Effects of equine grass sickness on sympathetic neurons in prevertebral and paravertebral ganglia.

The research article investigates how acute equine grass sickness (EGS) impacts specific types of neurons in horses. The study demonstrates that this fatal disease results in the destruction of autonomic neurons in the afflicted animals, and the damage seems to be more pronounced in certain ganglia than others.

Introduction and Aim

• The study was designed to inspect how EGS impacts neurons in two sympathetic ganglia in horses – the cranial cervical ganglion (CCG) and the coeliac/cranial mesenteric ganglion (CG/CMG).
• EGS is believed to be caused by ingestion of a neurotoxic agent that largely damages autonomic neurons.
• The researchers wanted to identify the differences in the disease’s effects on both ganglia types.

Methodology

• Post-mortem samples from horses affected with EGS and control samples were processed using single and double immunofluorescence labelling.
• Several markers were used for labelling, including PGP 9.5 and HuC/HuD for pan-neuronal markers, TUNEL and caspase 3 for apoptosis, VIP and galanin for injury following axotomy, and tyrosine hydroxylase (TH) for noradrenaline synthesis.

Results

• In control horses, all neurons contained PGP 9.5 and HuC/HuD. However, there was a significant loss of these markers in horses with EGS, which was more pronounced in the CG/CMG than the CCG.
• The researchers observed increased apoptosis in both ganglia in horses with EGS, as evidenced by an increase in caspase 3 and TUNEL cells. However, TUNEL activity in sympathetic neurons was significantly higher in the CG/CMG.
• While no VIP was observed in any of the ganglia, there was a significant increase in galanin-positive neurons in both ganglia of EGS-affected horses.
• TH activity was markedly different in the two ganglia. In the CCG, there was an increased fluorescence intensity for TH, contrasting with the significant reduction in the CG/CMG, aligning with the more significant loss of neurons.

Conclusion

• These findings illustrate that EGS triggers a cell body response similar to the one sympathetic neurons experience after exposure to a chemical neurotoxin.
• EGS also causes the loss of sympathetic neurons, with some of this damage occurring through apoptosis.
• The study found more pronounced changes in the CG/CMG than the CCG, suggesting that the prevertebral ganglia are hit earlier and suffer more substantial neurodegeneration in the disease process.