α2-Adrenoceptors mediate inhibition of withdrawal reflexes after remote noxious stimuli in the anaesthetised rabbit

Trinity College, Dublin (2003) J Physiol 551P, C20

Communications: α2-Adrenoceptors mediate inhibition of withdrawal reflexes after remote noxious stimuli in the anaesthetised rabbit

J. Harris, Rakhi Patel and R.W. Clarke

School of Biosciences, University of Nottingham, Sutton Bonington Campus, Loughborough LE12 5RD, UK

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Withdrawal reflexes in left hindlimb of anaesthetised rabbits are inhibited for ca 20 min after application of mustard oil to various body locations in distant parts of the body surface, including the snout and the contralateral medial gastrocnemius (MG) muscle. In the case of reflexes evoked in MG by stimulation at the heel, the same effect is evoked when mustard oil is applied to the ipsilateral metatarsophalangeal (MT) joint (Harris & Clarke, 2003). Previous studies from this laboratory have implicated adrenergic systems as probable mediators of such widespread, stimulus-evoked inhibition. The present study investigates the role of α2-adrenoceptors in inhibition evoked from the three sites mentioned above.

Experiments were performed on 10 rabbits under terminal pentobarbitone anaesthesia (average doses 45 mg kg-1 initially, followed by infusion at 16 mg kg-1 h-1). Reflexes were evoked in the flexor muscles tibialis anterior (TA) and semitendinosus (ST) by electrical stimulation of the toes with an average stimulus intensity of 3.4 ± 0.9 mA (mean ± S.E.M.) using 1 ms pulses. Reflexes were evoked in the extensor MG by stimulation at the heel with an average stimulus intensity of 6.7 ± 0.7 mA. Reflexes were recorded using percutaneous EMG electrodes in the left hindlimb. Mustard oil conditioning stimuli (100 µl of a 20 % mixture in paraffin oil) were applied in a random order to the snout, the right MG muscle, and the skin over the left MT joint. At least 1 h was allowed between conditioning stimuli. After a cycle of stimuli was completed, the selective α2-adrenoceptor antagonist RX 821002 was given intrathecally at 200-300 µg and the mustard oil stimuli reapplied close to, but not exactly at, the same locations as before. Booster doses of RX 821002 (100-150 µg) were given between stimuli.

The toes-ST reflex was significantly inhibited only by stimulation of contralateral MG, toes-TA was inhibited from this location and from the snout, and heel-MG was inhibited from all three sites (Friedman’s ANOVA, P < 0.01). The median duration of this effect was between 11 and 63 min and maximum inhibition was to values between 28 and 78 % of immediate pre-mustard oil levels. The two flexor reflexes were significantly facilitated from stimulation over the MT joint (Friedman’s ANOVA, P < 0.0001). After RX 821002, conditioning stimuli applied to any site failed to significantly influence any reflex (Friedman’s ANOVA, P > 0.05), i.e. both inhibition and facilitation were blocked.

These data suggest that the inhibition of reflexes from remote sites is the result of activation of adrenergic neurones in the brainstem. Why blockade of α2-receptors should also abolish facilitation of reflexes is more difficult to explain.

This work was supported by BBSRC.



Where applicable, experiments conform with Society ethical requirements.

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