Effect of reduced impulse activity on the development of identified motor terminals in Drosophila larvae

Abstract

In Drosophila larvae, motoneurons show distinctive differences in the size of their synaptic boutons; that is, axon 1 has type Ib ("big" boutons) terminals and axon 2 has type Is ("small" boutons) terminals on muscle fibers 6 and 7. To determine whether axon 1 develops large boutons due to its high impulse activity, we reduced impulse activity and examined the motor terminals formed by axon 1. The number of functional Na(+) channels was reduced either with the nap(ts) mutation or by adding tetrodotoxin (TTX) to the media (0.1 microg/g). In both cases, the rate of locomotion was decreased by approximately 40%, presumably reflecting a decrease in impulse activity. Locomotor activity was restored to above wild-type (Canton-S) levels when nap(ts) was combined with a duplication of para, the Na(+)-channel gene. Lucifer yellow was injected into the axon 1 motor terminals, and we measured motor terminal area, length, the number of branches, and the number and width of synaptic boutons. Although all parameters were smaller in nap(ts) and TTX-treated larvae compared to wild-type, most of these differences were not significant when the differences in muscle fiber size were factored out. Only bouton width was significantly smaller in both different nap(ts) and TTX-treated larvae: boutons were about 20% smaller in nap(ts) and TTX-treated larvae, and 20% larger in nap(ts); Dp para(+) compared to wild-type. In addition, terminal area was significantly smaller in nap(ts) compared to wild-type. Bouton size at Ib terminals with reduced impulse activity was similar to that normally seen at Is terminals. Thus, differences in impulse activity play a major role in the differentiation of bouton size at Drosophila motor terminals.

Mutations in aDrosophilaα2δ Voltage-Gated Calcium Channel Subunit Reveal a Crucial Synaptic Function

“…Changes in the size and morphology of the Drosophila neuromuscular junction have been shown to occur as a result of perturbations in both presynaptic activity (Lnenicka et al, 2003;Mosca et al, 2005) and regulatory signaling (Packard et al, 2002;Keshishian and Kim, 2004;Ruiz-Canada and Budnik, 2006). However, many other perturbations of synaptic function do not have these effects, including viable mutations in synaptotagmin, syntaxin and SNAP-25 (DiAntonio and Schwarz, 1994;Schulze et al, 1995;Vilinsky et al, 2002).…”

Dissection of synaptic excitability phenotypes by using a dominant-negative Shaker K + channel subunit

“…Both hyper-and hypoexcitability alter the development of the Drosophila NMJ (6,7,9,60). Electrical activity is also essential for regulating neuromuscular signaling through homeostatic feedback mechanisms that influence both presynaptic transmitter release and postsynaptic transmitter sensitivity (10,11,47).…”

Morphogens and synaptogenesis in Drosophila

“…The mechanisms that maintain synaptic homeostasis have been extensively studied, and clever genetic manipulations have shown that both anterograde (from motoneuron to muscle) and retrograde signaling (from muscle to motoneuron) is required for appropriate growth and function of the NMJ (Budnik et al, 1990;Jarecki and Keshishian, 1995;Petersen et al, 1997;DiAntonio et al, 1999;Baines et al, 2001;Paradis et al, 2001;Lnenicka et al, 2003). Over the past few years, two classical morphogens have been identified as essential regulators of synaptic growth.…”