2009
DOI: 10.1080/10253890802302908
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Modulation of stress by imidazoline binding sites: Implications for psychiatric disorders

Abstract: In this review, we present evidence for the involvement of imidazoline binding sites (IBS) in modulating responses to stress, through central control of monoaminergic and hypothalamo-pituitary-adrenal (HPA) axis activity. Pharmacological and physiological evidence is presented for differential effects of different IBS subtypes on serotoninergic and catecholaminergic pathways involved in control of basal and stress-stimulated HPA axis activity. IBS ligands can modulate behavioural and neuroendocrine responses i… Show more

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Cited by 24 publications
(25 citation statements)
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References 212 publications
(211 reference statements)
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“…RO5166017 did not affect NA neurons in the LC where harmane, a putative endogenous imidazoline binding sites ligand, increases firing activity (31). In contrast, it reduced the firing of DA neurons in the VTA, where no I 1 imidazoline binding sites were seen (31). Importantly, RO5166017 had no effect in Taar1 −/− mice, both in electrophysiological and behavioral studies.…”
Section: Discussionmentioning
confidence: 97%
See 1 more Smart Citation
“…RO5166017 did not affect NA neurons in the LC where harmane, a putative endogenous imidazoline binding sites ligand, increases firing activity (31). In contrast, it reduced the firing of DA neurons in the VTA, where no I 1 imidazoline binding sites were seen (31). Importantly, RO5166017 had no effect in Taar1 −/− mice, both in electrophysiological and behavioral studies.…”
Section: Discussionmentioning
confidence: 97%
“…However, I 1 imidazoline binding sites are unlikely to mediate the effects of RO5166017. RO5166017 did not affect NA neurons in the LC where harmane, a putative endogenous imidazoline binding sites ligand, increases firing activity (31). In contrast, it reduced the firing of DA neurons in the VTA, where no I 1 imidazoline binding sites were seen (31).…”
Section: Discussionmentioning
confidence: 99%
“…The first experiment investigated the effects of clonidine in the CeA and the second experiment investigated the effects of dexmedetomidine in the CeA on stress-induced reinstatement of nicotine seeking. Clonidine (Ki α2: 3.2 nM; Ki α1: 713 nM) and dexmedetomidine (Ki α2: 1.1 nM; Ki α1: 1750 nM) are potent α2-adrenergic receptor agonists and they also bind with a relatively low affinity to α1-adrenergic receptors and imidazoline 1 (I1) and I2 receptors (Smith et al, 2009; Virtanen et al, 1988). Dexmedetomidine is a somewhat more selective α2-adrenergic receptor agonist than clonidine.…”
Section: Introductionmentioning
confidence: 99%
“…Dexmedetomidine has a 7 fold greater selectivity for α2 over α1-adrenergic receptors than clonidine (Dexmedetomidine, α2/α1 ratio: 1620; Clonidine, α2/α1 ratio: 220) (Savola and Virtanen, 1991; Virtanen et al, 1988). Both the I1 and I2 receptor have been detected in the central nervous system (Dardonville and Rozas, 2004; Smith et al, 2009). Dexmedetomidine has a lower affinity for the I1 receptor than clonidine (Dexmedetomidine Ki: 637 nM; Clonidine Ki: 55 nM)(Piletz and Sletten, 1993).…”
Section: Introductionmentioning
confidence: 99%
“…There is a well-established role for MAO-A and GABA A receptors in the regulation of emotional processing and a significant body of evidence suggesting that imidazoline binding sites (I 1 and I 2 subtypes) may represent a novel therapeutic target for the treatment of psychiatric disorders (Smith et al, 2009a). Thus, increased understanding of the behavioural and neurobiological effects of harmane is warranted.…”
Section: Introductionmentioning
confidence: 98%