Behavioural and pharmacological characterization of the mouth movements induced by muscarinic agonists in the rat

Salamone, John D.; Lalies, M. D.; Channell, S.; Iversen, Susan D.

doi:10.1007/bf00178508

Cited by 95 publications

(53 citation statements)

References 11 publications

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“…In accordance with the findings of Salamone et al (1986), we have shown that in addition to pilocarpine, purposeless chewing behaviour can be induced by the cholinergic agonists oxotremorine and arecoline. We have shown further that chewing behaviour can be induced in a dose-related manner by the cholinergic agonist RS 86 (Palacios et al 1986).…”

Section: Discussionsupporting

confidence: 90%

“…Neuroleptic-induced chewing behaviour can be potentiated by cholinergic agonists and prevented by anticholinergic drugs. Purposeless chewing can also be directly induced by the acute administration of cholinergic agonists or cholinesterase inhibitors (Rupniak et al 1983;Salamone et al 1986); this effect is central in origin and can be inhibited by anticholinergic drugs. So, purposeless chewing induced by acute cholinergic agonist administration may provide a model of central cholinergic function.…”

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confidence: 99%

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Assessment of the muscarinic receptor subtype involved in the mediation of pilocarpine-induced purposeless chewing behaviour

1989

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Purposeless chewing behaviour in rats was enhanced by intraperitoneal administration of the muscarinic agonists pilocarpine (1.0-8.0 mg/kg), RS 86 (0.5-0.8 mg/kg), oxotremorine (1-2 mg/kg) and arecoline (2-32 mg/kg), but not by nicotine (0.1-3.2 mg/kg). Chewing behaviour was also induced by the ICV administration of the muscarinic agonists carbachol (12.5-100 micrograms) and pilocarpine (50-200 micrograms), but not by the putative M-1 receptor agonist McN-A-343 (50-200 micrograms) or AH 6405 (100-200 micrograms). The muscarinic receptor antagonists scopolamine (0.01-0.1 mg/kg SC), benzhexol (0.075-2.5 mg/kg SC), secoverine (1-10 mg/kg SC), and dicyclomine (1.25-10 mg/kg SC) antagonised purposeless chewing behaviour induced by pilocarpine (4 mg/kg IP). AF-DX 116 (2.5-100 mg/kg SC), an M-2 antagonist, partially inhibited the actions of pilocarpine (4 mg/kg IP). Based on ED40 values the rank order of potency following IP administration was scopolamine greater than benzhexol greater than secoverine greater than dicyclomine greater than AF-DX 116. The ICV administration of the muscarinic antagonists N-methylscopolamine (2.5-10 micrograms) and oxyphenonium (10-40 micrograms) antagonised chewing behaviour induced by pilocarpine (4 mg/kg IP) in a dose-related manner. The M-2 antagonist 4-DAMP (40-160 micrograms ICV), as well as AF-DX 116 (40-160 micrograms ICV), also inhibited the effects of pilocarpine (40-160 micrograms ICV). The putative M-1 receptor antagonist pirenzepine (80-320 micrograms ICV) did not antagonise chewing behaviour induced by pilocarpine (4 mg/kg IP).(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Discussionsupporting

confidence: 90%

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confidence: 99%

Assessment of the muscarinic receptor subtype involved in the mediation of pilocarpine-induced purposeless chewing behaviour

1989

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“…Conversely, muscarinic antagonists block the catalepsy induced by dopamine antagonists [15,16]. In addition to playing a role in mediation of psychomotor behavior via sites within the striatum, these receptors are also associated with cognitive function.…”

Section: Discussionmentioning

confidence: 99%

The striatum and cerebral cortex express different muscarinic receptor mRNAs

1988

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The existence of four distinct muscarinic acetylcholine receptor genes (ml -m4) has recently been demonstrated. cDNAs for three of these receptors have been cloned from brain (ml, m3, m4) and one from heart (m2). To gain some understanding of the physiological role of the brain muscarinic receptors, we mapped the distribution of their mRNAs in rat brain by in situ hybridization.These mRNAs are barely detectable in the hindbrain and cerebellum. Within forebrain, each mRNA has a strikingly different pattern of distribution.The highest levels of ml mRNA are in the cerebral cortex and hippocampus followed by the striatum. m3 mRNA is also prominent in the cerebral cortex, but has very low levels in the striatum. Conversely, the levels of m4 mRNA are highest in the striatum. Since the cognitive effects of muscarinic drugs have been localized to the cerebral cortex and hippocampus, and their psychomotor effects to the striatum, these data suggest that the muscarinic receptors which subserve these responses may be different gene products. Finally, we show that these muscarinic receptors can be distinguished pharmacologically, suggesting that it may be possible to develop drugs for the selective treatment of the psychomotor vs cognitive difficulties of Parkinson's and Alzheimer's disease, respectively.

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“…The number of VCM, along with number of orofacial burst (OB) and tongue protrusion (TP) was scored for the period of 1 h (Salamone et al, 1986).…”

Section: Behavioral Parametersmentioning

confidence: 99%

Reversal of haloperidol-induced orofacial dyskinesia byMurraya koenigiileaves in experimental animals

Patil¹,

Hiray²,

Shinde³

et al. 2011

Pharmaceutical Biology

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Behavioural and pharmacological characterization of the mouth movements induced by muscarinic agonists in the rat

Cited by 95 publications

References 11 publications

Assessment of the muscarinic receptor subtype involved in the mediation of pilocarpine-induced purposeless chewing behaviour

Assessment of the muscarinic receptor subtype involved in the mediation of pilocarpine-induced purposeless chewing behaviour

The striatum and cerebral cortex express different muscarinic receptor mRNAs

Reversal of haloperidol-induced orofacial dyskinesia byMurraya koenigiileaves in experimental animals

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