Involvement of the noradrenergic system in modulating the blink reflex in humans

Several researches have shown that the spinal reflex transmission in animal s, as well as humans, was inhibited by alpha(2)-agonists, due to a disfacil itation of tonic noradrenergic control on motoneuronal output, To understan d better the mechanisms regulating certain aspects of motor activity, here we reinvestigated the possible role of noradrenergic systems in modulating reflex activity of the brainstem in humans. To this aim, blink reflex respo nses (R1 and R2) evoked by electrical stimulation of the supraorbital nerve were electromyographically recorded in healthy volunteers. Both R1 and R2 areas were measured at 10-min intervals before and after i.v. injection of alpha(2)-agonist clonidine (0.5 mu g/kg). The substance induced consistent depression of R1, which reached its maximum 40 min after drug administratio n (-43% of the control values). Ipsilateral R2 area resulted little affecte d by clonidine (-15% at 50 min), whereas no effects were observed in contra lateral R2. Blood pressure values were never altered by drug injections. Th ese results, taken together with previous observations, support the hypothe sis that alpha(2)-agonist substances may cause a transient inactivation of nonadrenergic neurons, thus releasing neurons involved in the circuitry of the blink refer from a facilitatory drive. Since clonidine differentially m odulated blink reflex responses, it is likely to assume that such a disfaci litation concerns mostly pontine units mediating the R1. However, the compl exity of clonidine's effects at multiple pre- and postsynaptic sites does n ot allow us to exclude that other systems are involved in the alpha(2)-medi ated control of facial motoneurons. (C) 2000 Elsevier Science B.V. All righ ts reserved.