Role of central amygdaloid alpha-2 adrenergic receptors in the modulation of anxiety in the rat

It is commonly recognized that amygdala plays a critical role in the modulation of anxiety. Furthermore, alpha-2 adrenergic receptor activity has been suggested to be involved in anxiety modulation. The aim of this study was to ascertain whether the central amygdaloid nucleus, which represents the main anxiogenic output of amygdala is involved in such adrenergic actions. Elevated Plus-Maze and Shock-Probe-Burying paradigms were used to study the effects of sterotaxically-infused clonidine, a specific alpha 2 adrenergic agonist on anxiety. DSP-4, a toxin specifically destroying locus coeruleus noradrenergic neurons was used determine to which extent clonidine effects were induced by either pre- or post-synaptic actions. Curve dose-response studies showed that clonidine evoked anxiolytic effects at the dose of 1.25 ug/side in both anxiety paradigms and that these effects were counteracted by the previous i.p. yohibine (an alpha 2 adrenergic receptor antagonist) administration. In addition, the DSP-4 ablation of locus coeruleus noradrenergic neurons was able to prevent the clonidine effects suggesting an important role of presynaptic receptors in the clonidine anxiolytics effects. Our results suggest an important presynaptic involvement of amygdaloid alpha 2 adrenergic receptor in the modulation o anxiety. It remains to study whether interactions between alpha-2 noradrenergic receptors with some other neurotransmitter receptors i.e, oxytocinergic receptors are involved in the amygdaloid anxiolytic effects of clonidine demonstrated in this work.This work was supported by a grant IN 210024 from the Dirección General de Apoyo al Personal Académico, UNAM (MPM). Authors declare non-conflict of interest.