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PubMed1989

Occurrence of yawning and decrease of prolactin levels via stimulation of dopamine D2-receptors after administration of SND 919 in rats.

SND 919 [S)-2-amino-4,5,6,7-tetrahydro-6-propylamino-benzothiazole) is expected to have a potent and selective dopamine D2-receptor agonistic activity. From this information, the present study was performed to investigate effects of SND 919 on yawning behavior and prolactin secretion in rats. Subcutaneous injections of SND 919 (25-500 micrograms/kg, s.c.) elicited yawning responses. Its dose-response curve was bell-shaped with maximal effects at a dose of 100 micrograms/kg. Yawning behavior was also evoked by the putative dopamine autoreceptor agonists, talipexole (6-allyl-2-amino-5,6,7,8-tetrahydro-4H-thiazolo [4,5-d]azepine) (B-HT 920) (5-100 micrograms/kg, s.c.) and (+)-3-PPP ((+)-3-(3-hydroxyphenyl)-N-n-propylpiperidine) (5-15 mg/kg, s.c.). The yawning induced by SND 919 (100 micrograms/kg, s.c.) as well as talipexole (25 micrograms/kg, s.c.) was inhibited by pretreatment with dopamine D2-receptor antagonists such as spiperone (0.5 mg/kg, i.p.) and YM-09151-2 (cis-N-(1-benzyl-2-methylpyrrolidin-3-yl)-5-chloro-2-methoxy-4-met hylamino- benzamide) (0.1 mg/kg, i.p.), or the muscarinic receptor antagonist, scopolamine (0.5 mg/kg, i.p.). However, the yawning was not affected by the dopamine D1-receptor antagonist, SCH 23390 (R(+)-8-chloro-2,3,4,5-tetrahydro-3-methyl-5-phenyl-1H-3-benzazepine-7-o l) (0.5 mg/kg, i.p.). Stereotypy such as licking and biting was not observed following the administration of SND 919, talipexole and (+)-3-PPP. Administration of SND 919, talipexole or (+)-3-PPP in respective yawn-inducing doses caused a reduction in both the basal prolactin levels and the alpha-methyl-p-tyrosine-induced hyperprolactinemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Effects of adenosine agents on apomorphine-induced yawning in rats.

In the present work, adenosine agonists and antagonists on apomorphine-induced yawning in rats was investigated. Subcutaneous (SC) injection of apomorphine (0.02, 0.05 and 0.1 mg/kg) induced dose-dependent yawning behaviour in rats. Intracerebroventricular (ICV) administration of different doses of the drug (1, 3, 5 micrograms/rat) also caused a dose-related yawning. ICV administration of the adenosine receptor agonists 5-N-ethylcarboxamidoadenosine (NECA) and N6-cyclohexyladenosine (CHA) decreased apomorphine-induced yawning. The response induced by the adenosine agonists was reduced by 8-phenyladenosine (8-PT) pretreatment. The yawning induced by SC and ICV administration of apomorphine was decreased by ICV or IP injection of theophylline, respectively. It is concluded that at least A1 adenosine receptors may exert negative influence on the apomorphine-induced yawning. However, the exact mechanism(s) of adenosine receptors in this behaviour remain to be established.

Adenosine↗
PubMed1987

Permissive role of D-1 receptor stimulation by endogenous dopamine for the expression of postsynaptic D-2-mediated behavioural responses. Yawning in rats.

Low doses of BHT 920, LY 171555 and (+)3PPP, three dopamine agonists selective for D-2 receptors, induced yawning in rats. This effect was reduced by the selective D-1 antagonist SCH 23390 but the antagonism did not exceed a 50% reduction from the control values. In contrast, the selective D-2 antagonist (-)sulpiride completely abolished agonist-induced yawning. A 6 h reserpine pretreatment (5 mg/kg i.p.), which depletes brain dopamine (DA) by about 95%, reduced agonist-induced yawning by an extent similar to SCH 23390; in the reserpinized rats, SCH 23390 completely lost the property of blocking agonist-induced yawning while (-)sulpiride retained it. Two 5HT receptor antagonist, ketanserin and metergoline failed to influence agonist-induced yawning. The reportedly selective D-1 agonist, SKF 38393, failed to induce yawning in normal rats as well as in rats pretreated with reserpine 6 or 16 h earlier. If one excludes that SCH 23390 and the D-2 agonists interact with the same DA-receptors, the data are consistent with the possibility that stimulation of D-1 receptors by endogenous DA plays a permissive-facilitatory role for the behavioural expression of D-2 receptor activation.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1988

Prolactin-induced yawning behavior requires an intact nigro-striatal dopamine system.

Herein, we evaluate the importance of the nigro-striatal dopamine system in prolactin-, apomorphine-, and physostigmine-induced yawning behavior. Bilateral 6-OH-dopamine lesions of the substantia nigra were performed on male rats (2-4 months old). The lesioned as well as control rats were injected with either physiological saline, physostigmine (200 micrograms/kg), apomorphine (50 micrograms/kg), or ovine prolactin (0.25 micrograms/kg) 72 hours after the surgical procedure. The results show that bilateral lesions of the substantia nigra did not affect physostigmine-induced yawning whereas both apomorphine- and prolactin-induced yawning were reduced by the lesion. Following the observation period the caudate nuclei were removed and analyzed for dopamine (DA) and dihydroxyphenylacetic acid (DOPAC) content. The lesions reduced DA and DOPAC content in all treatment groups compared to the respective intact groups. Also, both DA and DOPAC concentrations were lower in the intact apomorphine and prolactin treated groups compared to intact saline controls, at times that were temporally related to the display of yawning behavior suggesting a decrease in dopamine activity following apomorphine and prolactin treatment. Interestingly, DA and DOPAC concentrations were higher in the lesioned apomorphine group compared to lesioned saline controls; however, in the lesioned prolactin group only the DA concentrations were higher when compared to lesioned saline controls. These results indicate that prolactin- and apomorphine-induced yawning require an intact nigro-striatal dopamine system and that these substances induce yawning by different mechanisms.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1989

GABAergic modulation of yawning behavior.

The hypothetical modulation by GABAergic neurons of yawning behavior in the rat was explored with GABA-active drugs. Gamma-acetylenic-GABA, a specific inhibitor of GABA-T, increases yawning frequency when injected at a dose of 7 mg/kg. Baclofen, a GABAB agonist (3 mg/kg), inhibits yawning completely; GABA antagonists, bicuculline and picrotoxin, at subconvulsant doses, also decrease yawning. All drugs were injected intraperitoneally with the exception of apomorphine, which was injected subcutaneously. It is suggested that GABAB receptors play a role in yawning behavior by modulating ACh release, and that GABAA receptors may modify yawning frequency by modulating inhibitory influences on ACh neurons.

4-Aminobutyrate Transaminase↗
PubMed1995

Atropine increases pilocarpine-induced yawning behavior in paradoxical sleep deprived rats.

Paradoxical sleep (PS) deprivation has been suggested to induce supersensitivity of postsynaptic dopamine (DA) receptors and subsensitivity of acetylcholine (ACh) receptors. Yawning behavior is reduced after PS deprivation and is believed to result from an interaction between ACh and DA systems. Concomitant treatment of PS deprived animals with DA agonists reverses PS deprivation effects on stereotypy and aggressiveness. To examine this possibility on yawning behavior, rats were treated, during the deprivation period, with atropine, methamphetamine, haloperidol or distilled water. Following PS deprivation, rats were injected with apomorphine or pilocarpine and number of yawns was recorded. Atropine increased yawning of PS deprived rats induced by pilocarpine, but not by apomorphine. Treatment with methamphetamine and haloperidol did not change PS deprivation effect on pilocarpine- and apomorphine-induced yawning. The data suggest that reversal of PS deprivation-induced yawning inhibition is mediated distinctly by both acetylcholine and dopamine systems.

Animals↗
PubMed1996

Involvement of catecholamine receptor activities in modulating the incidence of yawning in rats.

Possible involvement of catecholamine receptor activities in modulating the incidence of yawning, which involves activation of dopaminergic-cholinergic linked neuronal mechanism, was investigated in rats. Subcutaneous injection of talipexole (B-HT 920), a selective dopamine D2-receptor-agonist, elicited yawning behavior. This behavior was increased by prazosin and bunazosin, alpha 1-adrenoceptor antagonists, and by pindolol, a beta-adrenoceptor antagonist. The yawning induced by physostigmine, an anticholinesterase agent, and pilocarpine, a direct muscarinic receptor agonist, was increased by pindolol, but was unaffected by prazosin and bunazosin. In addition, the yawning induced by the dopaminergic agonists, but not by the cholinergic agonists, was markedly suppressed by ST587, an alpha 1-adrenoceptor agonist. All the yawning responses to dopaminergic and cholinergic agents were reduced not only by scopolamine, a muscarinic receptor antagonist, but also by idazoxan, rauwolscine, and yohimbine, alpha 2-adrenoceptor antagonists. The results suggest that catecholamine receptor activities seem to play different roles in inhibitory modulation of the occurrence of yawning caused by dopaminergic and cholinergic stimulation.

Adrenergic alpha-1 Receptor Agonists↗
PubMed1996

The new muscarinic M1-receptor agonist YM796 evokes yawning and increases oxytocin secretion from the posterior pituitary gland in rats.

The present experiments were performed to examine the effects of a new muscarinic M1-receptor agonist, (-)-YM796 ((-)-S-2,8-dimethyl-3-methylene-1-oxa-8-azaspiro[4.5]decane L-tartrate monohydrate), on yawning and oxytocin secretion from the posterior pituitary gland in rats YM796, at doses of 2.5-50 mg/kg (SC), elicited yawning. The yawning response was markedly increased by pretreatment with a beta-adrenoceptor antagonist, pindolol (20 mg/kg, IP), which per se did not elicit yawning. The yawning induced by YM796 (10 mg/kg, SC) in combination with pindolol (20 mg/kg, IP) was inhibited by scopolamine (0.5 mg/kg, SC), a muscarinic receptor antagonist, and pirenzcpine (300 micrograms/ rat, ICV) and EEDQ (N-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline) (5 mg/kg, IP), muscarinic M1-receptor antagonists, but not by spiperone (0.5 mg/kg, SC), a dopamine D2-receptor antagonist, 4-DAMP (4-diphenylacetoxy-N-methylpiperidine methiodide) (100 micrograms/rat, ICV), a muscarinic M3-receptor antagonist, and [d(CH2)5, Tyr(Mc)2, Orn8]-vasotocin (100 ng/rat, ICV), an oxytocin receptor antagonist. YM796 at 2.5-50 mg/kg (SC) did not exert an action on prolactin levels but increased oxytocin secretion from the posterior pituitary gland in rats. This augmentation of oxytocin secretion by YM796 was inhibited by scopolamine (0.5 mg/kg, SC) and pirenzepine (3 mg/kg, SC), but not by mecamylamine (1 mg/kg, IP), a nicotinic receptor antagonist. The present findings obtained with YM796 suggest that the muscarinic M2-receptor stimulation participates in causing yawning behavior and oxytocin secretion in rats.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

Influence of modified casomorphins on yawning behavior of rats.

Apomorphine-induced yawning was completely suppressed in animals treated with 5 nmol [D-Pro4]casomorphin (CM) (ICV), 10 nmol [D-Phe3]CM (ICV) or 10 nmol [D-Pip4]CM (ICV). The apomorphine-induced yawning was also decreased, by des-Tyr analogs, but only by about 50%. Physostigmine (0.15 mg/kg, IP) induced yawning. The physostigmine-induced yawning was suppressed by 5 nmol [D-Pro4]CM and 10 nmol [D-Phe3]CM. Both [des-Tyr-D-Phe3]CM and [des-Tyr-D-Pip4]CM were without effect, whereas [des-Tyr-D-Pro4]CM increased significantly the physostigmine-induced yawning. The results suggest that dopaminergic transmission can be modulated by beta-casomorphin derivatives, thus resulting in a decrease in yawning. In the case of the des-tyrosine derivatives, we can assume a dopaminergic modulation, too. An increase in serotonergic activity might be supposed for [des-Tyr-D-Pro4]CM.

Amino Acid Sequence↗
PubMedDate not supplied

Treatment with dexamethasone alters yawning behavior induced by cholinergic but not dopaminergic agonist.

Because stressful manipulations have been reported to modify drug-induced yawning, the present study investigated the effects of single and repeated treatment with a synthetic glucocorticoid, dexamethasone (DEXA) on apomorphine- and pilocarpine-induced yawning in male rats. Neither single nor repeated treatment with DEXA altered apomorphine-induced yawning. Single administration of DEXA, however, resulted in an increased number of yawns induced by pilocarpine. Conversely, repeated administration of DEXA led to a decreased number of yawns induced by pilocarpine. In conclusion, the present findings show that dopaminergic and cholinergic are distinctly altered by DEXA, in terms of yawning behavior when animals received DEXA.

Animals↗
PubMed2004

[The phylogeny, ethology and nosology of yawning].

Charles Darwin would have said that yawning was a useless piece of physiology. If so, then how should the survival of this very stereotyped behavior among the poikilothermal and homoeothermic vertebrates, from the basic brained reptiles to human primates, whether in the air, on the land or in the sea be understand? This issue of the ethnological, neurophysiologic and neuropsychological literature depicts yawning as being associated with an alternation of "awake-sleep" rhythms, sexuality, and nutrition, where it appears as a reference behavior of the mechanisms stimulating the state of vigilance. In pharmacology, yawning is used as an indicator of dopamine-ocytocinergic pathway activity, but in the Parkinson patient the neurologist sees it as an expression of therapeutic dopaminergic activity. J.M. Charcot and his school considered yawning as a clinical sign, long since forgotten. However, many patients complain about excessive yawning. Iatrogenic causes are the most frequent and can be found among many neurological diseases: vasovagal syncope, migraine, epilepsy, hypophyseal tumor, or stroke. Our ability to achieve motor and emotional behavior in resonance with others is deeply rooted in hominid evolution, and probably explains the strange phenomenon of contagious yawning.

Animals↗
PubMed2002

Grooming and yawning trace adjustment to unfamiliar environments in laboratory Sprague-Dawley rats (Rattus norvegicus).

The authors studied grooming and yawning caused by mild stress in laboratory Sprague-Dawley rats (Rattus norvegicus). Two groups received 3 and 6 sequences of 5 foot shocks at random intervals (RI) and fixed intervals (FI), respectively. A 3rd group was not shocked (NS). The groups were exposed for 60 min twice. Grooming did not differ among groups, but yawning diminished with RI. Yawning increased and grooming decreased with the 2nd exposure, except in RI in which grooming increased. In NS and FI, grooming prevailed during the first 20 and 30 min, respectively, whereas yawning dominated the remainder of the time. In RI, grooming occurred more than yawning. An upward shift on this scale causes grooming to substitute yawning, whereas a downward shift causes the reverse effect.

Animals↗
PubMed2001

Primary yawning headache.

To describe three patients with recurrent severe paroxysmal headache precipitated by yawning. Pain elicited by yawning is a well-recognized clinical phenomenon in patients with cranial neuralgia, temporomandibular joint dysfunction syndrome and Eagle syndrome. Clinical history, neurological and oral examinations, brain magnetic resonance imaging (MRI), cranial nerve electrophysiological testing and skull X-rays are reported. In all the patients pain was induced by yawning; in the third patient pain was also triggered by eructation. None had history of migraine. Facial gestures and forceful opening of the mouth did not reproduce the pain. The first patient had retroauricular pain, simvastatin-induced myopathy and subclinical axonal peripheral neuropathy; the second patient had a post-viral benign sensory neuropathy; and the third had retroauricular and facial pain and no underlying neurological illness. Cranial nerve testing and MRI of the brain were normal except for a coincidentally found pituitary adenoma on the first patient. Headache or cranial pain with yawning may occur in patients with no apparent cause (primary yawning headache). It is a chronic, benign condition that requires no specific treatment but needs to be distinguished from secondary yawning headache, of greater clinical relevance.

Adult↗
PubMed1989

Is yawning an arousal defense reflex?

Despite the fact that yawning is a reality of everyday life, its study is not included in the curriculum of medical schools, and most medical textbooks barely mention its existence. Two factors may help to explain this puzzling situation: (a) yawning's borderline position between psychology and neurology, and (b) researchers' lack of understanding as to why people yawn. After review of the literature and personal observation, it is concluded that yawning is a complex arousal defense reflex located in the reticular brainstem with a peripheral and central arche, whose aim is to reverse brain hypoxia. Yawning occurs with loss of interest (boredom) and may or may not be associated with fatigue. By reversing drowsiness, yawning avoids a decreased concentration capacity resulting from borderline hypoxia. It is hoped that this article will stimulate further research on the phenomenon.

Arousal↗
PubMed1996

Dopamine agonists increase nitric oxide production in the paraventricular nucleus of the hypothalamus: correlation with penile erection and yawning.

A low dose of apomorphine (80 micrograms/kg s.c.), a mixed D1/D2 agonist that induces penile erection and yawning, increased the concentration of NO2-from 1.12 +/- 0.45 microM to 3.8 +/- 0.75 microM and NO3-from 5.53 +/- 0.82 to 11.25 +/- 2.30 microM in the dialysate collected from the paraventricular nucleus of the hypothalamus of male rats by in vivo microdialysis. The NO2-concentration was also increased by LY 171555 (50 micrograms/kg s.c.), a D2 agonist that induces penile erection and yawning, but not by SKF 38393 (5 mg/kg s.c.), a D1 agonist with no effect on these responses. Conversely, apomorphine's effect on NO2-was prevented by haloperidol (0.5 mg/kg i.p.), a mixed D1/D2 antagonist and L-sulpiride (25 mg/kg i.p.), a D2 antagonist, but not by the D1 agonist SCH 23390 (50 micrograms/kg s.c.), although all three compounds prevented penile erection and yawning. The apomorphine effect on NO2-, penile erection and yawning was also prevented by the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester (200 micrograms i.c.v.). The nitric oxide scavenger haemoglobin (200 micrograms i.c.v.) also prevented the NO2-increase, but was ineffective against penile erection and yawning. In contrast, the oxytocin antagonist d(CH2)5Tyr(Me)-Orn8-vasotocin (1 microgram i.c.v.) and the guanylate cyclase inhibitor methylene blue (300 micrograms i.c.v.) had no effect on the NO2-increase, but did prevent the behavioural responses. We infer from this that dopamine agonists induce penile erection and yawning by acting on D2 receptors that increase nitric oxide synthase activity in the cell bodies of paraventricular oxytocinergic neurons projecting to extra-hypothalamic brain areas.

Animals↗
PubMed2007

Do your patients suffer from excessive yawning?

OBJECTIVE: Yawning has been described in relation to drugs such as serotonin reuptake inhibitors, levodopa, dopamine agonists, MAO B inhibitor, morphine, methadone, buprenorphine, dextromethorphan, benzodiazepine, lidocaine, and flecaine. This is a report of two patients, on long-term escitalopram therapy (more than 8 weeks) with stable dosing, who presented excessive yawning. Escitalopram is widely used in major depressive disorder and generalized anxiety disorder. METHOD: A clinical description of two cases. RESULTS: Two females (62 and 59 years old, respectively) developed excessive daytime yawning. It was not associated with sedation or a feeling of needing sleep. The dosage was reduced and yawning disappeared some hours later. The patients' depression did not recur. CONCLUSION: Yawning has been described in relation to different selective serotonin reuptake inhibitors and remitted following their discontinuation; it is interesting that the reported yawning in these two cases disappeared with the reduction of dosage, rather than the interruption of treatment.

Antidepressive Agents, Second-Generation↗
PubMed1991

Chronic D1-receptor blockade: effects on D2-receptor agonist-induced yawning in rats.

The effects of chronic treatment with the selective D1 dopamine receptor antagonist SCH 23390 (0.25 mg kg-1 s.c. twice daily for 18 days, 4 days withdrawal on yawning induced by the D2-receptor agonist quinpirole has been investigated. Low doses of quinpirole (20 and 50 micrograms kg-1 s.c.) induced dose-related yawning behaviour in rats. The yawning response to quinpirole was not significantly different in the presence or absence of SCH 23390 pretreatment. However, chronic treatment with SCH 23390 alone significantly suppressed yawning behaviour. The results suggest that chronic D1-receptor blockade with SCH 23390 does not alter the function of the D2-receptor population mediating yawning behaviour. However, after withdrawal it may result in behavioural activation as seen by suppression of yawning behaviour in the present study.

Animals↗
PubMed1993

Effect of scopolamine on spontaneous yawning in men.

The effect of scopolamine hydrobromide (0.4 mg s.c.) on spontaneous yawning was studied in 16 male volunteers in a double-blind study. Scopolamine (or placebo) was given 60 min before (-60 min) placebo (physiological saline s.c.) (time 0 min) and yawning monitored from -15 to +60 min by recording displacement of the lower jaw and storing the traces on diskettes. After placebo, the number of yawns was 5.3 +/- 1.4 (means +/- SE) and after scopolamine pretreatment 4.3 +/- 1.6 (p = NS). Drowsiness was assessed with the Stanford Sleepiness Scale and the Analog Sleepiness Scale at -15, 0, +20, +40, +60 min. There was no significant correlation between total sleepiness scores (area under the curve, 0 min to +60 min), peak sleepiness score or peak increment in sleepiness score and number of yawns on either scale. These data suggest that (a) spontaneous yawning in man is not mediated by a central muscarinic cholinergic link, and (b) the assumed relationship between drowsiness and yawning remains to be verified experimentally.

Adult↗