Banihashemi L, Rinaman L (2004) Noradrenergic inputs to the bed nucleus of the stria terminalis (BNST) contribute to yohimbine-induced activation of BNST neurons and hypothalamic CRH neurons in rats. Neuroscience 2004 Abstracts 426.10. Society for Neuroscience, San Diego, CA.
Summary: Noradrenergic (NA) inputs to the BNST and hypothalamus are implicated in behavioral and endocrine responses to stress and anxiety. Yohimbine (YO) increases transmitter release from NA terminals, which promotes anxiety and activates CRH neurons at the central apex of the HPA axis. We hypothesized that these effects require NA signaling within the BNST. To test this, saporin toxin conjugated to an antibody against dopamine beta hydroxylase (DSAP; 50-100 nl) was microinjected bilaterally into the BNST to eliminate its NA inputs in adult male Sprague-Dawley rats. After 2 weeks, DSAP-treated rats and intact control rats were injected with YO (0 or 5 mg/kg, i.p) and perfused with fixative 90 min later. Brain sections were processed to reveal DSAP lesion extent and YO-induced cFos activation. DSAP rats displayed nearly complete loss of NA terminals in the BNST, accompanied by moderate loss of hypothalamic NA terminals. Significantly fewer BNST neurons and hypothalamic CRH neurons were activated in DSAP rats after YO compared to activation in intact control rats, whereas parabrachial and central amygdala activation in DSAP rats was not diminished. We conclude that medullary NA neurons projecting to the lateral BNST collateralize to innervate the paraventricular hypothalamus, and that these NA projection neurons are necessary for YO to activate BNST and hypothalamic CRH neurons. Studies are ongoing to determine whether BNST-projecting NA neurons are necessary for YO to inhibit food intake or support conditioned flavor avoidance.
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