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The Journal of Neuroscience, September 22, 2004, 24(38):8198-8204; doi:10.1523/JNEUROSCI.0425-04.2004

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Cellular/Molecular
Noradrenaline Triggers GABA_A Inhibition of Bed Nucleus of the Stria Terminalis Neurons Projecting to the Ventral Tegmental Area

Éric C. Dumont and John T. Williams

Vollum Institute, Oregon Health Sciences University, Portland, Oregon 97239

The lateral part of the ventral bed nucleus of the stria terminalis (vlBNST) is a critical site for the antiaversive effects of noradrenergic drugs during opioid withdrawal. The objective of the present study is to identify the cellular action(s) of noradrenaline in the vlBNST after withdrawal froma5d treatment with morphine. The vlBNST is a heterogeneous cell group with multiple efferent projections. Therefore, neurons projecting to the midbrain were identified by retrograde transport of fluorescent microspheres injected in the ventral tegmental area (VTA). Whole-cell voltage clamp recordings of these neurons and of those sharing physiological properties were done in brain slices. Noradrenaline activated ₁-adrenergic receptors to increase GABA_A-IPSC frequency. Noradrenaline produced a similar increase in GABA_A-IPSCs during acute opioid withdrawal, but this increase resulted from activation of-adrenergic receptors, adenylyl cyclase, and protein kinase A, as well as ₁-adrenergic receptors. Given that neurons in the vlBNST send an excitatory projection to the VTA, noradrenaline may reduce excitatory drive to mesolimbic dopamine cells. This mechanism might contribute to the withdrawal-induced inhibition of dopamine neurons and explain how noradrenergic drugs microinjected into the vlBNST reduce aversive aspects of opioid withdrawal.

Key words: ₁- and -adrenergic receptors; withdrawal; electrophysiology; morphine; adenylyl cyclase; retrograde labeling

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Received Feb 5, 2004; revised July 15, 2004; accepted July 15, 2004.

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