Autoradiographic localisation of [3H]2-BFI imidazoline I2 binding sites in mouse brain

MacInnes, Nicholas; Handley, Sheila L.

doi:10.1016/j.ejphar.2005.04.006

Cited by 11 publications

(10 citation statements)

References 28 publications

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“…1998; Paterson et al . 2003; MacInnes and Handley 2005). The MAO‐A knockout mice used in the study contain a transgene inserted into the MAO‐A gene, resulting in non‐ or partial translation into protein (Cases et al .…”

Section: Discussionmentioning

confidence: 99%

“…[ 3 H]2‐BFI autoradiography in mouse brain indicates that this ligand recognizes a similar I 2 ‐BS population (Paterson et al . 2003; MacInnes and Handley 2005). This is further supported by the highly significant ( p < 0.0001; data not shown) correlation between the [ 3 H]2‐BFI and [ 3 H]idazoxan distributions achieved in the present study.…”

Section: Discussionmentioning

confidence: 99%

“…This is further supported by the highly significant ( p < 0.0001; data not shown) correlation between the [ 3 H]2‐BFI and [ 3 H]idazoxan distributions achieved in the present study. Small differences between the mouse and rat brain I 2 ‐BS do exist and these are thought to reflect the relatively higher level of MAO‐B expressed in the mouse brain compared with the rat brain (MacInnes and Handley 2005). In MAO‐A knockout mice, a significant reduction in [ 3 H]idazoxan and [ 3 H]2‐BFI binding was observed.…”

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Autoradiographical distribution of imidazoline binding sites in monoamine oxidase A deficient mice

Anderson¹,

Seif²,

Nutt³

et al. 2006

Journal of Neurochemistry

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Autoradiographical distribution of imidazoline binding sites in monoamine oxidase A deficient mice

Anderson¹,

Seif²,

Nutt³

et al. 2006

Journal of Neurochemistry

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“…These binding sites demonstrate a high affinity for imidazoline-class α2-adrenergic ligands but low affinity for known biogenic amines. Studies by several research groups indicate their presence in peripheral tissues and in both the central and peripheral nervous systems of various species (Campbell and Potter, 1994;Ernsberger and Haxhiu, 1997;Eglen et al, 1998;MacInnes and Handley, 2005 (Parini et al, 1996;Mourtada et al, 1997;Reis and Piletz, 1997;Eglen et al, 1998), subcellular location (Tesson et al, 1995;Ernsberger and Haxhiu, 1997;Zhang and Abdel-Rahman, 2006) and regional distribution (Ernsberger and Haxhiu, 1997;Lione et al, 1998;Robinson et al, 2002;MacInnes and Handley, 2005;Anderson et al, 2006).…”

Section: Imidazoline Binding Sitesmentioning

confidence: 99%

Modulation of stress by imidazoline binding sites: Implications for psychiatric disorders

Smith

Jessop

Finn

2009

Stress

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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 in animal models of stress, depression and anxiety, and a body of evidence exists for alterations in central IBS expression in psychiatric patients, which can be normalised partially or fully by treatment with antidepressants. Dysfunction in monoaminergic systems and the HPA axis under basal and stress-induced activation has been extensively reported in psychiatric illnesses. On the basis of the literature, we suggest a potential therapeutic role for selective IBS ligands in the treatment of depression and anxiety disorders.

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“…In vivo , systemic I 2 R agonist administration increases dopamine (DA), serotonin (5-HT), and norepinephrine (NE) levels in several CNS regions including striatum, frontal cortex, dorsal raphe, hippocampus, and spinal cord (Nutt et al ., 1995; Nutt et al ., 1997; Ugedo et al ., 1999; Sastre-Coll et al ., 2001; Finn et al ., 2002; Ferrari et al ., 2011). Investigations on the CNS distribution of I 2 Rs have shown that I 2 Rs are enriched in brain regions including arcuate nucleus of the hypothalamus (ArcN), interpeduncular nucleus (IPN), paraventricular nucleus of the thalamus (PVT), lateral mammillary nucleus (LMN), dorsal raphe (DR), nucleus accumbens (NAc), and medial habenula (MH) in rat and mouse brain (MacKinnon et al ., 1995; Lione et al ., 1998; MacInnes & Handley, 2005). Yet, while intracerebroventricular injections of 2-BFI produce antinociception (Thorn et al ., 2016a), the specific brain regions mediating this effect and other I 2 R-associated effects have not yet been demonstrated through functional studies.…”

Section: Introductionmentioning

confidence: 99%

Neuroanatomical characterization of imidazoline I₂ receptor agonist‐induced antinociception

Siemian

Jia

Liu

et al. 2018

Eur J of Neuroscience

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Chronic pain is a significant public health problem with a lack of safe and effective analgesics. The imidazoline I receptor (I R) is a promising analgesic target, but the neuroanatomical structures involved in mediating I R-associated behaviors are unknown. I Rs are enriched in the arcuate nucleus, dorsal raphe (DR), interpeduncular nucleus, lateral mammillary body, medial habenula, nucleus accumbens (NAc) and paraventricular nucleus; thus, this study investigated the antinociceptive and hypothermic effects of microinjections of the I R agonist 2-(2-benzofuranyl)-2-imidazoline hydrochloride (2-BFI). In rats, intra-DR microinjections produced antinociception in complete Freund's adjuvant- and chronic constriction injury-induced pain models. Intra-NAc microinjections produced antinociception and increased noxious stimulus-associated side time in a place escape/avoidance paradigm. Intra-NAc pretreatment with the I R antagonist idazoxan but not the D1 receptor antagonist SCH23390 or the D2 receptor antagonist raclopride attenuated intra-NAc 2-BFI-induced antinociception. Intra-NAc idazoxan did not attenuate systemically administered 2-BFI-induced antinociception. Microinjections into the other regions did not produce antinociception, and in none of the regions produced hypothermia. These data suggest that I R activation in some but not all I R-enriched brain regions is sufficient to produce antinociception and supports the theory that different I R-associated effects are mediated via distinct receptor populations, which may in turn be distributed differentially throughout the CNS.

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Autoradiographic localisation of [3H]2-BFI imidazoline I2 binding sites in mouse brain

Cited by 11 publications

References 28 publications

Autoradiographical distribution of imidazoline binding sites in monoamine oxidase A deficient mice

Autoradiographical distribution of imidazoline binding sites in monoamine oxidase A deficient mice

Modulation of stress by imidazoline binding sites: Implications for psychiatric disorders

Neuroanatomical characterization of imidazoline I₂ receptor agonist‐induced antinociception

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Autoradiographic localisation of [3H]2-BFI imidazoline I2 binding sites in mouse brain

Cited by 11 publications

References 28 publications

Autoradiographical distribution of imidazoline binding sites in monoamine oxidase A deficient mice

Autoradiographical distribution of imidazoline binding sites in monoamine oxidase A deficient mice

Modulation of stress by imidazoline binding sites: Implications for psychiatric disorders

Neuroanatomical characterization of imidazoline I2 receptor agonist‐induced antinociception

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Product

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Neuroanatomical characterization of imidazoline I₂ receptor agonist‐induced antinociception