Brainstem noradrenergic cell groups mediating autonomic responses to stress project to airway-related vagal preganglionic neurons (AVPNs). In ferrets, their activation produces withdrawal of cholinergic outflow to the airways via release of norepinephrine (NE) and activation of _2A-adrenergic receptors (_2AAR) expressed by AVPNs. In these studies we examined the effects of allergen exposure of the airway (AE) with ovalbumin (OA) on noradrenergic transmission regulating the activity of AVPNs and, consequently, airway smooth muscle tone. Experiments were performed in vehicle control (CON) and allergen exposed (AE) ferrets. Microperfusion of an _2A adrenergic receptor (_2AAR) agonist (guanabenz) in close proximity to AVPNs elicited more pronounced effects in CON than AE ferrets, including a decrease in unit activity and reflexly evoked responses of putative AVPN neurons with a corresponding decrease in cholinergic outflow to the airways. While no differences were found in the extent of noradrenergic innervation of the AVPNs, RT-PCR and Western blot studies demonstrated that AE and repeated exposure to antigen significantly reduced expression of _2AARs at message and protein levels. These findings indicate that, in an animal model of allergic asthma, sensitization and repeated challenges with a specific allergen diminishes central inhibitory noradrenergic modulation of AVPNs, possibly via downregulation of _2AAR expression by these neurons.