The brain’s noradrenergic system system provides essential modulation to neuronal activity, with well established roles in control of arousal and selective attention, as well as memory, learning and response to stress. We have generated a transgenic mouse, NR1DbhCre, with ablation of the essential NMDA receptor subunit NR1 (Grin1) in noradrenergic cells. Since no functional NMDA receptors may be formed in the absence of NR1, and their expression is restricted to the central nervous system, the NR1DbhCre mice have impaired glutamate-dependent plasticity in the central noradrenergic neurons, without observable alterations in the sympathetic system or the hypothalamus-pituitary-adrenal axis. Transgenic animals were born at expected ratios and developed normally, displaying no obvious impairments. The general anatomy of the noradrenergic system in the mutant mice was normal, no loss of cells was observed and noradrenaline content in the prefrontal cortex was not altered. Interestingly, preliminary electrophysiological analysis indicates that loss of functional NMDA receptors attenuates the spontaneous activity in current-clamped locus coeruleus noradrenergic neurons manually held at −50 mV potential. In summary the NR1DbhCre transgenic mice are a novel model for the study of the roles of the noradrenergic system in the central nervous system.
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