Frq2^V7 larvae show a reduction in the number of type 1s boutons at the neuromuscular junction, while the number of type 1b boutons is not significantly affected. The amplitude of the evoked excitatory junctional potential (EJP) at the neuromuscular junction is increased compared to wild type. The amplitude and frequency of spontaneous mEJPs is not affected in these flies. Quantal content of type 1b and type 1s boutons is increased in these flies compared to wild type.

Frq1¹ animals have a normal heart rate and rhythms and response to serotonin or norepinephrine is normal.

Mutant animals have a normal heart rate and rhythms and response to serotonin or norepinephrine is normal.

The motor nerve endings in mutant larvae have shorter and less numerous type I and type II processes than wild type. This phenotype shows variable expressivity both between and within individual larvae. There is a reduction in the number of boutons compared to control larvae. The appearance of the terminal boutons is similar to wild type. The size of the small clear vesicles (SCVs) is not different from wild type and the size and arrangement of microtubules in interbouton axonal regions and of intraterminal mitochondria is normal. The total terminal length of the motor nerve endings in larvae carrying Frq1^hs.PP and raised at 29[o]C is reduced compared to control larvae raised at 29[o]C. Single terminal branch length and the number of branches per ending are reduced. The phenotype is not altered if the larvae are also carrying T(1;Y)V7.

The delivery of a short electrical buzz to the brain has no significant effect on Frq1¹ mutant flies. Stimulation of the giant fibre (GF) fails to evoke dorsal longitudinal muscle potentials for slightly longer than is seen for wild-type flies following a long electrical buzz to the brain.

The delivery of a short electrical buzz to the brain has no significant effect on mutant flies. Stimulation of the giant fibre (GF) fails to evoke dorsal longitudinal muscle potentials for slightly longer than is seen for wild-type flies following a long electrical buzz to the brain.

Ca²⁺-dependent modulation of the type A K⁺ channel in larval muscle is absent in Frq1¹. This may result from an increase in frequenin altering intracellular cGMP-dependent pathways responsible for internal Ca²⁺ homeostasis.

Giant cervical axons show more than one action potential in response to a single stimulus (FBrf0037273). Larval neuromuscular junctions show increased neurotransmitter release under high frequency stimulation (FBrf0054505). Larval muscle fibres respond with large excitatory junction potentials (EJPs) to high frequency motor nerve stimulations.

I_A is present in rested Frq1¹ nerve endings but it can show a use-dependent depression causing membrane potential oscillations giving rise to repetitive presynaptic nerve firing and a late enhanced transmitter release in motor endings. Neuromuscular electrophysiological phenotype is caused by presynaptic membrane hyper-excitability, probably in relation with a Ca²⁺-dependent down-regulation of voltage-dependent K channels.

I[[A]] is present in rested nerve endings in mutant animals but it can show a use-dependent depression causing membrane potential oscillations giving rise to repetitive presynaptic nerve firing and a late enhanced transmitter release in motor endings. Neuromuscular electrophysiological phenotype is caused by presynaptic membrane hyper-excitability, probably in relation with a Ca[2+]-dependent down-regulation of voltage-dependent K channels.

K+ muscle current is unaffected.