Developmental consequences of neuromuscular junctions with impaired calcium channel function. Abst Soc Neurosci 30:502.11

KEY WORDS neurotransmission; neuromuscular junction; synapse; Drosophila; epilepsy; growth; development ABSTRACT Evoked neurotransmitter release at the Drosophila neuromuscular junction (NMJ) is regulated by the amount of calcium influx at the presynaptic nerve terminal, as for most chemical synapses. Calcium entry occurs via voltage-gated calcium channels. The temperature-sensitive Drosophila mutant, cacTS2, has a reduced amount of calcium entry during evoked stimulation. We have used this mutation to examine homeostatic regulatory mechanisms during development of the NMJ on muscle 6 within the developing larva. The amplitude of the excitatory postsynaptic potentials are reduced for both the Ib and Is motor neurons in 3rd instar larvae which have been raised at 338C from the 1st instar stage. Larvae raised at 258C and larvae pulsed at 338C from the late 2nd instar for various lengths of time show a reduced synaptic effi-cacy as a 3rd instar. The results indicate that the nerve terminal cannot fully compen-sate physiologically in the regulation of synaptic transmission during larval life for a reduced amount of evoked calcium entry. Morphological comparisons of Ib and Is termi-nals in relation to length and numbers of varicosities are significantly reduced in cacTS2, which also suggests a lack in homeostatic ability. These findings are relevant since many deficits in synaptic transmission in various systems are compensated for either physiologically or structural over development, but not in this case for reduced calcium entry during evoked transmission. Synapse 57:132–147, 2005. VC 2005 Wiley-Liss, Inc