Mutant third instar larvae show no significant increase in quantal content at the neuromuscular junction in the presence of the glutamate receptor antagonist philanthotoxin-433 (10μM), indicating a defect in synaptic homeostasis.
The morphology of the neuromuscular junction is normal in mutant third instar larvae.
ppk11[+]/ppk11f02053, ppk16MB11536 has abnormal neurophysiology | dominant | third instar larval stage phenotype
ppk11f02053/ppk16MB11536 transheterozygous third instar larvae show no significant increase in quantal content at the neuromuscular junction in the presence of the glutamate receptor antagonist philanthotoxin-433 (10μM), indicating a defect in synaptic homeostasis. In the absence of philanthotoxin-433, basal synaptic transmission is normal in these animals.