Key points• Here, in mouse brain slices, we examined the cellular effects of noradrenaline to better understand its influence on olfactory bulb processing.• β-and α 1 -adrenergic receptor activation increases GABA currents in mitral cells in an age-dependent manner; the β-adrenergic effect is prominent only during early postnatal weeks, while the α 1 effect is present at all ages.• This study focused on the α 1 -mediated increase in GABA inhibitory currents in mitral cells and found noradrenaline acts on the α 1A -adrenergic receptor subtype to produce long-lasting excitation of granule cells.• The enhancement of inhibition by noradrenaline was consistent across a broad concentration range; at all concentrations, noradrenaline increased inhibitory currents in mitral cells.• Our studies highlight the important role of α 1A -adrenergic receptor subtypes in increasing inhibition at dendrodendritic synapses, suggesting a synaptic mechanism for noradrenergic modulation of olfactory driven behaviours.Abstract By regulating inhibition at dendrodendritic synapses between mitral and granule cells (GCs), noradrenergic neurons extending from the brainstem provide an input essential for odour processing in the olfactory bulb (OB). In the accessory OB (AOB), we have recently shown that noradrenaline (NA) increases GABA inhibitory input on to mitral cells (MCs) by exciting GCs. Here, we show that GCs in the main OB (MOB) exhibit a similar response to NA, indicating a common mechanism for noradrenergic regulation of GC→MC inhibition throughout the OB. In GCs of the MOB, NA (10 μM) produced a robust excitatory effect that included a slow afterdepolarization that followed a train of action potentials evoked by a current stimulus. The depolarization and slow afterdepolarization in GCs were blocked by the α 1A -adrenergic receptor (AR) selective antagonist WB 4101 (30 nM) and mimicked by the α 1A -AR selective agonist A 61603 (1 μM). In recordings from MCs, A 61603 (30 nM-1 μM) produced a sizeable increase in the frequency of spontaneous and miniature IPSCs, an effect completely abolished by the GABA A receptor antagonist gabazine (5 μM). Likewise, activation of β-ARs increased the frequency of spontaneous IPSCs; however, this effect was smaller and confined to the first postnatal weeks. NA enhanced inhibition in MCs across a broad concentration range (0.1-30 μM) and its effects were completely abolished by a mixture of α 1 -and β-AR antagonists (1 μM prazosin and 10 μM propranolol). Furthermore, the general α 2 -AR agonist clonidine (10 μM) failed to affect sIPSC frequency. Thus, the NA-mediated increase in GC→MC inhibition in the OB results mostly from activation of the α 1A -AR subtype.