The
cam-1 null mutation did not eliminate synaptic ACR-16 receptors, as indicated by the residual ACR-16 synaptic fluorescence, and by the fact that the endogenous EPSC amplitude observed in
acr-16 mutants (48% wild-type, p < 0.001) were significantly smaller than those observed in
cam-1 null mutants. Thus, synaptic ACR-16 levels are reduced but not eliminated in
cam-1 mutants.