The Journal of Neuroscience, May 3, 2006, ():
Distinct Physiological Mechanisms Underlie Altered Glycinergic Synaptic Transmission in the Murine Mutants spastic, spasmodic, and oscillator
J. Neurosci. Graham et al.
26: 4880
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Supplementary Figure 1. Mechanisms underlying the effect of murine GlyR mutations on GlyR expression and assembly. A, schematic showing a synaptic connection between a glycinergic presynaptic bouton and a hypoglossal motoneuron. In the neuron on the left GlyR subunits accumulate intracellularly following transcription and translation. In adult animals, α1- (black ellipses) and β- (white ellipses) subunits are normally assembled into heteromeric α1/β GlyRs. These are first located in extrasynaptic membrane (small circle) and subsequently stabilized at synaptic loci (large circle) via the β subunit’s interaction with the anchoring molecule gephyrin (corrugated line). B, in the spastic mutant, functional β-subunit production is dramatically reduced (white ellipses) and α1-subunit (black ellipses) production is unchanged. Heteromeric α1/β GlyRs are targeted to synaptic loci (large circle), whereas the excess α1 subunits form homomeric receptors. These are subsequently inserted into extrasynaptic membrane (small circle) and remain there because they lack the β-subunit necessary for synaptic stabilization. C, the spasmodic mouse produces defective, and slightly reduced levels of α1-subunit (black rectangles). These defective subunits are assembled and expressed according to the mechanisms outlined in A, first in extrasynaptic membrane (small circle) and subsequently stabilized at synaptic loci (large circle).
