The olfactory receptor neurons of CspDG29203 mutants show a partial delay in degeneration of distal axons and synaptic terminals following surgical ablation of the antennae.
Csp[+]/CspDG29203 is an enhancer of abnormal neurophysiology phenotype of GluRIIASP16, cacS/cac[+]
CspDG29203, GluRIIASP16 has abnormal neurophysiology phenotype
One copy of CspDG29203 prevents the compensatory increase in quantal content seen in the NMJs of cacS/+; GluRIIASP16 mutant larvae that have reduced quantal size, resulting in impaired evoked neurotransmission. There is no increase in quantal content compared with cacS/+; CspDG29203/+ controls.
Synaptic homeostasis is impaired in the NMJs of GluRIIASP16 CspDG29203 double mutant larvae compared with either mutant alone. The double mutant larvae show the decreased quantal size seen in GluRIIASP16 mutants but the usual compensatory upregulation of quantal content is not seen: quantal content is not increased compared with CspDG29203 mutants alone. As a result, evoked postsynaptic excitation is impaired.
Df(3L)Exel6138 fails to complement the delay in axonal degeneration seen in CspDG29203 mutants, but the phenotype is more severe in Df(3L)Exel6138/CspDG29203 mutants than in CspDG29203 homozygotes.
CspX1 fails to complement the delay in axonal degeneration seen in CspDG29203 mutants, but the phenotype is more severe in CspDG29203/CspX1 mutants than in CspDG29203 homozygotes.