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Comment
. 2012 Nov 8;76(3):463-5.
doi: 10.1016/j.neuron.2012.10.022.

Flip-flopping to the membrane

Catherine L Salussolia  1 , Lonnie P Wollmuth
Affiliations
Comment

Flip-flopping to the membrane

Catherine L Salussolia et al. Neuron. .

Erratum in

  • Neuron. 2012 Dec 20;76(6):1238

Abstract

Excitatory synapses that use the neurotransmitter glutamate are highly dynamic, constantly changing their character in an activity-dependent manner. In this issue of Neuron, Penn et al. (2012) describe a novel mechanism that changes the fidelity of glutamate signaling to maintain homeostatic synaptic plasticity.

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Figures

Figure 1
Figure 1. Schematic of the Biogenic Pathway of Ionotropic Glutamate Receptors from Synthesis to Membrane Expression in the CA1 Region of the Hippocampus Either under Normal Conditions (Left Half) or following Chronic Deprivation of Activity using TTX (Right Half)
Following TTX treatment, the ratio of flip to flop is decreased for both GluA1 and GluA2, but the splicing transition occurs more rapidly for GluA1, favoring the earlier appearance of GluA1o. Because of the slower splicing transition for GluA2 and its longer half-life in the endoplasmic reticulum (ER), GluA2i persists in the biosynthetic pathway. GluA1o also forms heteromers more readily than GluA1i with GluA2i. All of these factors favor the formation of GluA1o/Glu2Ai heteromers that display reduced desensitization and a faster recovery from desensitization. At CA1 synapses the fidelity of transmission is maintained better following TTX (red) than in the control (black) with high-frequency stimulation, presumably reflecting the presence of GluA1o/GluA2i at the synapse. Accessory proteins, such as TARPs or cornichons (green cylinder), apparently do not contribute to the phenotype.
See this image and copyright information in PMC

Comment on

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