A startling role for synaptic zinc.
It has long been known that the synaptic vesicles of certain glutamatergic terminals, as well as some inhibitory terminals, are richly supplied with zinc ions, yet the functional role of this pool of zinc in synaptic transmission has remained elusive. In this issue of Neuron, Hirzel et al. provide direct in vivo evidence that endogenous zinc is required for proper functioning of neuronal circuitry in the brainstem and spinal cord. They show that knockin mice carrying a point mutation which eliminates zinc potentiation of alpha1-containing glycine receptors develop severe sensorimotor deficits characteristic of impaired glycinergic neurotransmission.
Kay
Alan R
AR
Biological Sciences, University of Iowa, Iowa City, Iowa 52242, USA..
Neyton
Jacques
J
Paoletti
Pierre
P
D000818:Animals; D002352:Carrier Proteins / Q000235:genetics; D027682:Cation Transport Proteins; D005998:Glycine / Q000378:metabolism*; D008565:Membrane Proteins / Q000235:genetics; D026901:Membrane Transport Proteins; D051379:Mice; D008822:Mice, Transgenic; D009154:Mutation / Q000235:genetics; D009433:Neural Inhibition / Q000235:genetics; D017729:Presynaptic Terminals / Q000378:metabolism* / Q000648:ultrastructure; D018009:Receptors, Glycine / Q000235:genetics; D013570:Synaptic Membranes / Q000235:genetics / Q000378:metabolism / Q000648:ultrastructure; D009435:Synaptic Transmission / Q000235:genetics*; D015032:Zinc / Q000378:metabolism*
D002352:Carrier Proteins; D027682:Cation Transport Proteins; D008565:Membrane Proteins; D026901:Membrane Transport Proteins; D018009:Receptors, Glycine; C491177:Slc30a3 protein, mouse; D015032:Zinc; D005998:Glycine