Differential activation of arginine-vasopressin receptor subtypes in the amygdaloid modulation of anxiety in the rat by arginine-vasopressin.

RATIONALE: The amygdala plays a paramount role in the modulation of anxiety and numerous studies have shown that arginine vasopressin (AVP) elicits anxiogenic effects following either its systemic or septal administration. OBJECTIVES: The aim of this paper was to study the involvement of vasopressinergic neurotransmission in the amygdaloid modulation of unconditioned anxiety and to ascertain whether or not AVP receptor subtypes may have a differential role in this modulation. METHODS: Anxiety behavior was evaluated both in Shock-Probe Burying Test and Light-Dark Box following the bilateral microinfusion of AVP alone or AVP together with either AVP 1a or AVP 1b receptor antagonists into the central amygdala (CeA). RESULTS: AVP microinfusion elicited at low (1 ng/side) but not at high doses (10 ng/side) anxiogenic-like responses in the Shock-Probe Burying Test but not in the Light-Dark Box. SSR149415, an AVP 1b antagonist unlike Manning compound, an AVP 1a antagonist, fully prevented AVP effects in the Shock-Probe Burying Test when it was administered simultaneously with AVP. In addition, oxytocin receptor blockade also failed to affect AVP effects. No effects of any AVP antagonist by itself were observed in both anxiety paradigms. CONCLUSIONS: Our results indicate that AVP 1b receptor contribute to the amygdaloid modulation of anxiety at least in the context of the Shock-Probe Burying Test since no effects were noticed in the Light-Dark Box. It remains to the future to ascertain whether AVP receptor subtypes have indeed differential actions either in the modulation of global or specific features of unconditioned anxiety.

The intercalated paracapsular islands as a module for integration of signals regulating anxiety in the amygdala.

The intercalated paracapsular (IPC) islands are clusters of dopamine-D1-and µ-opioid 1-receptor rich GABAergic neurons which surround the rostral half of the basolateral complex of the amygdala (BLA) giving rise to several subgroups which can be further subdivided. IPC cells are small-sized and have an axonal and dendritic pattern which differs according to the group they belong. Functionally, IPC neurons are endowed with unique properties that set them apart from other amygdaloid interneurons and allow them to participate in integrative functions. Consistent with this role IPC cells usually remain confined within the amygdala where they receive BLA and cortical inputs and interact synaptically with each other. They project into both the central (CeA) and medial (MeA) amygdaloid nuclei. Their main effect at the network level seems to control the trafficking of nerve impulses to the main input (BLA) and output (CeA) stations of the amygdala. Such a task seems to be accomplished by providing feedforward inhibition to BLA neurons from putative inputs of the medial prefrontal cortex (mPFC) and to CeA from both mPFC and BLA projections. Current experimental evidence will be discussed suggesting that through feedforward inhibitory effects on specific amygdaloid nuclei IPC neurons participate in the maintenance of basal anxiety as well as in the modulation of unconditioned and conditioned fear, and in the process of fear extinction. This article is part of a Special Issue entitled: Brain Integration.