Alpha(1)-adrenoceptor-mediated excitation of substantia nigra pars reticulata neurons.

The effect of noradrenaline was studied in principal neurons of the substantia nigra pars reticulata in rat brain slices using patch clamp recordings. Perfusion of noradrenaline or the alpha(1)-adrenoceptor agonist phenylephrine increased the spontaneous firing activity of reticulata cells. The alpha(1)-adrenoceptor antagonist prazosin counteracted the effects of noradrenaline. In contrast, the beta-adrenoceptor agonist isoproterenol did not affect the activity of reticulata cells and the beta-adrenoceptor antagonist pindolol did not prevent noradrenaline's effect. In whole-cell recordings, at -60 mV holding potential, noradrenaline caused a tetrodotoxin-resistant inward current with a time-course similar to the increase in firing activity. Analysis of the reversal potential of this current did not give homogeneous results. The net noradrenaline current could be associated with a conductance decrease or increase, or in some cases it did not reverse over a range from -120 to -30 mV. It is suggested that noradrenaline increases the excitability of substantia nigra reticulata cells through alpha(1)-adrenoceptors. Both a reduction and an increase in membrane conductance may mediate this effect. The increase in the tonic firing of principal reticulata cells caused by noradrenaline may have significant consequences in regulating the final output of the basal ganglia and consequently in motor-related behaviours.