mystery of yawning
Le bâillement, du réflexe à la pathologie
Le bâillement : de l'éthologie à la médecine clinique
Le bâillement : phylogenèse, éthologie, nosogénie
 Le bâillement : un comportement universel
La parakinésie brachiale oscitante
Yawning: its cycle, its role
Warum gähnen wir ?
 
Fetal yawning assessed by 3D and 4D sonography
Le bâillement foetal
Le bâillement, du réflexe à la pathologie
Le bâillement : de l'éthologie à la médecine clinique
Le bâillement : phylogenèse, éthologie, nosogénie
 Le bâillement : un comportement universel
La parakinésie brachiale oscitante
Yawning: its cycle, its role
Warum gähnen wir ?
 
Fetal yawning assessed by 3D and 4D sonography
Le bâillement foetal
http://www.baillement.com

 

 

 

 

 

 

 

 

 

 

mise à jour du
29 novembre 2011
Psychopharmacology (Berl)
1986;88(4):467-71.
Behavioural and pharmacological characterization of the mouth movements induced by muscarinic agonists in the rat
 
Salamone JD, Lalies MD, Channell SL, Iversen SD.

Chat-logomini

Abstract
 
Pilocarpine administered in doses of 1.25-10.0 mg/kg (IP) produced a variety of mouth movements in the rat. The most frequent of these movements was a chewing behaviour, which increased up to a mean frequency of over 40 per min at the highest doses. Tongue protrusion and gaping also showed dose-dependent increases. Yawning tended to increase in some doses, though these increases were not significant, and yawning was relatively infrequent. Pre-treatment with scopolamine reduced these responses, while pre-treatment with methyl scopolamine did not. Injections of oxotremorine or arecoline, but not carbachol, produced dose-related increases in mouth movements similar to those produced by pilocarpine. These results suggest that mouth movements in the rat are caused by stimulation of central muscarinic receptors. This may prove to be an important behavioural sign of central cholinomimetic activity.
 
 
Easily detectable behavioural signs of drug actions, such as stereotypy or catalepsy, are widely used in psychopharmacology. Such behaviours can help researchers identify drug effects consistent with an action upon a particular CNS neurotransmitter system. The current resurgence of interest in cholinergic psychopharmacology (Bartus et al. 1982; Rossor 1980) suggests that a simple behavioural test for CNS cholinomimetic actions would be valuable. The induction of various oral activities by muscarinic agonists could prove to be a useful cholinergic-related behaviour of this type.
 
It has been reported that cholinomimetics cause yawning in rats (Ushijima et al. 1984; Yamada and Furukawa 1980, 1981). This yawning was shown to be more frequent in young male rats (Urba-Holmgren et al. 1977). Ushijima et al. (1984) observed that yawning was frequently accompanied by tongue protrusion . Rupniak et al. (1983) also found that physostigmine and pilocarpine induced tongue protrusion. This observation was made in the context of investigating cholinergic modulation of perioral movements following chronic neuroleptic treatment. The anticholinergics scopolamine and atropine attenuated the frequency of these movements (Rupniak et al. 1983). The neuroleptic-induced oral movements were increased by physostigmine and pilocarpine. Acute treatment with the cholinomimetic drugs alone produced "chewing", gaping and tongue protrusion (Rupniak et al. 1983). Chronic administration of pilocarpine and physostigmine also produced mouth movements (Rupniak et al. 1985)
 
The present study was conducted to obtain a more detailed behavioural and pharmacological description of the oral activities induced by muscarinic agonists. The frequencies of several individual oral responses following injection of different doses of pilocarpine were recorded. In addition, a simpler behavioural procedure was developed, in which the durations of periods of mouth movements were used to assess the actions of pilocarpine, oxotremorine, arecoline, and carbachol, and the antagonism of pilocarpine-induced mouth movements with scopolamine.
 
4. Yawning. A gradual opening of the mouth, followed by a retention of the open position, frequently accompanied by a lifting back of the head, and usually finished with a closure of the mouth more rapid than the original opening
 
 
 
Discussion
 
The muscarinic agonist pilocarpine produces dose-related increases in a number of mouth movements in the rat. Chewing and tongue protrusion, both of which are seen in normal control animals, are increased in frequency in a dose-dependent manner. Gaping, which rarely occurs in untreated animals, is also induced reliably by pilocarpine.
 
These results are consistent with the initial work of Rupniak et al. (1983), who demonstrated that 4.0 mg/kg pilocarpine increased mouth movements. In our study, a dose-related graduation of effects was observed, such that gaping was observed only at relatively high doses, while chewing and tongue protrusion were increased even at lower doses.
 
No consistent increase in yawning was observed in this study. Ushijima et al. (1984) previously reported that pilocarpine increased yawning in rats. Their peak dose for obtaining this response was 4.0 mg/kg, so our data showing increases in yawning in some rats at 2.5 and 5.0 mg/kg were consistent with the results of their study. However, even though the increase in yawning reported by these authors was statistically significant, the mean frequency of yawning (16 yawns per 90 mm) was rather low. The use of a different strain of rats, or other methodological differences, could account for the greater reliability of yawning in the Ushijima et al. (1984) study. One should note that in the study of Ushijima et al. (1984), yawns were counted as "total number of mouth openings" (p 297). It is possible that some of the "gaping" responses that we observed were scored as "yawning" in the Ushijima study. The lack of consistency of yawning as a response, and its relatively low frequency, suggest that yawning alone might not be useful as a cholinergic-related behaviour across a wide variety of conditions.
 
The antagonism of pilocarpine effects by scopolamine is consistent with these behavioural effects being attributable to cholinergic stimulation. The lack of effect of the quaternary compound methyl scopolamine as an antagonist demonstrates that the oral activities probably stem from central rather than peripheral effects, as this compound is a potent antagonist of peripheral muscarinic receptors but does not cross the blood-brain barrier. This conclusion is supported by the absence of significant mouth movements following carbachol administration. Rupniak et al. (1983) found that neostigmine, which does not cross the blood brain barrier, did not produce oral activities, while physostigmine did. In the present work, doses of scopolamine as low as 0.125 mg/kg resulted in an almost total blockade of mouth movements induced by 10.0 mg/kg pilocarpine. However doses of methyl scopolamine as high as 4.0 mg/kg yielded no reduction. The lack of methyl scopolamine effect dissociates mouth movements from peripheral effects such as salivation, which methyl scopolamine blocked in doses as low as 0.0625 mg/kg. Thus, the mouth movements are not elicited reflexly as a by-product of excessive salivation.
 
Oral activities such as chewing, tongue protrusion and gaping could be useful behavioural signs of central cholinomimetic actions of drugs. These activities could be used to augment information gained from observation of other cholinergic responses such as salivation. Oxotremorine and arecoline produce movements similar to those seen with pilocarpine. The observation of mouth movements can yield information on the in vivo potency, efficacy and time course of cholinomimetics. In addition, it introduces a new behavioural model which may enable researchers to further explore brain cholinergic mechanisms. It is interesting to speculate on the relationship between cholinergic-related oral activities and those seen during stimulant-induced stereotypes. Though both types of movements involve the mouth and tongue, unpublished observations from our laboratory indicated that there are some topographical differences between the two types of behaviours which would allow observers to discriminate between them. The rapid chewing movements seen with cholinominetics do not seem to predominate with apomorphine or amphetamine. Stereotypy is usually directed at objects, and can be quantified by measuring gnawing (Redgrave et al. 1982). By definition, the oral activities observed in the present study were not directed at any objects. In addition, these responses appear to be pharmacologically distinct, since anticholinergic drugs antagonize the cholinergic-related mouth movements, but enhance apomorphine stereotypy (Scheel-Krflger 1970). It is possible that both types of movements reflect a cholinergic-dopaminergic imbalance, and that the specific pattern of activities depends upon which way the balance is shifted. Further studies comparing the response topographics and pharmacological manipulation of responses to cholinergic and dopaminergic agonists would be useful to clarify these points.
 
The finding that cholinergic agonists enhance the frequency of some movements and induce abnormal movements poses interesting questions for those who advocate the use of cholinomimetics for the treatment of Alzheimer's Disease. Rupniak et al. (1983) suggested that the oral activity induced by neuroleptics reflects an acute dystonic reaction. It is possible that the movements induced by pilocarpine are a type of dystonia, perhaps related to the induction of Parkinsonian symptoms. Researchers investigating the effects of cholinomimetics on memory in aged subjects should also carefully examine their patients for dystonic reactions