Repeated tail pinch leads to desensitization of postsynaptic alpha2-adrenoceptors which modulate the jaw-opening reflex in the rat.

There are few in vivo studies which have investigated the modulation of central postsynaptic alpha2-adrenoceptors functionality provoked by stress. We assessed in the rat the effects of either single or repeated tail pinch on clonidine-induced inhibition of the jaw-opening reflex (JOR) via activation of postsynaptic central alpha2-adrenoceptors. At the end of each experimental period, the progressive inhibition of the digastric electromyographic responses elicited by orofacial electrical stimulation after the i.v. administration of cumulative doses (x3.3) of clonidine (0.1-10000 microg/kg) was recorded. Single tail pinch did not significantly modify the ability of the agonist to inhibit the JOR, although there was a tendency to decrease the basal amplitude of the reflex (a 40% reduction) immediately after exposure to the single stressor. However, the dose-response curve for clonidine-induced inhibition of the JOR was clearly shifted to the right in rats exposed to repeated tail pinch (ED50 was increased by 152%, P < 0.0001) when compared with the unstressed control group, without affecting the slope of the inhibitory function and the estimated maximum effect for the agonist. These results show that repeated stress leads to a subsensitivity of the alpha2-adrenoceptors which modulate the JOR, suggesting the development of adaptive mechanisms in postsynaptic alpha2-adrenoceptors in response to stress.