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Developmental consequences of neuromuscular junctions with reduced presynaptic calcium channel function
Author(s) -
Xing Bin,
Long A. Ashleigh,
Harrison Douglas A.,
Cooper Robin L.
Publication year - 2005
Publication title -
synapse
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.809
H-Index - 106
eISSN - 1098-2396
pISSN - 0887-4476
DOI - 10.1002/syn.20165
Subject(s) - neuromuscular junction , neurotransmission , neuromuscular transmission , calcium , postsynaptic potential , synapse , excitatory postsynaptic potential , neuroscience , voltage dependent calcium channel , biology , neurotransmitter , calcium channel , synaptic plasticity , microbiology and biotechnology , biophysics , inhibitory postsynaptic potential , chemistry , central nervous system , endocrinology , biochemistry , receptor , organic chemistry
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, cac TS2 , 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 33°C from the 1st instar stage. Larvae raised at 25°C and larvae pulsed at 33°C from the late 2nd instar for various lengths of time show a reduced synaptic efficacy as a 3rd instar. The results indicate that the nerve terminal cannot fully compensate physiologically in the regulation of synaptic transmission during larval life for a reduced amount of evoked calcium entry. Morphological comparisons of Ib and Is terminals in relation to length and numbers of varicosities are significantly reduced in cac TS2 , 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. © 2005 Wiley‐Liss, Inc.