Vulnerability of motor nerve terminals to hypoxia

B. Baxter, T. H. Gillingwater, S. H. Parson

Research output: Contribution to conferencePosterpeer-review

Abstract

Damage to neurons caused by ischemia and/or ischaemiareperfusion injuries are now thought to contribute to the neurological defects seen as a consequence of surgery, cardio-pulmonary failure and stroke. There is growing evidence to indicate that the nerve terminal/synaptic compartment of neurons is more vulnerable to pathological stimuli than the axon and cell body, and therefore
more likely to demonstrate functional and morphological changes in response to perturbation. To investigate if nerve terminals are especially vulnerable to ischaemic-reperfusion injury we have developed an ex-vivo model utilizing the mouse neuromuscular junction. Preliminary work has investigated the hypoxic element of ischaemia as this is believed to be the most damaging. In this
model, isolated, intact tibial nerve and associated lumbrical muscles from the hind leg are maintained in a large volume of physiological saline/ringer bubbled with 95%:5% N2:CO2 for hypoxic and 95%:5%O2/CO2 for control and reperfusion conditions. Results show that 2 h of hypoxia followed by 2 h reperfusion can selectively trigger rapid disruption of motor nerve terminal morphology. The observed heterogeneity of the morphological responses to hypoxia, indicates that several mechanisms leading to nerve terminal disruption
may be active and that these mechanisms may, at least in part, be controlled locally. It is likely that these morphological changes will have an
adverse affect on synaptic function and connectivity, which may contribute to some of the punitive symptoms following ischaemia/ischaemiareperfusion injury to the peripheral nervous system.
Original languageEnglish
Pages81-81
Number of pages1
DOIs
Publication statusPublished - Jan 2008

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