Octopamine stabilizes conduction reliability of an unmyelinated axon during hypoxic stress.
Mechanisms that could mitigate the effects of hypoxia on neuronal signaling are incompletely understood. We show that axonal performance of a locust visual interneuron varied depending on oxygen availability. To induce hypoxia, tracheae supplying the thoracic nervous system were surgically lesioned and action potentials in the axon of the descending contralateral movement detector (DCMD) neuron passing through this region were monitored extracellularly. The conduction velocity and fidelity of action potentials decreased throughout a 45-min experiment in hypoxic preparations, whereas conduction reliability remained constant when the tracheae were left intact. The reduction in conduction velocity was exacerbated for action potentials firing at high instantaneous frequencies. Bath application of octopamine mitigated the loss of conduction velocity and fidelity. Action potential conduction was more vulnerable in portions of the axon passing through the mesothoracic ganglion than in the connectives between ganglia, indicating that hypoxic modulation of the extracellular environment of the neuropil has an important role to play. In intact locusts, octopamine and its antagonist, epinastine, had effects on the entry to, and recovery from, anoxic coma consistent with octopamine increasing overall neural performance during hypoxia. These effects could have functional relevance for the animal during periods of environmental or activity-induced hypoxia.
Department of Biology, Queen's University, Kingston, Ontario, Canada; and.
T G A
TG
Money
Department of Biology, Queen's University, Kingston, Ontario, Canada; and.
M K J
MK
Sproule
Centre for Neuroscience Studies, Queen's University, Kingston, Ontario, Canada.
K P
KP
Cross
Department of Biology, Queen's University, Kingston, Ontario, Canada; and Centre for Neuroscience Studies, Queen's University, Kingston, Ontario, Canada robertrm@queensu.ca.
R M
0000-0002-2666-7861
RM
Robertson
D000200:Action Potentials / Q000187:drug effects; D000316:Adrenergic alpha-Agonists / Q000494:pharmacology* / Q000627:therapeutic use; D000818:Animals; D004791:Enzyme Inhibitors / Q000494:pharmacology; D007839:Functional Laterality / Q000187:drug effects; D006110:Grasshoppers; D006931:Hyperbaric Oxygenation / Q000379:methods; D000860:Hypoxia / Q000473:pathology*; D008297:Male; D009068:Movement / Q000187:drug effects; D036421:Nerve Fibers, Unmyelinated / Q000187:drug effects* / Q000502:physiology; D009431:Neural Conduction / Q000187:drug effects*; D009655:Octopamine / Q000494:pharmacology* / Q000627:therapeutic use; D018408:Patch-Clamp Techniques; D010775:Photic Stimulation; D019810:Sodium Azide / Q000494:pharmacology; D013900:Thoracic Nerves / Q000473:pathology; D013997:Time Factors
D000316:Adrenergic alpha-Agonists; D004791:Enzyme Inhibitors; D009655:Octopamine; D019810:Sodium Azide
DCMD; action potential; conduction velocity; locust; sodium azide