Neurotransmitter-Induced Electrical Activity Identified As Key Regulator Of Synaptogenesis

cultured spinal neurons with tetrodotoxin Kirsch and Betz now found that electrical activity is required for glycine receptor clustering. In a second step, they investigated whether electrical activity induced by activation of the glycine receptor itself might be an important component in this process. Therefore, neuronal cultures were treated with the highly selective glycine receptor antagonist strychnine. This treatment abolished both gephyrin and glycine receptor clustering in a dose-dependent manner. Knowing that glycine receptor activation in embryonic neurons can result in membrane depolarization and the opening of voltage-gated calcium channels, spinal cord cultures were treated with calcium channel antagonists and again, receptor clustering was strongly reduced.

The data suggest the following model for postsynaptic membrane formation: Initially glycine receptors are diffusely distributed in the neuronal plasma membrane. Whenever receptors, encounter freely diffusing an active nerve terminal releasing the appropriate neurotransmitter, namely glycine, they open and the resulting ion flux generates a local change in membrane potential. This induces the opening of voltage-gated calcium channels. The resulting calcium influx triggers a second messenger cascade which together with additional presynaptic effectors causes the aggregation of gephyrin beneath the activated plasmamembrane. The aggregates of this peripheral membrane protein then act as a diffusion trap for additional glycine receptor polypeptides. This passive mechanism concentrates the receptors at the developing postsynaptic site.

In the forties, Donald Hebb postulated that the coincident activity of both pre- and

Contact: Joachim Kirsch & Heinrich Betz

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