Conclusions
NE inhibits bulbospinal RVL neurons by activating  alpha2-
adrenoceptors (a2-ARs) located postsynaptically and
presynaptically on glutamatergic terminals.
Contrary to our expectations, a2-ARs were also found on
GABAergic inputs to these cells.
 Unlike the postsynaptic effects, the decrease of synaptic
transmission by NE was not sensitive to barium, indicating that
different mechanisms of action are involved in the pre- and
postsynaptic effects of NE.
 Finally, all effects of NE were mimicked by the prototypical
imidazoline ligand moxonidine which was found to behave like
an a2-AR agonist.