Clonidine binds to imidazole binding sites as well as α2-adrenoceptors in the ventrolateral medulla

Ernsberger, Paul; Meeley, Mary P.; Mann, J. John; Reis, Donald J.

doi:10.1016/0014-2999(87)90125-7

Cited by 431 publications

(147 citation statements)

References 25 publications

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“…The latter three studies have all related their findings to I 2 sites (King et al 1995;Lione et al 1998;Mallard et al 1992). By convention, I-sites labeled with [ 3 H]-clonidine have been designated as I 1 sites (Ernsberger et al 1987). However, De Vos and colleagues (1994) used cautionary language when making an assignment of their nonadrenergic [ 3 H]-clonidine binding site as an I 1 subtype.…”

Section: Discussionmentioning

confidence: 99%

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Autoradiographic Comparison of [3H]-Clonidine Binding to Non-Adrenergic Sites and α2-Adrenergic Receptors in Human Brain

Piletz

Ordway

Zhu

et al. 2000

Neuropsychopharmacology

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Section: Discussionmentioning

confidence: 99%

“…Originally thought to be a selective agonist for ␣ 2 -adrenoceptors ( ␣ 2 AR), clonidine is now realized to possesses only slightly lower affinity for non-adrenergic imidazoline receptors (IR) compared to ␣ 2 AR (Bousquet et al 1984;Ernsberger et al 1987).…”

mentioning

confidence: 99%

Autoradiographic Comparison of [3H]-Clonidine Binding to Non-Adrenergic Sites and α2-Adrenergic Receptors in Human Brain

Piletz

Ordway

Zhu

et al. 2000

Neuropsychopharmacology

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“…Moreover, we have assessed the effects of a 2 antagonists in this regard. Yohimbine, a selective a 2 adrenoceptor antagonist (Goldberg and Robertsson, 1983) with very low affinity for I 1 binding sites (I 1 /a 2 affinity ratio ¼ 0.01; Ernsberger et al, 1987Ernsberger et al, , 1992Hamilton et al, 1988;Senard et al, 1990), with a dose of 0.005 mg/kg is incapable of affecting place preference or altering morphine CPP; however, it completely blocks the potentiating effect of agmatine on morphineinduced place preference. Yohimbine with higher doses is shown to induce CPA (File, 1986) and it tends to limit the place preference induced by morphine (Morales et al, 2001).…”

Section: Discussionmentioning

confidence: 99%

Agmatine Potentiates Morphine-Induced Conditioned Place Preference in Mice: Modulation by Alpha(2)-Adrenoceptors

Tahsili-Fahadan

Yahyavi-Firouz-Abadi

Khoshnoodi

et al. 2005

Neuropsychopharmacol

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The effects of agmatine, an endogenous polyamine metabolite formed by decarboxylation of L-arginine, and its combination with morphine on conditioned place preference (CPP) has been investigated in male mice. Our data show that subcutaneous administration of morphine (1-7.5 mg/kg) significantly increases the time spent in the drug-paired compartment in a dose-dependent manner. Intraperitoneal administration of agmatine (1-40 mg/kg) alone does not induce either CPP or conditioned place aversion, while combination of agmatine and subeffective doses of morphine leads to potent rewarding effects. Lower doses of morphine (0.1, 0.05, and 0.01 mg/kg) are able to induce CPP in mice pretreated with agmatine 1, 5, and 10 mg/kg, respectively. Concomitant intraperitoneal administration of UK 14 304 (0.5 mg/kg), a highly selective a 2 -agonist, with per se noneffective dose of morphine (0.5 mg/kg) and also its combination with noneffective doses of agmatine (1 mg/kg) plus morphine (0.05 mg/kg) produces significant CPP. UK 14 304 (0.05, 0.5 mg/kg) alone, or in combination with agmatine (1, 5 mg/kg) have had no effect. We have further investigated the possible involvement of the a 2 -adrenoceptors in the potentiating effect of agmatine on morphine-induced place preference. Selective a 2 -antagonists, yohimbine (0.005 mg/kg) and RX821002 (0.1, 0.5 mg/kg), block the CPP induced by concomitant administration of agmatine (5 mg/kg) and morphine (0.05 mg/kg). Yohimbine (0.001-0.05 mg/kg) or RX821002 (0.05-0.5 mg/kg) alone or in combination with morphine (0.05 mg/kg) or agmatine (5 mg/kg) fail to show any significant place preference or aversion. Our results indicate that pretreatment of animals with agmatine enhances the rewarding properties of morphine via a mechanism which may involve a 2 -adrenergic receptors.

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“…Clonidine is an agonist at I1Rs in addition to a2Rs (Bricca et al, 1993;De Vos et al, 1994;Ernsberger et al, 1993Ernsberger et al, , 1987Michel et al, 1989;Wallace et al, 1994). To determine if the above actions were because of actions at a2ARs, we studied the effect of UK14304, a specific a2-adrenoreceptor agonist with an I1 binding site/a2 binding site affinity ratio o0.01 (Andorn et al, 1988;Bricca et al, 1993;Buccafusco et al, 1995;Urban et al, 1995).…”

Section: Costimulation Of A2-adrenergic Receptors and I1rs Is Requirementioning

confidence: 99%

“…In the brain, clonidine binds with high affinity to I1Rs (Bricca et al, 1989;Ernsberger et al, 1987). Among other functions, the I1R has been implicated in the hypotensive effect of clonidine and other agents with similar structures (for a review see Bousquet, 2001).…”

Section: Introductionmentioning

confidence: 99%

Prolonged Activation of Mesolimbic Dopaminergic Neurons by Morphine Withdrawal Following Clonidine: Participation of Imidazoline and Norepinephrine Receptors

Georges

Aston‐Jones

2003

Neuropsychopharmacol

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The a2 adrenoceptor (a2R) agonist clonidine is used as a treatment for heroin addiction. Substantial evidence indicates that dopaminergic and noradrenergic systems have key roles in opiate dependence and withdrawal but the possible interactions between these two pathways remain unclear. The objective of this study was to establish the effects of clonidine pretreatment on ventral tegmental area dopaminergic (VTA DA) neuronal activity during morphine withdrawal. Responses of VTA DA neurons to withdrawal precipitated by naltrexone were characterized in anesthetized rats using extracellular recordings. As expected, withdrawal produced a marked inhibition of VTA DA neuronal activity. However, pretreatment with clonidine prevented this inhibition induced by withdrawal, and instead produced a long-lasting activation of firing rate (+50%) and burst firing (+19%). In contrast, pretreatment with a more selective a2R agonist, UK14304, did not prevent the inhibition of VTA DA neuron activity during withdrawal. We tested whether the high affinity of clonidine for imidazoline-1 receptors (I1Rs) was responsible for the difference between these two a2R agonists. In morphine-dependent rats pretreated with rilmenidine (mixed a2R/I1R agonist), precipitation of withdrawal elicited a 22% increase of VTA DA impulse activity. The action of clonidine on I1Rs was studied by coadministering clonidine with RX821002, a specific a2R antagonist. Pretreatment with RX821002 plus clonidine prevented the inhibition of VTA DA activity during withdrawal but failed to produce excitation. These results indicate that the pharmacological effects of clonidine on VTA DA neurons during morphine withdrawal is related to actions on I1Rs as well as a2Rs.

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Clonidine binds to imidazole binding sites as well as α2-adrenoceptors in the ventrolateral medulla

Cited by 431 publications

References 25 publications

Autoradiographic Comparison of [3H]-Clonidine Binding to Non-Adrenergic Sites and α2-Adrenergic Receptors in Human Brain

Autoradiographic Comparison of [3H]-Clonidine Binding to Non-Adrenergic Sites and α2-Adrenergic Receptors in Human Brain

Agmatine Potentiates Morphine-Induced Conditioned Place Preference in Mice: Modulation by Alpha(2)-Adrenoceptors

Prolonged Activation of Mesolimbic Dopaminergic Neurons by Morphine Withdrawal Following Clonidine: Participation of Imidazoline and Norepinephrine Receptors

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