| Abstract No.: | A-C1102 |
| Country: | Canada |
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| Title: | ALTERED SOMATOSENSORY PROCESSING PRIOR TO DISEASE ONSET IN EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS (EAE) |
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| Authors/Affiliations: | 1 Camille Olechowski*; 1 Bradley Kerr;
1 University of Alberta, Edmonton, AB, Canada
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| Content: | Objectives: Chronic pain is a significant problem for a large proportion of patients suffering from the autoimmune disease, Multiple Sclerosis (MS). While significant strides have been made in understanding the processes that lead to neurological impairment in this disease, the mechanisms underlying chronic pain remain unknown. To begin to address this question, we have used the animal model of multiple sclerosis (MS), experimental autoimmune encephalitis (EAE) and monitored changes in threshold responses to noxious and non-noxious sensory stimuli to fully characterize how somatosensory processing is affected in this model.
Materials and Methods: EAE was induced by immunizing female C57/BL6 mice with 50 µg of myelin oligodendrocyte glycoprotein (MOG35-55) emulsified in complete Freund’s adjuvant (0.5mg/ml). Mice were treated with 300ng of Pertussis toxin intraperitoneally on the day of induction and 48 hours later. Mice were monitored daily and clinical signs of EAE were graded using a standard 5 point scale. Mice were tested on alternate days for changes in sensitivity to noxious heat using the Hargreaves test. Changes in sensitivity to punctate mechanical stimuli were assessed using calibrated von Frey hair monofilaments and the development of cold allodynia was assessed using the Acetone test.
Results: Prior to symptom onset, the majority of mice with EAE showed significant changes in their threshold responses to cold and mechanical stimuli while the threshold response to noxious heat remained unchanged. EAE mice displayed an approximate twofold increase in the duration of their response to acetone applied to the hindpaws compared to control mice. Mechanical allodynia was also apparent, as the mean force required to elicit nociceptive withdrawal responses in EAE mice was nearly half of that required in controls. EAE mice also showed signs of spontaneous pain behaviours (caudally directed overgrooming) that were never observed in ‘adjuvant-only’ treated controls.
Conclusions: In addition to the characteristic effects on locomotor function, our results illustrate that EAE also leads to significant alterations in somatosensory processing. Changes in sensory thresholds are apparent even before the onset of ‘classical’ neurological symptoms such as flaccid tail and hindlimb weakness in this model. These findings are an important validation of using the EAE model to study MS-related pain.
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