The imidazoline receptor ligand 2-(2-benzofuranyl)-2-imidazoline is a dopamine-releasing agent in the rat striatum in vivo

Sastre-Coll, Antoni; Esteban, Susana; Miralles, Antonio; Zanetti, Rosana; Garcı́a-Sevilla, Jesús A.

doi:10.1016/s0304-3940(01)01599-3

Cited by 19 publications

(16 citation statements)

References 13 publications

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“…Several studies have shown however, that I 2 receptor ligands such as 2-BFI significantly modulate monoamine levels in rat brain (Nutt et al, 1995;Sastre-Coll et al 2001). Nevertheless, the present results suggest that I 2 receptors are unlikely to play a role in quinpirole sensitization since 2-BFI did not alter quinpirole-induced sensitization, nor did it induce sensitization when administered alone.…”

Section: Sigma and I 2 Receptors In Development Of Sensitizationcontrasting

confidence: 81%

Clorgyline-induced switch from locomotion to mouthing in sensitization to the dopamine D2/D3 agonist quinpirole in rats: role of sigma and imidazoline I2 receptors

Culver

Szechtman

2003

Psychopharmacology

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Because Ro 41-1049 produced the same effects as clorgyline, and 2-BFI had no effects on quinpirole sensitization, it is unlikely that clorgyline exerts its effects via an action at sigma or I(2) receptors. Our results are consistent with the suggestion that clorgyline and Ro 41-1049 affect the behavioral response to quinpirole via the MAOI-displaceable quinpirole binding (MQB) site, and the hypothesis that the MQB site selects what motor output becomes sensitized to repeated injections of quinpirole.

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Section: Sigma and I 2 Receptors In Development Of Sensitizationcontrasting

confidence: 81%

Clorgyline-induced switch from locomotion to mouthing in sensitization to the dopamine D2/D3 agonist quinpirole in rats: role of sigma and imidazoline I2 receptors

Culver

Szechtman

2003

Psychopharmacology

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“…It follows that one possible explanation for the ipsiversive rotational behaviour seen here with 2-BFI and BU224 is that these I 2 -site ligands may also act to release dopamine in the striatum of the intact hemisphere. That I 2 -site ligands may act as 'dopamine releasers' has been suggested previously (Sastre-Coll et al, 2001) and is backed up by the in vivo microdialysis studies of Hudson et al (1999), which showed that acute administration of similar doses of 2-BFI and BU224 as used here (20 mg kg À1 ) increased extrasynaptic levels of dopamine in the striatum by 0.5-and 2.5-fold above baseline, respectively. That this N. MacInnes & S. Duty I 2 -site-specific ligands in 6-OHDA-lesioned rats increase in striatal dopamine levels is small compared to the 10-fold increase above baseline that would be achieved by 5 mg kg À1 amphetamine (Lamensdorf et al, 1999) is consistent with the level of rotations achieved with 2-BFI and BU224 being small compared to that produced by amphetamine.…”

Section: Discussionsupporting

confidence: 64%

Locomotor effects of imidazoline I₂‐site‐specific ligands and monoamine oxidase inhibitors in rats with a unilateral 6‐hydroxydopamine lesion of the nigrostriatal pathway

MacInnes

Duty

2004

British J Pharmacology

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1 The present study examined the ability of the selective imidazoline I 2 -site ligands 2-(-2-benzofuranyl)-2-imidazoline (2-BFI) and 2-[4,5-dihydroimidaz-2-yl]-quinoline (BU224) and selected monoamine oxidase (MAO) inhibitors to evoke locomotor activity in rats bearing a lesion of the nigrostriatal pathway. 2 Male Sprague-Dawley rats were injected with 12.5 mg 6-hydroxydopamine (6-OHDA) into the right median forebrain bundle to induce a unilateral lesion of the nigrostriatal tract. After 6 weeks, test drugs were administered either alone or in combination with L-DOPA (L-3,4-dihydroxyphenylamine) and the circling behaviour of animals was monitored as an index of anti-Parkinsonian activity. ) significantly increased either the duration or total number of contraversive rotations emitted over the testing period in comparison to L-DOPA alone. 5 These data suggest that I 2 -specific ligands have dual effects in the 6-OHDA-lesioned rat model of Parkinson's disease; a first effect associated with an increase in activity in the intact hemisphere, probably via an increase in striatal dopamine content, and a secondary action which, through the previously documented inhibition of MAO-A and/or MAO-B, increases the availability of dopamine produced by L-DOPA.

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“…Similarly, in rodents, a moderate density of these receptor subtypes has been demonstrated (Kamisaki et al, 1990;Ruggiero et al, 1998) (but see Vauquelin et al, 1999). Evidence that I 2 -imidazoline receptor binding is altered in the putaminal tissue taken postmortem from patients with Huntington's disease (Reynolds et al, 1996) and that the I 2 -imidazoline receptor ligand 2-(2-benzofuranyl)-2-imidazoline increases dopamine release in the striatum shown in vivo (Sastre-Coll et al, 2001) indicates that imidazoline receptors may influence neuronal function in the striatum. However, no study has provided direct evidence of modulatory roles for I 1 -and/or I 2 -imidazoline receptors detected electrophysiologically in the striatum.…”

Section: Introductionmentioning

confidence: 93%

“…The endogenous ligands may reach both I 1 -and I 2 -imidazoline receptors in the striatum. Activation of I 2 -imidazoline receptors inhibits monoamine oxidase (Carpéné et al, 1995;Ozaita et al, 1997;Lalies et al, 1999) and elicits dopamine release (Sastre-Coll et al, 2001), both of which can result in an increase of extracellular dopamine. Hence, it is plausible that the endogenous ligands facilitate the striatal direct output pathway via both I 1 -imidazoline receptormediated disinhibition and I 2 -imidazoline receptor-mediated increase in dopamine.…”

Section: Physiological Implicationsmentioning

confidence: 99%

Presynaptic I₁-Imidazoline Receptors Reduce GABAergic Synaptic Transmission in Striatal Medium Spiny Neurons

et al. 2006

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Imidazoline receptors are expressed widely in the CNS. In the present study, whole-cell patch-clamp recordings were made from medium spiny neurons in dorsal striatum slices from the rat brain, and the roles of I 1 -imidazoline receptors in the modulation of synaptic transmission were studied. Moxonidine, an I 1 -imidazoline receptor agonist, decreased the GABA A receptor-mediated IPSCs in a concentration-dependent manner. However, glutamate-mediated EPSCs were hardly affected. The depression of IPSCs by moxonidine was antagonized by either idazoxan or efaroxan, which are both imidazoline receptor antagonists containing an imidazoline moiety. In contrast, yohimbine and SKF86466 (6-chloro-2,3,4,5-tetrahydro-3-methyl-1H-3-benzazepine), which are ␣2-adrenergic receptor antagonists with no affinity for imidazoline receptors, did not affect the moxonidine-induced inhibition of IPSCs. Moxonidine increased the paired-pulse ratio and reduced the frequency of miniature IPSCs without affecting their amplitude, indicating that this agent inhibits IPSCs via presynaptic mechanisms. Moreover, the sulfhydryl alkylating agent N-ethylmaleimide (NEM) significantly reduced the moxonidine-induced inhibition of IPSCs. Thus, the activation of presynaptic I 1 -imidazoline receptors decreases GABA-mediated inhibition of medium spiny neurons in the striatum, in which NEM-sensitive proteins such as G i/o -type G-proteins play an essential role. The adenylate cyclase activator forskolin partly opposed IPSC inhibition elicited by subsequently applied moxonidine. Furthermore, the protein kinase C (PKC) activator phorbol 12,13-dibutyrate attenuated and the PKC inhibitor chelerythrine potentiated the moxonidineinduced inhibition of IPSCs. These results suggest that IPSC inhibition via presynaptic I 1 -imidazoline receptors involves intracellular adenylate cyclase activity and is influenced by static PKC activity in the striatum.

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The imidazoline receptor ligand 2-(2-benzofuranyl)-2-imidazoline is a dopamine-releasing agent in the rat striatum in vivo

Cited by 19 publications

References 13 publications

Clorgyline-induced switch from locomotion to mouthing in sensitization to the dopamine D2/D3 agonist quinpirole in rats: role of sigma and imidazoline I2 receptors

Clorgyline-induced switch from locomotion to mouthing in sensitization to the dopamine D2/D3 agonist quinpirole in rats: role of sigma and imidazoline I2 receptors

Locomotor effects of imidazoline I₂‐site‐specific ligands and monoamine oxidase inhibitors in rats with a unilateral 6‐hydroxydopamine lesion of the nigrostriatal pathway

Presynaptic I₁-Imidazoline Receptors Reduce GABAergic Synaptic Transmission in Striatal Medium Spiny Neurons

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The imidazoline receptor ligand 2-(2-benzofuranyl)-2-imidazoline is a dopamine-releasing agent in the rat striatum in vivo

Cited by 19 publications

References 13 publications

Clorgyline-induced switch from locomotion to mouthing in sensitization to the dopamine D2/D3 agonist quinpirole in rats: role of sigma and imidazoline I2 receptors

Clorgyline-induced switch from locomotion to mouthing in sensitization to the dopamine D2/D3 agonist quinpirole in rats: role of sigma and imidazoline I2 receptors

Locomotor effects of imidazoline I2‐site‐specific ligands and monoamine oxidase inhibitors in rats with a unilateral 6‐hydroxydopamine lesion of the nigrostriatal pathway

Presynaptic I1-Imidazoline Receptors Reduce GABAergic Synaptic Transmission in Striatal Medium Spiny Neurons

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Locomotor effects of imidazoline I₂‐site‐specific ligands and monoamine oxidase inhibitors in rats with a unilateral 6‐hydroxydopamine lesion of the nigrostriatal pathway

Presynaptic I₁-Imidazoline Receptors Reduce GABAergic Synaptic Transmission in Striatal Medium Spiny Neurons