P{lacW}corak08713 is inserted into the second intron of the cora gene.
Homozygous corak08713, corak08713/cora5, and corak08713/Df(2R)BSC26 mutants show electrophysiologically detectable loss of glutamate receptors.
Homozygous corak08713 mutants exhibit a glutamate-gated current amplitude that is approximately half that found in wild-type.
sEJC (spontaneous excitatory junction currents) amplitudes, which reflect the number of functional glutamate receptors localised specifically to synapses, are reduced to approximately 80pA in corak08713 mutants, compared to approximately 154pA in wild-type. sEJC frequency is reduced in corak08713 mutants, although not to a significant level. sEJC decay time is significantly reduced in corak08713 mutants, consistent with a specific loss of A-type receptors.
The single glutamate receptor channel amplitude is similar in both control and corak08713 mutants.
Homozygous corak08713 mutants exhibit an average cluster size of A-type glutamate receptors that is reduced to approximately one-half of the wild-type size. The cluster size of B-type glutamate receptors, however, is not reduced in corak08713 mutants compared with controls.
While in wild-type dynamic filamentous actin is required for maintenance of postsynaptic function, in corak08713 mutants this requirement is abolished, as exemplified by treatment with latrunculin A or cofilin having no effect.
Treatment with latrunculin A has no effect on the size of A-type receptor clusters in corak08713 mutants (compared to a reduction in wild-type). More specifically, treatment with latrunculin A has no effect on the size of GluRIIA receptor clusters in corak08713 mutants (compared to a reduction in wild-type).
I. Kiss.
Complements: ena02029.