In vivo synaptic scaling is mediated by GluA2-lacking AMPA receptors in the embryonic spinal cord
| Autor: | Miguel Angel Garcia-Bereguiain, Ellie Butler, Casie Lindsly, Peter Wenner, Atlantis Wilkins Hill, Carlos Gonzalez-Islas |
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| Jazyk: | angličtina |
| Rok vydání: | 2013 |
| Předmět: |
Patch-Clamp Techniques
Biophysics AMPA receptor Chick Embryo Tetrodotoxin Biology Article GABA Antagonists Homeostatic plasticity Animals Patch clamp Receptors AMPA Anesthetics Local Receptor Motor Neurons Synaptic scaling GABAA receptor General Neuroscience Excitatory Postsynaptic Potentials Gene Expression Regulation Developmental Lidocaine GABA receptor antagonist Electric Stimulation Pyridazines nervous system Spinal Cord Synapses Excitatory postsynaptic potential Neuroscience Excitatory Amino Acid Antagonists |
| Popis: | When spiking activity within a network is perturbed for hours to days, compensatory changes in synaptic strength are triggered that are thought to be important for the homeostatic maintenance of network or cellular spiking activity. In one form of this homeostatic plasticity, called synaptic scaling, all of a cell's AMPAergic miniature postsynaptic currents (mEPSCs) are increased or decreased by some scaling factor. Although synaptic scaling has been observed in a variety of systems, the mechanisms that underlie AMPAergic scaling have been controversial. Certain studies find that synaptic scaling is mediated by GluA2-lacking calcium receptors (CP-AMPARs), whereas others have found that scaling is mediated by GluA2-containing calcium-impermeable receptors (CI-AMPARs). Spontaneous network activity is observed in most developing circuits, and in the spinal cord this activity drives embryonic movements. Blocking spontaneous network activity in the chick embryo by infusing lidocainein vivotriggers synaptic scaling in spinal motoneurons; here we show that AMPAergic scaling occurs through increases in mEPSC conductance that appear to be mediated by the insertion of GluA2-lacking AMPA receptors at the expense of GluA2-containing receptors. We have previously reported thatin vivoblockade of GABAAtransmission, at a developmental stage when GABA is excitatory, also triggered AMPAergic synaptic scaling. Here, we show that this form of AMPAergic scaling is also mediated by CP-AMPARs. These findings suggest that AMPAergic scaling triggered by blocking spiking activity or GABAAreceptor transmission represents similar phenomena, supporting the idea that activity blockade triggers scaling by reducing GABAAtransmission. |
| Databáze: | OpenAIRE |
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