Journal
JOURNAL OF NEUROSCIENCE
Volume 24, Issue 38, Pages 8198-8204Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.0425-04.2004
Keywords
alpha(1)- and beta-adrenergic receptors; withdrawal; electrophysiology; morphine; adenylyl cyclase; retrograde labeling
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Funding
- Canadian Institutes of Health Research [49878-1] Funding Source: Medline
- NIDA NIH HHS [DA08163, R01 DA008163] Funding Source: Medline
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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 from a 5 d 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 alpha(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 beta-adrenergic receptors, adenylyl cyclase, and protein kinase A, as well as alpha(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.
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