The evoked excitatory junctional potential amplitude at the Csp^X1/Csp^U1 mutant third larval instar neuromuscular junction is reduced compared to controls at 23^oC and severely reduced compared to controls at 30^oC.

Csp^U1 homozygotes and Csp^U1/Csp^U1w transheterozygotes exhibit a significantly reduced lifespan as compared to controls.

Spontaneous central nervous system generated bursts of electrical activity can occur at nonpermissive temperatures (35^oC) in muscle 6 of mutant larvae. EJP amplitudes evoked by low-frequency nerve stimulation are reduced at room temperature (21^oC) in mutant larvae (compared to wild type) and are completely absent at 32^oC. High stimulation frequencies at the nonpermissive temperature can partially rescue the block in synaptic transmission. The ability of the central nervous system to generate motor rhythms at any temperature is compromised in mutant larvae. The motor rhythms are reduced in frequency in the mutants and the rate at which rhythm frequency changes with temperature is most affected in the mutant at low temperatures.

The EJP amplitudes recorded from mutant neuromuscular junctions (NMJs) are reduced to about a third of control amplitudes.

Mutants lose evoked responses at 32^oC, but retain mESCs (miniature excitatory synaptic currents).

Mutant boutons are physiologically less able to cope with Ca²⁺ loads than control boutons and more easily compromised by adverse conditions such as high temperature. The relative increase of intraterminal Ca²⁺ is generally larger in mutants than in controls, the recovery (clearance) of intraterminal Ca²⁺ at high temperature is slower, and the reduction of neurotransmitter release cannot be entirely explained by loss of Ca²⁺ entry into the nerve terminal. Levels of intraterminal Ca²⁺ are not significantly different from controls at room temperature, but higher than controls at 34^oC. An aberrant time course of Ca²⁺ signal is observed at 34^oC. Ca²⁺ clearance after stimulation is deficient, and this effect is exacerbated at higher temperatures.

Homozygotes are viable at 18^oC, although they develop more slowly than wild-type animals. Adults have a severely reduced lifespan at 18^oC, during which they lay fewer eggs than wild-type. Towards the end of their life, the flies show a wide variety of neurological conditions, including uncoordinated movement, staggering, shaking and spasmic extension of hind legs, before they become paralysed. Viability is dramatically reduced at all stages beyond late embryogenesis at 23^oC or higher, and only a few escapers survive to adulthood. Temperature shift to the restrictive temperature after eclosion produces the neurological symptoms and death over a period of a few minutes to a few days, depending on the temperature. The symptoms are reversible on return to 18^oC if heat exposure is sufficiently short.