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Yawning: its cycle, its role
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Le bâillement : de l'éthologie à la médecine clinique
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La parakinésie brachiale oscitante
Yawning: its cycle, its role
Warum gähnen wir ?
 
Fetal yawning assessed by 3D and 4D sonography
Le bâillement foetal
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mystery of yawning 

 

 

 

 

 

 

 

 

 

 

mise à jour du
3 janvier 2014
Behav Brain Res
1990;36(1-2):65-72
 Yawning behavior in male rats is associated with decreases in in vivo DOPAC efflux from the caudate nucleus.
 
Laping NJ, Ramirez VD.
 
Department of Physiology and Biophysiology, University of Illinois, Urbana

Chat-logomini

-Laping NJ, Ramirez VD Prolactin-induced yawning behavior requires an intact nigro-striatal dopamine system Pharmacol Biochem Behav 1988;29(1):59-62
-Laping NJ, Ramirez VD Prolactin induces yawning and the stretching yawning syndrome in young adulte male rats. Hormones & Behavior 1986;20:49-59
-Laping NJ, Ramirez VD.Yawning behavior in male rats is associated with decreases in in vivo DOPAC efflux from the caudate nucleus. Behav Brain Res. 1990;36(1-2):65-72.
 
Abstract
 
Young adult male rats were implanted with a push-pull cannula aimed at the dorsal and rostral areas of the caudate nucleus. Perfusate samples were collected at two-minute intervals for approximately one hour and assayed for DOPAC concentrations. Simultaneously, yawning, penile erections and grooming behavior were recorded. Yawns were induced by systemic prolactin or apomorphine injections. While mean DOPAC efflux was elevated following prolactin (PRL) and apomorphine decreased mean DOPAC efflux as expected, yawns and penile erections induced by both compounds were associated with rapid momentary decreases in DOPAC efflux in these living animals. Although yawning was associated with significant decreases in DOPAC output, not every momentary DOPAC decrease was associated with a yawn, suggesting that the 'yawning generator' most likely requires additional inputs for the expression of a yawn.
 
INTRODUCTION
 
Yawning is a curious and still little understood behavior which is displayed in many vertebrate species. At least in humans it has been shown that neither oxygen nor carbon dioxide levels contribute to yawning rates. While the physiologic importance of yawning behavior is still not clear, it is nonetheless a discrete and easily quantifiable behavioral event that can be used as a model for understanding how various CNS structures interact to initiate and execute a behavior. Current models based on pharmacological experiments suggest that cholinergic systems, of which a subset is under dopaminergic inhibitory control, stimulate yawning. This is evident by the findings that yawning is induced by cholinomimetics as well as by low doses of dopamine (DA) agonists or DA agents which preferentially bind to DA autoreceptors and thus reduce DA transmission.
 
Further support for this model are findings that muscarinic antagonists block yawning induced by both classes of compounds. Previous studies including work in our own laboratory have revealed that low doses of the DA receptor agonist, apomorphine (APO), as well as low doses of the pituitary hormone prolactin (PRL), can induce yawning in young adult male rats. Both compounds induce yawning in a dose-dependent bell-shaped manner. Systemic administration of either agent at relatively low doses (50 #g/kg APO, 0.25 ~tg/kg PRL) induces yawning, whereas higher and much lower doses do not. A potentially important CNS site where APO and PRL can act to induce this behavior in the caudate nucleus (CN) since lesion studies of the nigrostriatal DA system, as well as local injections of APO or PRL into the CN, have profound effects on yawning behavior. Specifically, 6-hydroxydopamine (6-OHDA) lesions of the substantia nigra or the CN greatly reduce APO- and PRL-induced yawning, while local infusions of APO or PRL into the CN evoke yawning behavior. It should be noted, however, that yawning can also be induced by local injections of APO into the septum and the paraventricular nucleus, suggesting that in vivo DA activity in these areas may also be related to the display of yawning behavior.
 
In order to examine the relationship between this discrete behavioral event and rapid changes in dopaminergic activity, we have utilized a push-pull perfusion technique in which we collect samples at two-minute intervals with minimal perfusion artifacts. Since low extracellular concentrations of DA preclude consistent determination of in vivo DA release under these conditions, in the present experiments we examined 3,4-dihydroxyphenylacetic acid (DOPAC) output, as an index of DA metabolism. It has been shown that 80% of DA released is converted to DOPAC. Also, within our own laboratory several studies have indicated that with the push-pull perfusion technique, DOPAC effiux is a good indicator of DA release under normal physiological conditions, though under pharmacological conditions this may not be the case. The purpose of this study was to focus on the CN and examine the relationship between yawning behavior and the in vivo release of DOPAC from the CN of young adult male rats following low systemic injections of APO or PRL.
 
DISCUSSION
 
These experiments have demonstrated that yawning behavior and penile erections but not grooming behavior are associated with negative changes in DOPAC effiux in male rats injected with PRL or APO. While yawning can occur when mean levels of DOPAC output are high or low, the data analysis in terms of rapid changes in DOPAC efflux have shown that yawning events are associated with momentary decreases in DOPAC efflux. Interestingly, penile erections and DOPAC effiux changes follow the same pattern in animals receiving either PRL or APO. This is not entirely surprising as it has been shown that the same agents that induce yawning can induce penile erections as well, and the frequency of yawns has been positively correlated with the frequency of penile erections 15. Additional evidence for this relationship are the agonistic effects of testosterone and antagonistic effects of estrogen on yawning behavior. Perhaps the same CNS structures that are involved in yawning are also important in this particular aspect of male sexual function.
 
It should be noted that the use of DOPAC as an index of dopaminergic activity needs to be taken cautiously since DOPAC efflux is a function of both DA release, re-uptake and monoamine oxidase activity and under certain pharmacological conditions in vivo DA and DOPAC release rates, as determined by microdialysis, do not follow the same trends 36. However, similar responses between DA and DOPAC were observed following treatment with APO, or a specific D2 agonist, or via cholinergic stimulation. Moreover, since 80% of DA released is converted to DOPAC and we have previously observed that under push-pull perfusion conditions of stimulated DA release DOPAC release closely follows changes in DA output, we assume that determinations of DOPAC release under the present experimental conditions provide an index of increases or decreases in dopaminergic activity. While we are concerned whether DOPAC is truly an index of DA release, the interpretation of these results support the hypothesis generated by pharmacological experiments. The hypothesis that momentary lifting of dopaminergic inhibition of cholinergic neurons can induce yawning, is consistent with these results if DOPAC is an index of DA release.
 
However, arguments have been made that DOPAC decreases reflect increases in DA activity. This would indicate that yawning behavior requires DA release for its activation. Most evidence indicates that cholinergic activation is required for yawning behavior; it is then required that DA stimulate acetylcholine release. There is some evidence that this might be the case in some areas of the CN. The viability of either hypothesis will be shown when DA itself can be measured under this experimental paradigm. At any rate the negative decreases in DOPAC output were significant only when penile erections or yawns occur, regardless of the compound used to induce yawning behavior. Moreover, increased DOPAC output was only observed concomitant with grooming behavior. This also supports findings that grooming behavior is activated by DA activation.
 
Not every decrease in DOPAC efflux from the CN resulted in a yawn or a penile erection. This indicates that these behaviors require inputs from additional neuronal systems for their expression. The site or sites of integration for these behaviors most likely compute these additional signals with the information from the CN when activation of the yawning sequence is appropriate. Other CNS sites that are most likely required are the paraventricular nucleus of the hypothalamus and possibly the septum. For, not only do chemical lesions of the nigrostriatal DA system eliminate PRL- and APO-induced yawning, but lesions of the paraventricular nucleus block APOand oxytocin-induced yawning as well~. In addition, local infusions of APO into the septum induce yawning. It would be interesting to discover the common pathway or site to which these nuclei project in the yawning sequence. Of importance is the observation that PRLinduced yawns occur when the mean DOPAC levels were higher than preinjection levels, while APO-induced yawns occur when the mean DOPAC levels were significantly lower than preinjection levels. Regardless, the yawning events under both conditions occurred during momentary but clear decreases in DOPAC efflux. The differences in mean DOPAC levels and latencies at which these behaviors occurred suggest different mechanisms for APO- and PRL-induced yawns. The APO effect is more easily explained by the activation of DA autoreceptors which can decrease DA release and synthesis and thus affect DOPAC efflux. This decrease in DA transmission would lift the inhibitory tonus on the cholinergic neurons and in this way increase the probability that a yawn occurs. PRL on the other hand has been shown to increase DA release. In the present experiments PRLinduced yawns occurred during heightened DOPAC levels, probably reflecting higher DA release rate. It has been shown that a population of cholinergic neurons exist in the dorsal region of the CN that can be stimulated by DA. Therefore, it is reasonable to postulate that activation of DA terminals controlling this sub-population of cholinergic neurons could occur following low doses of PRL.