Adrenergic Enhancement of Inhibitory Transmission in the Accessory Olfactory Bulb

Abstract

Noradrenergic modulation of dendrodendritic synapses between the mitral and granule cells in the accessory olfactory bulb (AOB) is postulated to play a key role in the formation of memory in olfactory-mediated behaviors. Current models propose that noradrenaline (NA) increases excitation of mitral/tufted cells (M/TCs) by decreasing the release of GABA from granule cells. However, surprisingly little is known about the actions of NA at the cellular level in the AOB. Here, in recordings from AOB slices, we show that NA decreases the firing frequency of M/TCs in response to stimulation. This effect is attributable to an increase in the GABA inhibitory input to M/TCs. Application of NA (10 M) produced an ϳ20-fold increase in the frequency of GABA-induced miniature IPSCs (mIPSCs) without changing their amplitude. A pharmacological analysis indicated that the increase in mIPSCs frequency results from activation of ␣1 adrenergic receptors. In addition to increasing the mIPSC frequency, NA also potentiated GABA inhibitory currents induced by direct stimulation of granule cells. Together, our results suggest that NA increases the release of GABA from granule cells by acting on presynaptic receptors. Thus, the role of the noradrenergic activity in the AOB may be opposite than suggested previously: we find that the overall effect of NA in the AOB is inhibition of M/TCs.

Muscarinic receptor type 1 (M1) stimulation, probably through KCNQ/Kv7 channel closure, increases spontaneous GABA release at the dendrodendritic synapse in the mouse accessory olfactory bulb

“…This implies the existence of alternative candidates for the facilitation of the learning. The carbachol effect in our study was similar to the actions of noradrenaline in the AOB (Araneda and Firestein, 2006). It is possible that acetylcholine and noradrenaline cooperate to facilitate learning in the AOB, as they do in the visual cortex (Kasamatsu, 1991).…”

“…Glutamate is released from the mitral cell, while GABA is released from the granule cell (Jia et al, 1999;Taniguchi and Kaba, 2001). Spontaneous release of GABA from granule cells can be recorded as chloride currents in mitral cells using whole-cell recording; neuromodulators can increase the spontaneous mIPSC frequency via stimulation of noradrenergic !1 receptors (Araneda and Firestein, 2006) or mGluR1 metabotropic glutamate receptors (Castro et al, 2007).…”

General organization of the perinatal and adult accessory olfactory bulb in mice

“…In addition, our data suggest that the conventional plexiform layers of the main olfactory bulb are not present in the accessory bulb. Anat Rec Part A, 288A: 1009-1025, 2006. 2006 Key words: vomeronasal system; accessory olfactory bulb; growth; anatomy; mouse…”

“…Albeit during the last 2 decades, progress in the knowledge of the VNS in general and of the AOB in particular has been considerable (Hayashi et al, 1993;Taniguchi and Kaba, 2001;Araneda and Firestein, 2006), there are still some specific aspects of the AOB that require further exploration. Among the issues in need of precision is the exact morphology of the AOB, especially when it is obtained from mice.…”

α2-Adrenergic receptor activation promotes long-term potentiation at excitatory synapses in the mouse accessory olfactory bulb

“…Concerning the role of the AR subtypes in information processing in the AOB, studies on mouse AOB slices have shown that stimulation of α 1 -ARs, but not α 2 -ARs, increases the release of GABA from GCs and subsequently inhibits MC activity (Araneda and Firestein 2006;Smith et al 2009). In contrast, our study revealed that α 2 -AR activation decreased the inhibitory feedback from GCs, thereby disinhibiting MCs.…”