract

Homeostatic synaptic plasticity ensures that networks maintain specific levels of activity by regulating synaptic strength in a compensatory manner. When spontaneous network activity was blockedin vivoin the embryonic spinal cord, compensatory increases in excitatory GABAergic synaptic inputs were observed. This homeostatic synaptic strengthening was observed as an increase in the amplitude of GABAergic miniature postsynaptic currents. We find that this process is mediated by an increase in chloride accumulation, which produces a depolarizing shift in the GABAergic reversal potential (EGABA). The findings demonstrate a previously unrecognized mechanism underlying homeostatic synaptic scaling. Similar shifts inEGABAhave been described following various forms of neuronal injury, introducing the possibility that these shifts inEGABArepresent a homeostatic response.