Central noradrenergic lesioning using anti-DBH-saporin: anatomical findings
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2020, Experimental NeurologyCitation Excerpt :To verify the role of NA signaling using our capsaicin-induced DNIC behavioral assay, we lesioned the LC prior to testing in naïve SD rats. Anti-dopamine beta-hydroxylase saporin (αDBH), a toxin that selectively destroys noradrenergic neurons of the LC and its projections, was injected unilaterally into the lateral ventricles 3 weeks prior to EPM testing (Picklo et al., 1994; Rohde and Basbaum, 1998; Wrenn et al., 1996). Data in Fig. 3B reveals that the loss of coeruleospinal noradrenergic inhibitory control resulted in DNIC failure with main effects of drug (F = 75.29, p = 1.2 × 10−5) and time (F = 6.16, p = 2.0 × 10−4).
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2019, Physiology and BehaviorNoradrenergic terminals are the primary source of α <inf>2</inf> -adrenoceptor mediated dopamine release in the medial prefrontal cortex
2019, Progress in Neuro-Psychopharmacology and Biological PsychiatryCitation Excerpt :Moreover, to clarify the relative involvement of α2-autoreceptors and α2-heteroreceptors in α2-adrenoceptor blockade, we examined if noradrenergic denervation modified the inhibitory effect of clonidine (an α2-adrenoceptor agonist) on DA release in the mPFC. Central noradrenergic denervation was induced by intraventricular injection of the immunotoxin anti-dopamine-β-hydroxylase saporin (aDBH), which is known to specifically target noradrenergic neurons, unlike other catecholamine neurotoxins (Wrenn et al., 1996; Rohde and Basbaum, 1998). Furthermore, because aDBH-induced destruction of noradrenergic terminals is expected to eliminate NET, which is the principal mechanism believed to control DA clearance from extracellular fluid in the mPFC (Carboni et al., 1990; Pozzi et al., 1994; Moron et al., 2002), it should also be able to remove putative α2-adrenoreceptor-mediated inhibitory control by NE on DA release (Gresch et al., 1995; Gobert et al., 1997; Pozzi et al., 1994).
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2018, Neurochemistry InternationalCitation Excerpt :Thus, the first goal of the current study was to produce a model of PD that demonstrated both DA and NE cell loss more akin to that seen in human PD. To do this, we targeted central NE neurons using the ribosomal inactivating neurotoxin αDBH, which is known to potently and selectively destroy NE neurons (Picklo et al., 1995, 1994; Wrenn et al., 1996). At the same time, we destroyed DA neurons by administering 6-OHDA unilaterally into the MFB.