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PubMed1995

Effects of stress on drug-induced yawning: constant vs. intermittent stress.

Effects of stress on drug-induced yawning: Constant vs. intermittent stress. PHYSIOL BEHAV 58(1) 181-184, 1995.--Experiment 1 tested whether chronic exposure to immobilization, foot shock or forced swimming would result in suppression of apomorphine-, pilocarpine-, and physostigmine-induced yawning. Immobilization caused suppression of yawning, whereas foot shock and swimming resulted in increased number of yawns. Since interstressor interval was long in the two latter stressors, animals could have recovered and the increase in yawning could be due to the last (acute) exposure to stress. In Experiment 2 we recorded the number of yawns induced by pilocarpine in animals exposed to 1 h of swimming or foot shock. No differences between control and acutely stressed animals were detected. These results suggest that yawning is differently altered by constant and intermittent stressors (i.e., diminished by constant and increased by intermittent stress).

Animals↗
PubMed1989

Potentiation by serotonergic inhibition of yawning induced by dopamine receptor agonists in rats.

Low doses of the dopamine D2-receptor agonist, B-HT 920 (25 micrograms/kg, SC), and the dopamine D1/D2-receptor agonists, apomorphine (50 micrograms/kg, SC) and piribedil (1 mg/kg, SC), evoked yawning. However, the dopamine D1-receptor agonist, SK&F 38393 (2 mg/kg, SC), failed to induce yawning. The yawning responses induced by B-HT 920, apomorphine or piribedil were markedly increased without eliciting stereotypy by pretreatment with reserpine (5 mg/kg, IP, 24 hr). These yawning responses were also enhanced by p-chlorophenylalanine (PCPA) (300 mg/kg, IP, 72 hr), but not by alpha-methyl-p-tyrosine (300 mg/kg, IP, 6 hr). The yawning induced by B-HT 920 given alone and in combination with reserpine or PCPA was inhibited by spiperone (0.5 mg/kg, IP) or scopolamine (0.5 mg/kg, IP), but not by SCH 23390 (0.5 mg/kg, IP). The present results suggest that yawning is evoked by stimulation of dopamine D2-receptors having a high affinity and consequent muscarinic activation, and that the yawning induced by dopamine receptor agonists is potentiated by decreases in serotonergic neuron activity.

Animals↗
PubMed1990

Yawning and suppression of exploration induced by dopamine agonists: no relation to extracellular striatal levels of dopamine.

The present study was aimed at testing the hypothesis that yawning and suppression of exploration induced by low doses of dopamine agonists in the rat are caused by a reduction of synaptic dopamine levels. The decrease in extracellular levels of dopamine in the corpus striatum induced by alpha-methyl-p-tyrosine (alpha MPT, 50-200 mg/kg IP), reserpine (2-5 mg/kg SC) and apomorphine (APO, 0.05 mg/kg SC) was measured in microdialysis experiments. Reserpine and alpha MPT reduced the dopamine levels to the same extent as APO. Exploratory behaviour was suppressed by APO, but not by alpha MPT (50 and 100 mg/kg) when tested in a separate experiment. Reserpine (2 mg/kg) suppressed exploration after 4 hr, but not after 3 hr. Changes in extracellular levels of dopamine were tested simultaneously with changes in yawning in another group of rats implanted with guide cannulae for microdialysis probes. There was a discrepancy in the time-course for the induction of yawning as compared to the changes in extracellular dopamine levels after APO (0.05 mg/kg) as well as after pergolide (0.02 mg/kg SC). Yawning appeared before and lasted shorter than the decrease in dopamine. The time-courses for APO-induced suppression of exploration and yawning were similar. The dose-response curve for APO-induced yawning was not changed by alpha MPT (200 mg/kg), while the suppression of exploration induced by APO, but not by pergolide, was enhanced by pretreatment with alpha MPT. The results show that yawning and suppression of exploration induced by dopamine agonists are not related to changes in extracellular levels of dopamine. It is proposed that these behaviours may be mediated by postsynaptic receptors.

Animals↗
PubMed1993

Effects of streptozotocin-induced diabetes on dopaminergic functioning in the rat: analysis of yawning behavior.

Apomorphine, a dopamine receptor agonist, causes yawning in rats. It has been suggested that the analysis of yawning behavior provides an index of dopamine autoreceptor function. Dopamine turnover in the substantia nigra of diabetic rats has been shown to be decreased following administration of amphetamine or apomorphine (17,21). Yawning behavior after 4 weeks of streptozotocin (STZ)-induced diabetes in Wistar rats was significantly lowered when compared with their age-matched normal controls. Yawning behavior was not further diminished after an 8-week duration of diabetes mellitus; however, a significant recovery in yawning was seen by 20 weeks of diabetes. Yawning in rats after 20 weeks of STZ-induced diabetes mellitus is not significantly different from that seen in normal control rats. The results suggest that in STZ-induced diabetes of only 4 weeks duration a measurable change in the substrate for yawning has occurred.

Amphetamine↗
PubMed1996

Partial agonistic effects of OPC-14597, a potential antipsychotic agent, on yawning behavior in rats.

The present experiments were performed to examine the behavioral effects of OPC-14597, which acts on dopamine receptors in rats. OPC-14597 administered subcutaneously (SC) at doses of 0.1-5 mg/kg elicited yawning, as did OPC-4392 (0.5-2 mg/kg, SC) and (-)-3-PPP (2.5-10 mg/kg, SC). These yawning responses were blocked by intraperitoneal (IP) pretreatment with haloperidol (0.5 mg/kg) but were increased by pindolol (20 mg/kg, IP) or reserpine (5 mg/kg, IP), which per se did not elicit yawning. The yawning induced by talipexole, a selective dopamine D2 receptor agonist, was inhibited by OPC-14597 (0.5-5 mg/kg, SC) and (-)-3-PPP (10 mg/kg, SC). Apomorphine (0.5 mg/kg, SC), a dopamine D1/D2 receptor agonist, elicited stereotypy such as sniffing and licking but OPC-14597 (5-20 mg/kg, SC) did not induce this behavior. The stereotypy induced by apomorphine was inhibited not only by haloperidol (0.5 mg/kg, IP) and (-)-3-PPP (10 mg/kg, SC) but also by OPC-14597 (5-20 mg/kg, SC), without being affected by OPC-4392 (2 mg/kg, SC). In 6-hydroxydopamine (6-OHDA)-treated rats, apomorphine (0.5 mg/kg, SC) elicited rotation behavior whereas OPC-14597, OPC-4392 and (-)-3-PPP did not produce this behavior. These findings suggest that OPC-14597 provokes yawning without causing stereotypy and rotation but markedly antagonizes the talipexole-induced yawning and apomorphine-induced stereotypy, and that OPC-14597 thus exerts partial agonistic effects on yawning behavior but antagonistic effects on stereotypy in rats.

Animals↗
PubMed1990

Yawning behavior in male rats is associated with decreases in in vivo DOPAC efflux from the caudate nucleus.

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.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1993

Two inbred rat sublines that differ in spontaneous yawning behavior also differ in their responses to cholinergic and dopaminergic drugs.

This work compares the sensitivities of high-yawning (HY) and low-yawning (LY) sublines of Sprague-Dawley rats to dopaminergic and cholinergic yawning-inducing drugs. HY animals are significantly more sensitive to apomorphine and (-)3PPP than LY animals. Physostigmine is a less effective yawning-inducer in HY than in LY rats. With pilocarpine no differences were detected between both sublines in regard to its yawning-inducing activity. Since yawning behavior is subject to dopaminergic (inhibitory) and cholinergic (excitatory) influences, it is suggested that the genetic differences between these sublines affect the dopaminergic pathways that normally regulate yawning frequency.

Animals↗
PubMed2004

Genotype-dependent effect of ACTH1-24 on grooming and yawning in two inbred strains of rats.

It has long been known that the intracerebroventricular administration of ACTH1-24 increases the duration of grooming episodes and the frequency of yawning in rats. The objective of this study was to investigate in what way these episodes are prolonged and whether and to what extent genotype influences such effects. We compared the effect of increasing doses of intracerebroventricular injections of ACTH1-24 on grooming and yawning in males of two inbred strains of Sprague-Dawley rats with distinct yawning frequency, high-yawning (HY) and low-yawning (LY). In LY rats the duration of grooming episodes increased, while in HY rats grooming episodes augmented both in number and duration. In LY rats the duration of grooming components increased likewise, in HY rats however, neither the number nor the duration of the components changed. The grooming rate in both strains of rats was slowed, though more so in LY than in HY rats. Yawning increased in LY rats but not in HY rats. We conclude therefore that ACTH1-24 increases the duration of grooming episodes by slowing the grooming rate according to genotype, and may or may not alter the frequency of yawning.

Adrenocorticotropic Hormone↗
PubMed2003

Behavioral differences between selectively bred rats: D1 versus D2 receptors in yawning and grooming.

We used SKF 38393 and quinpirole for determining whether activation of D(1) and D(2) receptors, respectively, is involved in behaviors of rats selectively bred for high or low rates of yawning. After injection of SKF 38393, yawning diminished more markedly in high-yawning (HY) than in low-yawning (LY) rats, whereas this drug increased the number and duration of grooming episodes similarly in both strains. After injection of quinpirole, yawning increased more markedly in HY than in LY rats, whereas this drug decreased the number and duration of grooming episodes similarly in both rat strains. After coadministration of SKF 38393 and quinpirole, yawning increased similarly in both rat strains, whereas the combination of drugs failed to reliably affect grooming behavior. We interpret our findings as indicating that D(2) receptors are more important than D(1) receptors for differences in yawning behavior between HY and LY rats.

Animals↗
PubMed2000

Yawning responses induced by local hypoxia in the paraventricular nucleus of the rat.

Yawing was induced by microinjections of L-glutamate, cyanide and a nitric oxide-releasing compound (NOC12) into the paraventricular nucleus of the hypothalamus (PVN) in anesthetized, spontaneously breathing rats. To evaluate physiological aspects of yawning, we monitored intercostal electromyogram (EMG) as an index of inspiratory activity, digastric EMG, blood pressure and electrocorticogram (ECoG). Microinjection of L-glutamate in the medial parvocellular subdivision (mp) elicited a stereotyped yawning response, i.e. an initial depressor response and an arousal shift in ECoG followed by a single large inspiration with mouth opening. The same sequential events were observed during spontaneous yawning, indicating that the mp is responsible for triggering yawning. Microinjection of cyanide into the mp caused the same yawning responses as the ones elicited by microinjection of L-glutamate, suggesting that the mp is sensitive to chemical hypoxia or ischemia within the PVN. Microinjection of NOC12 into the mp elicited a single large inspiration with a variable onset delay, suggesting that diffusible nitric oxide (NO) within the mp may act as a paracrine agent to cause a yawning response. We hypothesize that the mp of the PVN contains an oxygen sensor that causes a yawning response.

Animals↗
PubMed1993

A critical view of the yawn-sigh as a voice therapy technique.

The purpose of this study was to take a critical look at a voice therapy technique known as the yawn-sigh. The voiced sigh as an approach in voice therapy has had increased use in recent years, particularly with problems of vocal hyperfunction. In this study, the physiology of the yawn-sigh was studied with video nasoendoscopy in eight normal subjects; their taped voices were also studied acoustically for possible fundamental frequency and format changes in producing selected vowels under normal and sigh conditions. Although each subject was given a model by the examiner of a yawn-sigh, one of the eight subjects could not produce a true yawn-sigh. Endoscopic findings for seven of the eight subjects performing the yawn-sigh demonstrated retracted elevation of the tongue, a lower positioning of the larynx, and a widened pharynx. Acoustic analyses for the seven subjects producing the sigh found a marked lowering of the second and third formants. Implications for using the yawn-sigh in voice therapy are given, such as using a modified "silent" yawn-sigh, as an easy method for producing greater vocal tract relaxation.

Adult↗
PubMed2005

[Physiology, role and neuropharmacology of yawning].

Yawning is a physiological event that can be divided into three distinct phases: a long inspiratory phase, a brief acme and a rapid exspiration. The reason for yawning is not yet well defined. However this semi-voluntary event increases vigilance and aims to alert when drowsiness occurs. Yawning may have an important role for social communication. The neuropharmacology of yawning is complex and knowledge of its mechanisms is incomplete. While under the control of several neurotransmitters, yawning is largely affected by dopamine. Dopamine may activate oxytocin production in the paraventricular nucleus of the hypothalamus, oxytocin may then activate cholinergic neurotransmission in the hippocampus, and finally acetylcholine might induce yawning via the muscarinic receptors of the effectors. In fact, this scheme is simplified. Many other molecules can modulate yawning, such as nitric oxide, glutamate, GABA, serotonin, ACTH, MSH, sexual hormones and opium derivate peptides.

Acetylcholine↗
PubMed1997

Alterations of physostigmine-induced yawning by chronic lithium administration in rats.

The effect of chronic lithium pretreatment on physostigmine-induced yawning was investigated in male rats. Intraperitoneal administration of physostigmine to rats induced yawning in a biphasic manner. However the maximum response was obtained by 0.2 mg/kg of the drug. Intracerebroventricular administrations of a putative M1 and M2 muscarinic receptor antagonists, pirenzepine and methoctramine decreased physostigmine-induced yawning. Intraperitoneal administration of a non-selective muscarinic receptor antagonist, atropine, also decreased the physostigmine-induced yawning significantly. Chronic lithium pretreatment (30 days) reduced yawning induced by physostigmine. The inhibitory effect of pirenzepine, methoctramine and atropine on physostigmine-induced yawning increased in rats pretreated with chronic lithium. These findings indicate that yawning is induced by a central cholinergic mechanism and that chronic pretreatment of lithium may interact with the cholinergic-induced behaviour.

Animals↗
PubMed1999

Yawning: role of hypothalamic paraventricular nitric oxide.

Yawning is a phylogenetically old, stereotyped event that occurs alone or associated with stretching and/or penile erection in humans, in animals from reptiles to birds and mammals, under different conditions. Several neurotransmitters and neuropeptides are involved in its control at the central level. One of these at the level of the paraventricular hypothalamic nucleus (PVHN) is nitric oxide (NO). First, NO synthase inhibitors injected into this hypothalamic nucleus prevent yawning induced by dopamine agonists, oxytocin or N-methyl-D-aspartic acid (NMDA), which induce yawning by activating PVHN oxytocinergic neurons projecting to extra-hypothalamic brain areas. The inhibitory effect of NO synthase inhibitors was not observed when these compounds were given concomitantly with L-arginine, the precursor of NO. Second, dopamine agonists, NMDA and oxytocin given at doses that induce yawning, increase NO production in the PVHN, as determined by in vivo microdialysis. Conversely, the opiate morphine, which prevents yawning induced by dopamine agonists, oxytocin and NMDA, also prevents the increase in the paraventricular NO production induced by these compounds. Third, NO donors, such as nitroglycerin, sodium nitroprusside and hydroxylamine, induce yawning when injected into the PVHN apparently by activating oxytocinergic transmission. Since guanylate cyclase inhibitors and NO scavengers (hemoglobin) injected into the PVHN do not prevent drug-induced yawning, nor 8-Br-cGMP injected into the PVHN induces this behavioral response, it is likely that NO acts as an intracellular rather than an intercellular modulator inside the PVHN oxytocinergic neurons in which NO is formed to facilitate the expression of this phylogenetically old event by guanylate cyclase-independent mechanisms.

Animals↗
PubMed1984

Assessment of dopamine autoreceptor agonist properties of apomorphine, (+)-3-PPP and (-)-3-PPP by recording of yawning behaviour in rats.

Yawning behaviour in rats was studied by direct observation. Apomorphine dose dependently induced yawning: 0.05 mg/kg was most effective, 0.2 mg/kg induced locomotor and sniffing behaviour but less yawning. Sulpinide (2 and 10 mg/kg) dose dependently blocked the apomorphine (0.05 mg/kg)-induced yawning. (+)-3-PPP (1-10 mg/kg) induced yawning in a manner similar to that of apomorphine but (-)-3-PPP (1-10 mg/kg) did so only weakly. Yawning induced by (+)-3-PPP was blocked by sulpiride 10 mg/kg. It is concluded that (+)-3-PPP but not (-)-3-PPP is at least as effective as apomorphine to induce yawning in rats, indicating that (+)-3-PPP, but not (-)-3-PPP, is a pure agonist on dopamine autoreceptors.

Animals↗
PubMed1986

Antagonism of drug-induced yawning and penile erections in rats.

A number of centrally active drugs were tested for antagonism of physostigmine- or apomorphine-induced yawning and for apomorphine-induced penile erections. The alpha 2-adrenoceptor antagonists piperoxan and idazoxan inhibited the yawning response without affecting the penile erections. The 5HT agonist quipazine and the histamine antagonist dexchlorpheniramine inhibited the yawning response more effectively than the penile erections. Dexchlorpheniramine even enhanced the apomorphine-induced penile erections and induced penile erections in physostigmine-treated rats. The 5HT antagonists metergoline and methysergide blocked the apomorphine-induced penile erections without affecting the yawning response. The alpha 2-adrenoceptor agonist clonidine, the dopamine antagonist sulpiride, the antihistaminic mepyramine and the benzodiazepine chlordiazepoxide inhibited both yawning and penile erections at the same dose level. The alpha 1-adrenoceptor antagonists prazosin and phenoxybenzamine were inactive. It is concluded that yawning and penile erections can be differentially affected by drug treatments. Also, while concomitant yawning and penile erections can be selectively induced by a class of dopamine receptor agonists, the same selectivity does not apply to antagonism of these induced behaviours.

Adrenergic alpha-Agonists↗
PubMed1984

Muscarinic and nicotinic effects on yawning and tongue protruding in the rat.

Physostigmine, an anticholinesterase agent, elicited yawning with a marked protrusion of the tongue and teeth chattering. Yawning and chattering were also observed after pilocarpine, a cholinergic agonist predominantly acting upon muscarinic receptors. Apomorphine at low doses (0.1-0.5 mg/kg), which preferentially activates presynaptic dopamine autoreceptors, elicited yawning, whereas at high doses (1-2 mg/kg) it produced stereotypy. Yawning induced by both cholinergic agonists and apomorphine was inhibited by scopolamine, a muscarinic receptor blocking agent, but not by methylscopolamine, a peripheral anticholinergic agent and mecamylamine, a nicotinic receptor blocking agent. Low dose (0.02 mg/kg) of haloperidol, which has been reported to block presynaptic dopamine autoreceptors, inhibited apomorphine-induced yawning but did not affect cholinergic agonist-induced yawning. Physostigmine-elicited tongue protruding was inhibited by mecamylamine. The results imply that yawning behavior is essentially associated with the stimulation of central muscarinic receptors, and that physostigmine also induces tongue protruding by activating the central nicotinic receptors.

Animals↗
PubMed1984

Timing of yawns induced by a small dose of apomorphine and its alteration by naloxone.

The report examines the temporal sequence of yawns induced by apomorphine and whether the opiate antagonist, naloxone, affects it. Before administering apomorphine (0.075 mg/kg) or saline, rats (n = 8) were pretreated with naloxone (1 mg/kg) or saline. Each subject received all 4 possible treatments (saline-saline, saline-apomorphine, naloxone-saline, and naloxone-apomorphine) in random order. Results indicate that yawning induced by apomorphine seems to come in fits; that is, there is a series of yawns spaced closely together and followed by a period of quiescence before the start of another cluster of yawns. Naloxone reduced the number of apomorphine-induced yawns, and the occurrence of very short inter-yawn intervals. It is suggested that the timing of yawns may provide useful information regarding some pathologies and that opiates may potentiate the action of dopaminergic systems.

Animals↗