Acetylcholine-mediated axon-glia signaling in the developing insect olfactory system

Area of Science:

• Neuroscience
• Cell Biology
• Insect Physiology

Background:

• Neuropil glial cell migration in the Manduca sexta olfactory system is initiated by olfactory receptor axons.
• Intraglial Ca(2+) signaling is essential for this migration, but the communication mechanism between axons and glial cells remains unclear.
• The role of Ca(2+) signaling as a consequence of this communication is not fully understood.

Purpose of the Study:

• To investigate the communication between olfactory receptor axons and glial cells in Manduca sexta.
• To determine if Ca(2+) signaling in glial cells is a result of this axonal-glial communication.
• To elucidate the role of cholinergic signaling in glial cell migration during olfactory system development.

Main Methods:

• Studied Ca(2+) increases in glial cells in vivo and in situ using electrical stimulation of axons and odor stimulation of neurons.
• Utilized nicotinic acetylcholine receptor antagonists, acetylcholine, carbachol, external Ca(2+) removal, and voltage-gated Ca(2+) channel blockers.
• Monitored glial cell migration following in vivo injections of nicotinic antagonists during development.

Main Results:

• Axonal activity induced Ca(2+) increases in neuropil glial cells, which were blocked by nicotinic antagonists and mimicked by acetylcholine.
• Ca(2+) transients were dependent on external Ca(2+) and voltage-gated Ca(2+) channels.
• Acetylcholine-mediated Ca(2+) signaling began at developmental stage 6, coinciding with glial cell migration initiation.
• Glial cell migration was significantly reduced by nicotinic antagonist application.

Conclusions:

• Acetylcholine release from olfactory receptor axons triggers Ca(2+) signaling in glial cells via nicotinic acetylcholine receptors and voltage-gated Ca(2+) influx.
• Cholinergic signaling is essential for initiating and regulating neuropil glial cell migration in the developing Manduca sexta olfactory system.