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At least 19 recordsLinked to original sources
PubMed1986

Prolactin induces yawning and the stretch-yawning syndrome in young adult male rats.

Herein we report that subcutaneous injection of low doses of ovine prolactin (oPRL) induce yawning in young adult male rats. The most effective dose of oPRL in evoking yawning was 0.25 microgram/kg body weight (5.2 yawns/60 min at 1000 hr vs 0.3 in control animals). Doses of 0.025, 0.05, 2.5, 25, and 250 micrograms/kg were less effective. Interestingly, yawning in response to oPRL changes over the course of one circadian cycle with highest frequency at 1600 hr (11 yawns/80 min vs 2 yawns/80 min in animals injected with boiled oPRL). The onset of yawning in most oPRL-treated rats began approximately 40 min after oPRL injection, whereas with apomorphine the latency to the response was about 10 min. These results indicate that oPRL in addition to other hypophysial peptides such as ACTH and MSH can stimulate yawning. It is proposed that PRL after initial activation of the nigrostriatal dopamine system secondarily induces yawning by inhibition of this system via an autoreceptor-mediated negative feedback mechanism. This may explain the long latency to the response.

Animals↗
PubMed1989

SKF 38393 potentiates yawning induced by LY 171555: further evidence against the autoreceptor hypothesis of yawning.

The effect of concurrent D-1 receptor stimulation by SKF 38393 on the expression of yawning elicited by D-2 receptor stimulation with LY 171555 was studied in the rat. A low dose of SKF 38393 (2.5 mg/kg SC), while failed to elicit yawning, potentiated the effectiveness of LY 171555 in eliciting yawning at all the doses tested (12.5, 25 and 50 micrograms/kg SC) and this effect was abolished by SCH 23390 (0.012 mg/kg SC). The results indicate that in analogy with typical post-synaptic dopaminergic effects (hypermotility-stereotypy), yawning elicited by a D-2 agonist is facilitated by concurrent stimulation of D-1 receptors and therefore is consistent with previous evidence that yawning in response to a D-2 agonist is not mediated by autoreceptors.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1985

Characteristics of yawning behavior induced by apomorphine, physostigmine and pilocarpine.

Apomorphine, a dopamine receptor agonist, physostigmine, an anticholinesterase agent and pilocarpine, a cholinergic receptor agonist, produced yawning in rats, with the most effective doses being 0.25 mg/kg, 0.2 mg/kg and 4 mg/kg, respectively. The yawning induced by these drugs is characterized by differences in direction of head moving, tongue protruding and duration of the yawn. The apomorphine-induced yawn was characterized by a slow and wide opening of the mouth with the head moving mainly downward and with a marked protrusion of the tongue. The apomorphine-induced yawn was 3.6 sec in duration. Physostigmine elicited a similar yawn to that seen with apomorphine, except for moving of the head in the upward direction. The pilocarpine-induced yawn was characterized by the head moving forward with a high frequency but without tongue protrusion and lasted 1.8 sec. The frequency of physiological yawning was low, but the behavioral posture was almost similar to that of physostigmine-induced yawning. The characteristics of yawns induced by these agents were unchanged at all doses of the drugs. Different doses altered the frequency of yawning. After pretreatment with mecamylamine, the apomorphine- and physostigmine-induced tongue protruding was inhibited and the duration of the yawning induced by the both drugs was shortened. The results suggest that the behavioral features of yawning induced by apomorphine, physostigmine and pilocarpine differ from one another, and that physiological yawning as well as physostigmine-induced yawning may be mediated by endogenous acetylcholine which stimulates both muscarinic and nicotinic receptors.

Animals↗
PubMed1989

Interactions of drugs acting on central dopamine receptors and cholinoceptors on yawning responses in the rat induced by apomorphine, bromocriptine or physostigmine.

1. Yawning was induced by subcutaneous (s.c.) injection of low doses of apomorphine to rats. This effect decreased with increasing doses of the drug. 2. Intraperitoneal (i.p.) pretreatment of animals with sulpiride (D2-receptor blocker) reduced the frequency of the yawns induced by apomorphine, while SCH 23390 (D1-receptor blocker, s.c.) pretreatment increased the small number of yawns which was induced by higher doses of apomorphine. Administration of SCH 23390 alone to rats also produced a low degree of yawning. 3. Apomorphine-induced yawning was decreased in animals treated with SK&F 38393 (D1-agonist, i.p.), atropine (i.p.) or theophylline (i.p.). 4. Intraperitoneal injection of bromocriptine (D2-agonist) in rats also induced dose-dependent yawning. The effect was decreased in animals pretreated with sulpiride, while SCH 23390 pretreatment did not change bromocriptine-induced yawning significantly. Pretreatment of animals with SK&F 38393, atropine or theophylline reduced the number of yawns induced by bromocriptine. 5. Physostigmine (i.p.) but not neostigmine (i.p.) also induced yawning. The effect was antagonized by atropine or theophylline but not by sulpiride. Administration of SK&F 38393 decreased yawning induced by physostigmine. This inhibitory influence of SK&F 38393 was reduced by SCH 23390 in pretreated animals. Treatment of animals with SCH 23390 or bromocriptine increased the frequency of yawns induced by physostigmine. 6. It is concluded that D2-receptor activation elicits yawning through influence on cholinergic mechanisms, whereas D1-receptor stimulation decreases yawning behaviour by a negative influence on the cholinergic system.

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

Multifocal sites of action involved in dopaminergic-cholinergic neuronal interactions in yawning.

Bromocriptine (BRC), a dopamine D-2 receptor agonist, physostigmine, an anticholinesterase agent and pilocarpine, a muscarinic cholinergic receptor agonist, produced yawning in rats, with the most effective doses being 2.5 mg/kg, 0.2 mg/kg and 4 mg/kg, respectively. BRC-induced yawning was inhibited by high doses of SK&F38393 (5 and 10 mg/kg), a selective D-1 receptor agonist. BRC or SK&F38393 alone did not induced stereotyped behaviors. However, when BRC was administered after SK&F38393 (5.0 and 10 mg/kg), stereotyped behaviors occurred; i.e., mainly sniffing at 2.5 and 5.0 mg/kg BRC, and mainly licking and biting 10 and 20 mg/kg BRC. A high dose of apomorphine (4 mg/kg IP) completely inhibited physostigmine-induced yawning (physostigmine yawning) but did not affect pilocarpine-induced yawning (pilocarpine yawning). BRC (2.5 20 mg/kg) increased physostigmine yawning in an additive fashion. Pilocarpine yawning was completely blocked by either low or high doses of BRC. The inhibitory effect of BRC on pilocarpine yawning was reversed by sulpiride (20 mg/kg). alpha-Methyl-p-tyrosine (alpha-MPT; 100 and 200 mg/kg) did not affect physostigmine yawning but diminished pilocarpine yawning. Furthermore, physostigmine (0.2 mg/kg) inhibited apomorphine (4.0 mg/kg)-induced hyperlocomotion and sniffing but not licking and biting, whereas pilocarpine (4.0 mg/kg) had the opposite effect.(ABSTRACT TRUNCATED AT 250 WORDS)

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1984

Modification of apomorphine-, physostigmine- and pilocarpine-induced yawning after long-term treatment with neuroleptic or cholinergic agents.

Chronic treatment with haloperidol, physostigmine and scopolamine exerted different effects on the frequency of yawning induced by apomorphine (0.25 mg/kg, i.p.), physostigmine (0.2 mg/kg, i.p.) and pilocarpine (4 mg/kg, i.p.) as compared with chronic treatment with saline. Haloperidol decreased the apomorphine- and physostigmine-induced yawning but not the pilocarpine-induced yawning. Physostigmine reduced only the pilocarpine-induced yawning without affecting the apomorphine- and physostigmine-induced yawning. However, physostigmine showed the most rapid onset- and peak-time of yawning induced by a high dose of physostigmine (0.75 mg/kg, i.p.) as well as that of pilocarpine (8 mg/kg, i.p.), and potentiated apomorphine (1 mg/kg, i.p.)-induced stereotypy, as compared with that observed in the saline group. Scopolamine potentiated the physostigmine- and pilocarpine-induced yawning but not the apomorphine-induced yawning. A single pretreatment with scopolamine (0.5 mg/kg, i.p.), however, depressed these yawning responses. The results suggest that yawning induced by physostigmine, but not by pilocarpine, may be modified by long-term treatment with haloperidol. The stereotypy mediated by the postsynaptic dopaminergic system, but not the yawning mediated by the presynaptic system, may be altered by chronic treatment with physostigmine, while long-term treatment with scopolamine seems to produce a supersensitivity to cholinergic receptors.

Animals↗
PubMed1990

Yawning induced by apomorphine, physostigmine or pilocarpine is potentiated by dihydropyridine calcium channel blockers.

Previous studies have shown that dihydropyridine (DHP) calcium channel blockers can potentiate yawning induced by apomorphine in rats. The present study was undertaken to examine whether or not this interaction was seen with other compounds that induce yawning or if it represented a specific interaction with dopaminergic mechanisms. Yawning induced by apomorphine (40 micrograms/kg SC), physostigmine (50 micrograms/kg SC) or pilocarpine (1 mg/kg SC) was dose-dependently potentiated by the DHP calcium channel blocker nifedipine (1.25-10 mg/kg IP). Nimodipine (1.25-5 mg/kg IP) and nitrendipine (1.25-5 mg/kg IP) also significantly increased the yawning response. The DHP calcium channel blockers alone induced only a low incidence of yawning. The effects of nifedipine on physostigmine-induced yawning were reversed by the DHP calcium channel activator BAY K 8644 which also inhibited yawning induced by physostigmine (100 micrograms/kg SC) and pilocarpine (2 mg/kg SC). In contrast to the DHP compounds, diltiazem (2.5-10 mg/kg IP) and verapamil (2.5-10 mg/kg IP) failed to potentiate yawning. Sulpiride (10 mg/kg SC) antagonised the nifedipine potentiation of apomorphine-induced yawning but not that of physostigmine-induced yawning; atropine (2.5 mg/kg SC) antagonised both effects. These results support the hypothesis that this effect of dihydropyridine compounds is not dependent on, nor mediated through, dopaminergic mechanisms.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1987

Yawning: no effect of 3-5% CO2, 100% O2, and exercise.

Using human college-age subjects, the present study tested the commonly cited but previously untested hypothesis that yawning is facilitated by higher than normal levels of CO2 or lower than normal levels of O2 in the blood by comparing the effect on yawning of breathing 100% O2 and gas mixtures with higher than normal levels of CO2 (3 or 5%) with compressed air, the control condition. If yawning is a response to heightened blood CO2, the CO2 mixtures should increase yawning rate and/or duration. If low blood O2 produced yawning, breathing 100% O2 should inhibit yawning. The CO2/O2 hypothesis was rejected because breathing neither pure O2 nor gases high in CO2 had a significant effect on yawning although both increased breathing rate. A second study found that exercise sufficient to double breathing rate had no effect on yawning. The two studies suggest that yawning does not serve a primary respiratory function and that yawning and breathing are triggered by different internal states and are controlled by separate mechanisms.

Adolescent↗
PubMed1989

Involvement of central beta-adrenoceptors in the regulation of yawning responses.

A behavioral study was performed in an attempt to understand the role of central beta-adrenoceptors in yawning in rats. Yawning was evoked by apomorphine and piribedil, mixed dopamine D1/D2-receptor agonists, but not by SK&F 38393 [1-phenyl-2,3,4,5-tetrahydro-(1H)-3-benzazepine-7,8-diol], a dopamine D1-receptor agonist. The apomorphine-induced yawning was increased by pindolol, propranolol, indenolol, alprenolol and bukumolol which block the central beta-adrenoceptors, but not by the peripheral beta-adrenoceptor antagonists, carteolol and atenolol. These beta-adrenoceptor antagonists given alone did not elicit yawning. Conversely, the yawning was inhibited by salbutamol, a beta-adrenoceptor agonist, without being affected by prazosin, an alpha-adrenoceptor antagonist. The combined administration of SK&F 38393 and the beta-adrenoceptor antagonists did not induce yawning. The yawning elicited by either apomorphine or piribedil in combination with pindolol was suppressed by spiperone and YM-09151-2 [cis-N-(1-benzyl-2-methyl-pyrrolidin-3-yl)-5- chloro-2-methoxy-4-methylamino-benzamide], dopamine D2-receptor antagonists, and scopolamine, a muscarinic receptor antagonist, but not by SCH 23390 [R(+)-8-chloro-2,3,4,5-tetrahydro-3-methyl-5-phenyl-1H-3- benzazepine-7-ol], a dopamine D1-receptor antagonist. Physostigmine or pilocarpine induced yawning, which was also enhanced by pindolol and propranolol. This enhanced yawning was inhibited by scopolamine, but not by spiperone, YM-09151-2 and SCH 23390.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1986

Involvement of septal and striatal dopamine D-2 receptors in yawning behavior in rats.

A behavioral study was performed in an attempt to understand the neuronal mechanisms involved in yawning behavior in rats. Subcutaneous injections of low doses of apomorphine (0.05-0.25 mg/kg) or piribedil (0.2-1.0 mg/kg), which preferentially activate presynaptic dopamine autoreceptors at those doses, evoked yawning. Marked yawning responses were also elicited by both 3-PPP (5-20 mg/kg, SC) and TL-99 (1-2 mg/kg, SC). SK & F 38393, a dopamine D-1 receptor agonist, at doses ranging from 0.1 to 8.0 mg/kg (SC) induced neither yawning nor stereotypy. However, bromocriptine (0.5-32.0 mg/kg, SC), a dopamine D-2 receptor agonist, induced yawning for which the dose-response curves showed a bell-shaped form. After a higher dose of 32 mg/kg (SC) bromocriptine, some rats occasionally showed sniffing and sawdust chewing. Yawning responses induced by systemic injection of apomorphine, piribedil, 3-PPP or bromocriptine were wholly suppressed after treatment with sulpiride (10 mg/kg SC), a dopamine D-2 receptor antagonist. Bilateral injections of apomorphine (20 micrograms/side X 2), piribedil (100 micrograms/side X 2) or 3-PPP (50, 100 micrograms/side X 2) into the striatum or septum also elicited marked yawning. The results indicate that low doses of apomorphine, piribedil, 3-PPP, TL-99 or bromocriptine elicit yawning by stimulating dopamine D-2 receptors and striatal and septal dopaminergic systems may be related to the occurrence of yawning behavior.

Animals↗
PubMed1995

Involvement of beta-adrenoceptors in regulation of the yawning induced by neuropeptides, oxytocin and alpha-melanocyte-stimulating hormone, in rats.

The present study was undertaken to investigate whether beta-adrenoceptors are involved in regulation of yawning responses to oxytocin and alpha-melanocyte-stimulating hormone (alpha-MSH) in rats. Oxytocin administered intracerebroventricularly (ICV) at doses of 50 and 100 ng/rat elicited yawning. alpha-MSH (20 micrograms/rat, ICV) elicited not only yawning but also stretching and body shaking. RS-86 (2-ethyl-8-methyl-2,8-diazaspiro-(4,5)-decan-1,3-dion hydrobromide), a putative muscarinic M1 receptor agonist, administered ICV at a lower dose of 100 micrograms/rat and subcutaneously (SC) at doses of 0.25-2.5 mg/kg also elicited yawning. The yawning responses produced by these agents were markedly increased by intraperitoneal (IP) pretreatment with a beta-adrenoceptor antagonist, pindolol (20 mg/kg), which per se did not elicit yawning. The yawning induced by oxytocin (50 ng/rat, ICV) plus pindolol, but not that by alpha-MSH (20 micrograms/rat, ICV) or RS-86 (0.5 mg/kg, SC) plus pindolol, was inhibited by [d(CH2)5,Tyr(Me)2,Orn8]-vasotocin (100 ng/rat, ICV), an oxytocin receptor antagonist. The yawning induced by oxytocin, alpha-MSH, or RS-86 administered in combination with pindolol was inhibited by scopolamine (0.5 mg/kg, SC), a mucarinic receptor antagonist, without being affected by spiperone (0.5 mg/kg, SC), a dopamine D2 receptor antagonist. The results suggest that the yawning produced by the neuropeptides oxytocin and alpha-MSH is modulated by beta-adrenoceptor activity in an inhibitory manner as that produced by muscarinic M1 receptor agonists, and that it involves cholinergic, but not dopaminergic, activation.

Animals↗
PubMed1987

A simple method for the study of yawning in man induced by the dopamine receptor agonist, apomorphine.

Apomorphine (Apo), a dopamine (DA) receptor agonist, induces yawning by stimulating central DA autoreceptors. Few data are available on Apo-induced yawning in man. A simple method for recording and measuring Apo-induced yawning by measuring the displacement of the lower jaw using a pair of linearlized magnetometers with one sensor attached to the forehead just below the hairline and the other under the chin is described. The output of the magnetometers is fed into a DC amplifier and displayed on a strip chart recorder. Complete concordance between evaluators reading the tracings and between observed yawning and recorded yawns was found. Measuring Apo-induced yawning may provide a simple approach to evaluating DA autoreceptor function in normal subjects and in patients with psychiatric and neurological disorders. Preliminary data show that Apo-induced yawning is more marked in women than in men. This is in contrast to spontaneous and drug-induced yawning in animals which is predominantly a male phenomenon. Sleep appears to inhibit Apo-induced yawning.

Apomorphine↗
PubMed1980

Direct evidence for involvement of dopaminergic inhibition and cholinergic activation in yawning.

A behavioral study was performed in an attempt to understand the neurological mechanism involved in yawning in rats. Intraperitoneal injections of low doses (0.25 mg/kg) of apomorphine, which preferentially activate presynaptic dopamine autoreceptors, elicited yawning. Whereas apomorphine, at a high dose of 2 mg/kg, produces stereotypy which has been thought to be mediated by stimulation of postsynaptic dopamine receptors. The yawning and stereotypy did not occur simultaneously in the rat. The apomorphine-induced yawning was completely inhibited by pretreatment with fluphenazine (9 mg/kg, IM) or scopolamine (0.5 mg/kg IP), but markedly increased by reserpine (5 mg/kg, SC), however it was not affected by methylscopolamine (0.5 mg/kg, IP). Both physostigmine (0.2 mg/kg, IP), an indirect acetylcholine agonist, and pilocarpine (4 mg/kg, IP), a direct acetylcholine agonist, also induced yawning. This was abolished by scopolamine (0.5 mg/kg, IP) and increased by reserpine (5 mg/kg, SC). Fluphenazine (9 mg/kg, IP) did not affect the pilocarpine-induced yawning but increased the physostigmine-induced yawning. The results indicate that apomorphine elicits yawning by stimulating presynaptic dopamine receptors, and that dopaminergic inhibition and cholinergic activation are concomitantly involved in the yawning.

Animals↗
PubMed1983

Pharmacological characteristics of dopamine receptors involved in the dual effect of dopamine agonists on yawning behaviour in rats.

Increasing doses of apomorphine (APO) induced the dose-dependent appearance of yawns in rats at doses up to 0.1 mg X kg-1 and their disappearance from 0.1 to 0.6 mg X kg-1. A similar biphasic effect on yawning was observed with increasing doses of n-propyl norapomorphine, piribedil, S 584, bromocriptine, lergotrile, lisuride, CQ 32084 and L-DOPA. APO, n-propyl norapomorphine, piribedil and CQ 32084 had similar ED50 on the induction of sniffing and on the disappearance of yawns. All the neuroleptics tested antagonized the yawns induced by 0.1 mg X kg-1 APO. Increasing doses of haloperidol, chlorpromazine, mezilamine, metoclopramide and thioridazine made the yawns reappear in rats injected with 0.6 mg X kg-1 APO. The ID50 were similar to those for the antagonism of sniffing. On the other hand, increasing doses of clozapine, (+/-)- or (-)-sulpiride, veralipride and DAN 2163 did not make the yawns reappear in rats injected with 0.6 mg X kg-1 APO although sniffing was antagonized. These results are discussed in terms of the ability of sulpiride, veralipride and DAN 2163 to distinguish between the dopamine (DA) receptors involved in the appearance of yawns at low doses of DA agonists and in their disappearance at higher doses. The decreased APO-induced yawning observed concomitantly with increased sniffing in rats with 6-hydroxydopamine-lesioned olfactory tubercles suggests that yawning and sniffing could be mutually exclusive.

Animals↗
PubMed1981

Serotonergic and dopaminergic effects of yawning in the cat.

The serotonergic agents LSD (0.01-0.05 mg/kg) and lisuride (0.025 and 0.05 mg/kg) elicited a high frequency of limb flicking in the cat after IP doses; LSD, but not lisuride, elicited a significantly increased frequency of yawning as well. In combination, LSD plus lisuride (0.025 mg/kg each) gave additive frequencies of limb flicking, but the frequency of yawning was half that after LSD alone. The dopamine agonist apomorphine had no significant effect on either yawning or limb flicking over the dose range 0.006 to 3.2 mg/kg. Pretreatment of cats with 1.0 mg/kg of apomorphine (but not with 0.05 mg/kg) significantly reduced the frequency of yawning elicited by 0.01 or 0.025 mg/kg of LSD, but had no effect on limb flicking. The dopamine antagonist haloperidol had no effect on limb flicking at doses from 0.008 to 0.512 mg/kg, but produced a significantly increased frequency of yawning at 0.256 mg/kg, an effect antagonized by lisuride administration. Given that lisuride has more potent dopamine agonist properties than LSD, these results are consistent with serotonergic elicitation of yawning, dopaminergic inhibition of yawning, and with their concomitant interaction in the expression of drug-induced yawning in the cat. The behavioral pharmacologies of limb flicking and yawning are different in this species.

Analgesics↗
PubMed1980

Interaction of cholinergic and dopaminergic influences on yawning behavior.

The possible interaction between cholinergic and dopaminergic influences in the induction of yawning behavior in the rat is explored resorting to several experimental approaches: comparison of the ontogeny of yawning behavior induced by physostigmine (0.15 mg/kg) and apomorphine (0.05 mg/kg); simultaneous injection of both drugs; "crossed blocking" experiments, in which the action of the cholinomimetic agent is examined after injection of spiroperidol (0.05 mg/kg) and that of apomorphine after scopolamine (0.25 mg/kg). While physostigmine-elicited yawning is highest in early postnatal days and tends to decline from the 7th day onwards, reaching its lowest level around 3 wk, yawning induced by apomorphine begins around the 9th day and increases thereafter to a plateau that is reached in the third week. No synergism on yawning behavior is observed by simultaneous injection of optimal or suboptimal doses of physostigmine and apomorphine. Scopolamine blocks apomorphine-induced yawning; spiroperidol blocks apomorphine- but potentiates physostigmine-induced yawning, both in 15-day-old and young adult rats. Two 5-HT uptake blockers, citalopram (10-20 mg/kg) and fluoxetin (10-20 mg/kg) potentiate physostigmine - but not apomorphine-elicited yawning. On the basis of these results a tentative model of "in series" organization of dopaminergic and cholinergic influences on yawning behavior is proposed.

Animals↗
PubMed1990

Possible involvement of differing classes of dopamine D-2 receptors in yawning and stereotypy in rats.

The present experiments were performed to investigate differences in the properties of the dopamine D-2 receptors related to yawning and stereotypy. Subcutaneous injection of talipexole (B-HT 920) (10-250 micrograms/kg) or SND 919 ((S)-2-amino-4,5,6,7-tetrahydro-6-propylamino-benzothiazole) (25-500 micrograms/kg) evoked yawning behavior with bell-shaped responses. However, SK&F 38393 (1-phenyl-2,3,4,5-tetrahydro-(1H)-3-benzazepine-7,8-diol) (0.5-10 mg/kg SC) did not elicit yawning and decreased yawning responses to low doses of talipexole (25 micrograms/kg SC) or SND 919 (100 micrograms/kg SC). These low but effective doses for inducing yawning of talipexole or SND 919 in combination with SK&F 38393 (0.5-10 mg/kg SC) did not elicit stereotypy. In contrast, yawning behavior was not produced after very high doses of talipexole (500 micrograms/kg SC) or SND 919 (1000 micrograms/kg SC) given alone or in combination with SK&F 38393 (0.5-10 mg/kg SC). These extremely high doses of talipexole or SND 919 evoked slight stereotypy, which was enhanced by the combined treatment with SK&F 38393. The present results suggest that the dopamine D-2 receptors related to yawning are more sensitive to dopamine receptor agonists than those related to stereotypy, and that concurrent stimulation of postsynaptic dopamine D-1 receptors with D-2 receptors reduces the incidence of yawning but enhances that of stereotypy.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1995

Apomorphine-induced yawning in the rat: influence of fasting and time of day.

Yawning behavior is an experimental tool to study physiological responses, to elucidate the mechanisms of action of some drugs and hormones, and it is also a paradigm for some diseases and for dopamine (DA) agonists' clinical use. In this study, the effects of 24- and 48-h fasting as well as the influence of the light-dark cycle on apomorphine (APO)-induced yawning were evaluated. Initially, control and 48-h-fasted adult male rats were tested for yawning induced by APO (50, 100, 150 micrograms/kg, SC). The most effective dose tested was 100 micrograms/kg. Fasting significantly lowered yawning in all doses tested. Comparison between 24- and 48-h-fasted rats for APO (100 micrograms/kg)-induced yawning showed no significant difference between groups. Ad lib-fed groups were tested for APO (100 micrograms/kg)-induced yawning in both the light and in the dark phases of the cycle. Total number of yawnings increased significantly in the dark period. The present data show that fasting reduces and dark period increases APO-induced yawning in rats, suggesting that these conditions modulate the expression of this behavior.

Animals↗