Quantitative autoradiography of M2 muscarinic receptors in the rat brain identified by using a selective radioligand [3H]AF-DX 116

Wang, Jian xin; Roeske, William R.; Hawkins, Kumiko N.; Gehlert, Donald R.; Yamamura, Henry I.

doi:10.1016/0006-8993(89)91421-2

Cited by 31 publications

(12 citation statements)

References 21 publications

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“…The observed predominant location of M2 receptors in the main projection areas of basal forebrain nuclei, hippocampal formation and frontal cortex, concurs with this assumption. Most previous studies analysing M2 receptors have also found significant reductions in these cortical areas (Araujo et al, 1988;Aubert et al, 1992a;Mash et al, 1985;Quirion et al, 1986Quirion et al, , 1989Rinne et al, 1989;Wang et al, 1989). All these data would confirm that the loss of M2 receptors in some cortical areas is secondary to the extensive loss of neurones occurring in the basal forebrain in AD (McGeer et al, 1984;Whitehouse et al, 1981Whitehouse et al, , 1982.…”

Section: Discussionsupporting

confidence: 68%

“…There are currently five genetically defined MR subtypes that have been cloned and expressed in multiple types of cells, designated as m1-m5 and four subtypes of pharmacologically characterised MR, named as M1-M4 (for review, see Bonner, 1989 (Araujo et al, 1988;Aubert et al, 1992a;Caulfield et al, 1982;Dekosky et al, 1992;Lange et al, 1989;Mash et al, 1985;Palacios, 1982;Probst et al, 1988;Quirion et al, 1989;Rinne et al, 1989;Vanderheyden et al, 1987), decreases (Araujo et al, 1988;Nordberg et al, 1992;Perry et al, 1987b;Rinne et al, 1989), or increases (Aubert et al, 1992a;Svensson et al, 1992 Perry et al, 1990), decreases (Araujo et al, 1988;Aubert et al, 1992b;Mash et al, 1985;Perry et al, 1987b;Quirion et al, 1986Quirion et al, , 1989Rinne et al, 1989;Wang et al, 1989), and no changes (Aubert et al, 1992b;Svensson et al, 1992) have been described in cortical areas of AD brains as compared with control brains.…”

Section: H]qnb) and [ 3 H]n-methyl-scopolamine ([ 3 H]nms)mentioning

confidence: 99%

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Autoradiographic distribution of M1, M2, M3, and M4 muscarinic receptor subtypes in Alzheimer's disease

Rodrı́guez-Puertas

Pascual

Vilaró

et al. 1997

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105

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Section: Discussionsupporting

confidence: 68%

Section: H]qnb) and [ 3 H]n-methyl-scopolamine ([ 3 H]nms)mentioning

confidence: 99%

Autoradiographic distribution of M1, M2, M3, and M4 muscarinic receptor subtypes in Alzheimer's disease

Rodrı́guez-Puertas

Pascual

Vilaró

et al. 1997

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105

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“…Oxotremorine has been proposed to act mainly on muscarinic M 2 acetylcholine receptors (Bräuner-Osborne and Brann 1996). Muscarinic M 2 acetylcholine receptors are abundant in the thalamus (Wang et al 1989;Flynn and Mash 1993;Wei et al 1994). In this study, we administered oxotremorine directly into the NRT and VPM, and found that oxotremorine dose dependently decreased neocortical HVSs when administered into the NRT or VPM.…”

Section: Discussionmentioning

confidence: 86%

“…Muscarinic M 2 acetylcholine receptors are abundant in the thalamus (Wang et al 1989;Flynn and Mash 1993;Wei et al 1994). No studies have so far investigated the e¤ects of local intrathalamic administration of muscarinic acetylcholine receptor subtype speciÞc drugs on neocortical HVSs.…”

Section: Introductionmentioning

confidence: 99%

Oxotremorine suppresses thalamocortical oscillations via thalamic muscarinic acetylcholine receptors

et al. 1998

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We investigated whether the local intrathalamic infusion of a muscarinic acetylcholine receptor agonist (oxotremorine) at either the reticular nucleus of thalamus (NRT) or the ventroposteromedial nucleus of thalamus (VPM) suppresses thalamocortically generated neocortical high-voltage spindles (HVSs). In addition, we studied whether the intracerebroventricular (ICV) infusion of a selective muscarinic M2 acetylcholine receptor antagonist (methoctramine) could block the suppression of HVSs induced by either systemic (IP) administration of an anticholinesterase drug [tetrahydroaminoacridine (THA)] or ICV infusion of oxotremorine in rats. Intrathalamic administration of oxotremorine at 3 and 15 microg in the NRT, and at 15 microg in the VPM suppressed HVSs. ICV oxotremorine at 30 and 100 microg and IP THA at 3 mg/kg decreased HVSs. ICV methoctramine at 100 microg increased HVSs and completely blocked the decrease in HVSs produced by oxotremorine 100 microg and THA 3 mg/kg. The results suggest that activation of muscarinic M2 acetylcholine receptors in thalamic nuclei (NRT and VPM) can suppress thalamocortical oscillations and that ICV or systemically administered drugs that activate either directly (oxotremorine and methoctramine) or indirectly (THA) the muscarinic M2 acetylcholine receptors may modulate neocortical HVSs via the thalamus.

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“…In our previous study, pilocarpine was more potent in suppressing HVSs in adult rats than AF102B (predominantly a muscarinic M 1 acetylcholine receptor agonist), which in turn was more potent than oxotremorine (Riekkinen Jr et al 1993a). It is relevant to note that there are more muscarinic M 2 acetylcholine receptors than the M 1 type in many of the thalamic nuclei which are considered to participate in the generation and modulation of thalamocortical oscillations (Wang et al 1989;Flynn and Mash 1993;Wei et al 1994). In the present study with aged rats, and in our previous study with adult rats , systemic administration of both pilocarpine and oxotremorine e¤ectively decreased HVSs.…”

Section: Discussionmentioning

confidence: 95%

Activation of acetylcholine receptors and 5-HT 2 receptors have additive effects in the suppression of neocortical high-voltage spindles in aged rats

et al. 1997

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We investigated if activation of the muscarinic or nicotinic acetylcholine receptors and serotonin (5-hydroxytryptamine; 5-HT) subtype 2 receptors would have additive or synergistic effects on the suppression of thalamocortically generated rhythmic neocortical high-voltage spindles (HVSs) in aged rats. The 5-HT2 receptor antagonist, ketanserin, at a moderate dose (5 mg/kg) prevented the ability of a muscarinic acetylcholine receptor agonist, (oxotremorine 0.1 mg/kg), and a nicotinic acetylcholine receptor agonist (nicotine 0.1 mg/kg), to decrease HVSs. At a higher dose (20 mg/kg), ketanserin completely blocked the decrease in HVSs produced by moderate doses of muscarinic acetylcholine receptor agonists (pilocarpine 1 mg/kg and oxotremorine 0.1 mg/kg), and by a high dose of nicotine (0.3 mg/kg), though not that produced by high doses of pilocarpine (3 mg/kg) and oxotremorine (0.9 mg/kg). The ability of a 5-HT2 receptor agonist, (+/-)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI) (0.1-1.0 mg/kg), to suppress HVSs was non-significantly modulated by the nicotinic acetylcholine receptor antagonist, mecamylamine (1-15 mg/kg), and the muscarinic acetylcholine receptor antagonist, scopolamine (0.03-0.3 mg/kg). The effects of the drugs on behavioral activity could be separated from their effects on HVSs. The results suggest that activation of the muscarinic or nicotinic acetylcholine receptors plus 5-HT2 receptors has additive effects in the suppression of thalamocortical oscillations in aged rats.

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Quantitative autoradiography of M2 muscarinic receptors in the rat brain identified by using a selective radioligand [3H]AF-DX 116

Cited by 31 publications

References 21 publications

Autoradiographic distribution of M1, M2, M3, and M4 muscarinic receptor subtypes in Alzheimer's disease

Autoradiographic distribution of M1, M2, M3, and M4 muscarinic receptor subtypes in Alzheimer's disease

Oxotremorine suppresses thalamocortical oscillations via thalamic muscarinic acetylcholine receptors

Activation of acetylcholine receptors and 5-HT 2 receptors have additive effects in the suppression of neocortical high-voltage spindles in aged rats

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