Proceedings of The Physiological Society

Physiology 2016 (Dublin, Ireland) (2016) Proc Physiol Soc 37, PCA275

Poster Communications

Investigation of Possible Alpha Adrenergic Modification of Acute Pain Sensitivity in Absence Epileptic WAG/Rij Rats

A. Ayar1, O. KALKAN1, A. KURT1, O. Gedikli1, S. Velioglu1,2, M. YILDIRIM1

1. Physiology, Karadeniz Technical University, TRABZON, Turkey. 2. Neurology, Karadeniz Technical University, Trabzon, Select One, Turkey.


Aim: The aim of this study was to investigate possible modulatory role of noradrenergic system in absence epileptic WAG/Rij Rat model, which determined to have changed (increased) pain sensitivity. Methods: Experimental pain was induced in adult WAG/Rij epileptic rats by thermal and mechanical stimulation and effects of intraperiotenally administered yohimbine, an alpha-2 receptor antagonist, treatment on acute interictal (confirmed by simultaneous electroencephalography through intracranial implanted electrodes) pain threshold was assessed at 15, 30 and 60 minutes in vivo nociceptive behavioral "plantar (heat-induced)" and "electronic von Frey (mechanical stimulus) tests by comparing their prospective basal pain threshold values. Statistical analysis of normalised pain threshold values were performed by use of Shapiro-Wilk test followed by repeated measure of paired sampled t test for normally distributed data. P<0.05 value was accepted statistically significant. The protocols of this study was approved by local Ethic Committee. Results: Administration of yohimbine caused dose-dependent increase, although not statistically significant, in pain sensitivity in von Frey test: mechanical pain threshold values were 1±0.0 before and 1.50±0.9, 1.56±0.8 and 1.8±0.9 after 15, 30 and 60 minutes after 1 mg/kg yohimbine (n=6, p>0.05 for all). 1 mg/kg yohimbine did not cause any significant difference in thermal stimulated pain latencies either; pain threshold values were 1±0.0 before and 1,1±0.3, 1,2±0.1 and 1,1±0.2 after 15, 30 and 60 minutes after 1 mg/kg yohimbine (n=6, p>0.05 for all). Mechanical pain threshold values were 1±0.0 before and 1,5±0.6, 1,1±0.6 and 1,3±0.5 after 15, 30 and 60 minutes after 3 mg/kg yohimbine (n=7, p>0.05 for all). 3 mg/kg yohimbine significantly reduced thermal stimulated pain latencies; pain threshold values were 1.0±0.0 before and 0.9±0.2 (p>0.05), 0.7±0.2 (p<0.005) and 0.7±0.2 (p<0.005) after 15, 30 and 60 minutes after 1 mg/kg yohimbine (n=7 for all). Conclusion: Results from this study indicate that, noradrenergic pain modulation is probably (alpha-2 sensitive mechanism being only tested) involved in pain modulation in rat model of absence epileptic WAG/Rij and detailed explanation of this modulation, although other endogenous pain modulating system olse needs to be considered, may contribute our current understanding of increased/chronic pain development.

Where applicable, experiments conform with Society ethical requirements