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PubMed1986

Oxytocin-induced penile erection and yawning: site of action in the brain.

Microinjection of oxytocin into the paraventricular nucleus of the hypothalamus or into the CA1 field of the hippocampus induced a dose-dependent increase in the number of penile erection and yawning episodes in male rats. The minimal effective dose of oxytocin injected into the paraventricular nucleus was 3 ng. This dose induced the above-mentioned behaviors in 60% of the treated rats. Doses of 9 ng or higher induced the symptomatology in more than 85% of the animals. On the other hand, when the peptide was injected into the CA1 field of the hippocampus, 9 ng bilaterally were necessary to elicit penile erection and yawning in 62% of the rats. Arg8-vasopressin, which only differs from oxytocin in two amino acids, induced penile erection and yawning when injected either into the paraventricular nucleus or into the hippocampus, but was 5-10 times less potent than oxytocin. Oxytocin injection into the lateral septum, caudate nucleus, subiculum, preoptic area, ventromedial nucleus and supraoptic nucleus, was ineffective. The powerful effect of oxytocin on the induction of yawning and penile erection, suggests a physiological role of hypothalamic and hippocampal oxytocin in the regulation of such responses.

Animals↗
PubMed1987

Apomorphine-induced penile erection and yawning: site of action in brain.

Microinjection of the dopamine (DA) agonist apomorphine into the paraventricular nucleus of the hypothalamus (PVN) induced penile erection and yawning in rats. A significant effect was elicited by a dose of apomorphine as low as 5 ng. The symptomatology usually began within 5 min after the microinjection, lasted for 30-50 min, and was identical to that induced by the systemic administration of the drug. Stereotypy and hypermotility were never observed after apomorphine microinjection into the PVN, even at the highest dose tested (1 microgram). Microinjections of the same doses of apomorphine into the hypothalamic ventromedial and dorsomedial nucleus, preoptic area, caudate nucleus, nucleus accumbens and substantia nigra, were ineffective. LY 171555, a specific D2 Da receptor agonist, and (+)-3-PPP, but not (-)-3-PPP nor the specific D1 DA receptor agonist SKF 38393, were as effective as apomorphine when injected into the PVN. Apomorphine-induced penile erection and yawning were antagonized by pretreatment with neuroleptic drugs, such as haloperidol, (-)-sulpiride, a specific D2 DA antagonist, and SCH 23390, a specific D1 DA antagonist. The present results suggest that the PVN is the brain area where D2 DA agonists act to induce penile erection and yawning. Moreover, since the PVN contains the cell bodies of a group of incerto-hypothalamic DA neurons, the above results suggest for the first time a possible involvement of the incerto-hypothalamic DA system in the expression of penile erection and yawning.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1986

Oxytocin: an extremely potent inducer of penile erection and yawning in male rats.

The intracerebroventricular (i.c.v.) injection of oxytocin, in doses ranging from 5 to 90 ng (5-90 pmol) induced penile erection and yawning in male rats. Such response was not induced by doses of the peptide higher than 100 ng, nor by equimolar doses of i.c.v. [Arg8]vasopressin, ACTH-(1-24), alpha-MSH, rat corticotropin-releasing factor (rCRF), delta sleep-inducing peptide, neurotensin or substance P. Oxytocin-induced penile erection and yawning were prevented by atropine and morphine, but not by methylatropine or the opiate antagonist naloxone. Haloperidol, a dopamine receptor antagonist, was ineffective at low doses; it partially prevented penile erection but not yawning at high doses. Since oxytocin is present not only in the neurohypophysis but also in other brain areas, our results suggest that oxytocin is implicated in the regulation of penile erection and yawning, and provide further evidence that oxytocin acts as a neuropeptide in the central nervous system.

Amino Acid Sequence↗
PubMed1989

Evidence that apomorphine induces penile erection and yawning by releasing oxytocin in the central nervous system.

Oxytocin (10 and 30 ng) injected into a lateral ventricle (i.c.v.) or the dopamine agonist apomorphine (40 and 80 micrograms/kg) injected subcutaneously induced repeated episodes of penile erection and yawning in male rats. The concomitant administration of the two substances did not produce any further increase in the number of penile erection and yawning episodes. Penile erection and yawning induced by either oxytocin or apomorphine were antagonized in a dose-dependent manner by i.c.v. pretreatment with the oxytocin antagonists [d(CH2)5Tyr(Me)-Orn8]vasotocin, [Pen1,Phe(Me)2,Thr4,Orn8]oxytocin and [d(CH2)5Tyr(Me)-Arg8]vasopressin, with a rank order of potency that follows their antioxytocic activity. (i.e. [d(CH2)5Tyr(Me)-Orn8]vasotocin congruent to [Pen1,Phe(Me)2,Thr4,Orn8]-oxytocin greater than [d(CH2)5Tyr(Me)-Arg8]vasopressin). The results suggest that apomorphine induces penile erection and yawning by releasing oxytocin in the central nervous system.

Animals↗
PubMed1989

The effects of the enantiomers of the dopamine agonist N-0437 on food consumption and yawning behaviour in rats.

The enantiomers of the potent and selective dopamine (DA) D-2 receptor agonist 2-(N-propyl-N-thienylethyl-amino)-5-hydroxytetralin, N-0437, were tested for their effects on palatable food consumption and yawning behaviour in rats. (-)-N-0437 (1.0 and 5.0 mumols/kg). This confirms the agonistic action of (-)-N-0437 on postsynaptic receptors as food consumption is considered to be related to stimulation of postsynaptic DA receptors. Yawning behaviour was stimulated by (-)-N-0437 (0.5 mumol/kg) and could be antagonized by the autoreceptor-selective antagonist (+)-UH 232 (25 mumols/kg), which suggests an agonistic action on DA autorecptors. (+)-N-0437 (5.0 and 10.0 mumols/kg) also reduced food consumption and the effect could be antagonized by YM 09151-2 (0.03 mumol/kg). The weaker effect of (+)-N-0437 on food intake in comparison to that induced by (-)-N-0437 can be explained if it assumed that (+)-N-0437 is a partial agonist. (+)-N-0437 did not induce yawning behaviour in rats, suggesting that autoreceptors mediating the release of DA may be involved in stimulating yawning by DA agonists.

Animals↗
PubMed1991

Yawning produced by dopamine agonists in rhesus monkeys.

Yawning was recorded from five rhesus monkeys restrained in a chair after i.m. injection of dopaminergic compounds: apomorphine (0.03 mg/kg), quinpirole (0.01 mg/kg), and (-)-3-(3-hydroxyphenyl)-N-(1-propyl)piperidine (1 mg/kg). SKF 38393 or physostigmine produced no yawning. Yawning from apomorphine was blocked by chlorpromazine or SCH 23390 (0.03 mg/kg). Sulpiride (10 mg/kg) was ineffective. The difference between rats and monkeys in their yawning response to dopaminergic compounds is discussed.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1991

Effects of yawning and related activities on skin conductance and heart rate.

Accompanying physiological changes may clarify the functions of yawning, an act that is ubiquitous in the animal kingdom. The skin conductance, muscle tension, and heart rate of 30 young adult humans were recorded before, during, and after their yawns. These measures were also taken in 20 control subjects who merely opened their mouths or took deep breaths. Yawning, mouth opening and deep breathing each increased arousal initially, as measured by skin conductance. Some cumulative effects of successive yawns were found.

Adult↗
PubMed1987

Monosodium glutamate does not alter ACTH- or apomorphine-induced penile erection and yawning.

The effect of the intracerebroventricular (ICV) injection of ACTH 1-24 (1, 5 and 10 micrograms) or the subcutaneous administration of apomorphine (20 and 80 micrograms/kg SC) on spontaneous penile erection and yawning was studied in rats treated with monosodium glutamate (MSG), a treatment that depletes hypothalamic ACTH, alpha-MSH and endorphin-like peptides. Neonatal MSG treatment failed to antagonize either apomorphine- or ACTH-induced yawning in male and female rats, or to alter the number of penile erection episodes induced by the two substances in male rats. In contrast, hypophysectomy, that does not alter the concentration of hypothalamic ACTH and alpha-MSH, caused a marked prevention of apomorphine- and ACTH-induced responses, in agreement with previous studies. The results suggest that the integrity of opiomelanotropinergic neurons in the hypothalamus is not necessary for the induction of yawning and penile erection by ACTH-derived peptides, and that apomorphine and other dopamine agonists apparently do not induce penile erection and yawning by releasing an ACTH-derived peptide in brain.

Adrenocorticotropic Hormone↗
PubMed1989

The effect of pre- and postoperative procedures on physostigmine- and apomorphine-induced yawning in rats.

Previous experiments have shown that the potentiation of physostigmine-induced yawning by nifedipine is abolished by sham-lesioning procedures in rats, whereas the nifedipine potentiation of apomorphine-induced yawning is unaffected. The present results demonstrate that either the presurgical drug treatment (desmethylimipramine and pentobarbital) or 7 days isolation was alone sufficient to reduce the yawning response to physostigmine and abolish its potentiation by nifedipine. The sham-lesioned rats responded normally to a combination of apomorphine and nifedipine. These results suggest that the stress associated with standard operative procedures can differentially affect drug interactions with yawning induced by either apomorphine or physostigmine and that caution should be exercised when interpreting results from animals that have been similarly stressed.

Animals↗
PubMed1990

Omega-conotoxin prevents apomorphine- and oxytocin-induced penile erection and yawning in male rats.

The effect of the intracerebroventricular (ICV) administration of omega-conotoxin GVIA on penile erection and yawning induced by oxytocin or by the dopaminergic agonist apomorphine was studied in male rats. The peptide toxin, 1-10 ng given ICV 5 min before oxytocin (30 ng ICV) or apomorphine (80 micrograms/kg SC), but not its carboxymethylated (CM) derivative, prevented the above behavioral responses in a dose-dependent manner. Similarly, omega-conotoxin (5 ng) unilaterally injected in the paraventricular nucleus of the hypothalamus (PVN) prevented penile erection and yawning induced by the microinjection of oxytocin (10 ng) or apomorphine (50 ng) in the PVN. omega-Conotoxin injected in the PVN, but not in the preoptic area, prevented also penile erection and yawning induced by systemic apomorphine (80 micrograms/kg SC). ICV omega-conotoxin was unable to prevent stereotypy induced by apomorphine (500 micrograms/kg SC). The present results provide further evidence that calcium plays a major role in the expression of penile erection and yawning and that apomorphine and oxytocin induce these behavioral responses by mobilizing calcium through omega-conotoxin-sensitive (N-type) calcium channels.

Animals↗
PubMed1991

Ontogenic homologous supersensitization of quinpirole-induced yawning in rats.

Yawning in male rats is a behavior that may be induced by a group of dopamine receptors when low doses of dopamine-receptor agonists are administered. To determine whether agonist treatments during postnatal development could produce a long-lived supersensitization of these dopamine receptors, rats were treated daily for the first 28 days from birth with quinpirole HCl (3.0 mg/kg/day, IP), an agonist that acts at D2 and D3 receptors. At 8 to 10 weeks from birth the dose-effect curve for quinpirole-induced yawning demonstrated that a supersensitization of dopamine receptors for yawning behavior had occurred. Yawning at the optimal dose of quinpirole HCl (100 microgram/kg, IP) was increased 2-fold. The Bmax and Kd for D2 receptor binding in rat striatum were unaltered in this group of rats. These findings indicate that dopamine receptors can be ontogenically "primed" or supersensitized, and that the phenomenon apparently is not related to changes in striatal D2 receptor binding characteristics.

Aging↗
PubMed1993

Low-dose quinpirole ontogenically sensitizes to quinpirole-induced yawning in rats.

It is known that dopamine (DA) receptors can be sensitized by repeated treatments with quinpirole during postnatal development. This study was undertaken to determine whether low-dose quinpirole treatments might sensitize receptors to quinpirole-induced yawning behavior. Rats were treated with quinpirole HCl (50 micrograms/kg per day) or saline at four different periods of ontogeny: a) the 10th day of gestation to day of birth; b) 1st-11th days after birth; c) 12th-22nd days from birth; or d) 23rd-33rd days from birth. The numbers of yawns occurring in 1 h after a challenge dose of quinpirole HCl (50 micrograms/kg, IP) was determined at 6 weeks. Rats exposed prenatally to quinpirole demonstrated increased numbers of yawns following the third dose of quinpirole (2-day interval between doses). In rats exposed postnatally to quinpirole, there was a 70-300% increase in the yawning response, with the greatest response occurring in the group treated with quinpirole from birth to 11 days from birth. The findings demonstrate that quinpirole receptors are sensitized by a low dose of quinpirole, 60-fold lower than previously shown. It is suggested that sensitized receptors are of the DA D3 subclass.

Animals↗
PubMed1995

Effects of putative dopamine D3 receptor agonists, 7-OH-DPAT, and quinpirole, on yawning, stereotypy, and body temperature in rats.

7-OH-DPAT ((+/-)-2-(dipropylamino)-7-hydroxy-1,2,3,4-tetrahydronaphthalene) was recently identified as a dopamine receptor agonist having a > 100-, 1,000- and > 10,000-fold higher affinity for dopamine D3 than for D2, D4 and D1 receptors, respectively. Quinpirole (LY 171555) has also been reported to have a 113-fold greater affinity for dopamine D3 receptors than for D2 receptors. Therefore, we investigated the effects of these putative dopamine D3 receptor agonists on yawning, stereotypy and rectal temperature in rats (N = 424). 7-OH-DPAT and quinpirole administered subcutaneously (SC) at respective low doses of 10-250 micrograms/kg and 25-500 micrograms/kg elicited yawning behavior. The yawning induced by these agents was blocked by spiperone (0.5 mg/kg, SC) and scopolamine (0.5 mg/kg, SC) but was increased by intraperitoneal (IP) administration of pindolol (20 mg/kg). The yawning was also potentiated after treatment with reserpine. 7-OH-DPAT and quinpirole at respective high doses of 0.25 mg/kg (SC) and 0.5 mg/kg (SC) evoked slight stereotypy such as sniffing and licking, and this effect was enhanced by a selective dopamine D1 receptor agonist, SK&F 38393 (1-phenyl-2,3,4,5,-tetrahydro-(1H)-3-benzazepine-7,8-diol). 7-OH-DPAT (0.5 mg/kg, SC) and quinpirole (0.5 mg/kg, SC) decreased, but SK&F 38393 (10 mg/kg, SC) increased body temperature. However, the hyperthermia induced by SK&F 38393 was interestingly enhanced by 7-OH-DPAT and quinpirole.(ABSTRACT TRUNCATED AT 250 WORDS)

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMedDate not supplied

Penile erection and yawning induced by oxytocin and related peptides: structure-activity relationship.

The potency of several oxytocin-related peptides in inducing penile erection and yawning after injection into a lateral ventricle of male rats was compared. Substitution of two amino acids in the oxytocin molecule or deletion of the C-terminal glycinamide as in des-GlyNH2-oxytocin [oxytocin(1-8)] reduced oxytocin potency in inducing both effects, the rank order being: oxytocin greater than [Thr4,Gly7]-oxytocin congruent to isotocin [( Ser4,Ile8]-oxytocin) greater than vasopressin [( Phe3,Arg8]-oxytocin) greater than des-GlyNH2-oxytocin. Oxytocin's ability to induce penile erection and yawning was abolished by permanent opening of the disulfide bridge by reduction and carboxymethylation. Oxytocin(1-6) and oxytocin(7-9) were also inactive. Penile erection and yawning induced by oxytocin-related peptides were antagonized in a dose-dependent manner by nonapeptide antagonists with a rank order of potency that follows their antioxytocic activity (d[(CH2)5Tyr(Me)Orn8]-vasotocin congruent to [Pen1,Phe(Me)2,Thr4,Orn8]-oxytocin greater than d[(CH2)5Tyr(Me)Arg8]-vasopression). Carboxymethylated oxytocin, oxytocin(1-6), and oxytocin(7-9) were devoid of antagonistic activity. The present results suggest that central oxytocin receptors mediating the expression of penile erection and yawning are structurally related to those present in the uterus and in the mammary gland.

Animals↗
PubMed1989

Apomorphine: clinical studies on erectile impotence and yawning.

1. The erectile response to the short-acting dopamine (DA) receptor agonist, apomorphine (Apo) HCl (0.25, 0.5, 0.75 and 1.0 mg sc), and placebo was evaluated in 28 impotent patients and penile circumference monitored using a mercury strain gauge and strip chart recording. 2. A full erection (increment in penile circumference greater than 2 cm and lasting at least one minute) occurred in 17 patients with Apo; no erection developed after placebo. An erection occurred in 6/8 patients with impaired glucose tolerance, 2/6 patients with diabetes mellitus and in both patients on lithium. 3. Nine patients who responded to Apo were treated in an open trial with bromocriptine; 6 reported improvement in potency. 4. Impairment in DA function may play a role in idiopathic impotence and in impotence associated with impaired glucose tolerance and diabetes mellitus. 5. An erectile response to Apo may predict therapeutic response to bromocriptine or other long acting dopaminergic agents. 6. Lithium, which inhibits DA-sensitive adenylate cyclase, does not prevent Apo-induced erections. This provides further support indicating that Apo induces erections by an effect on D2 receptors. 7. The yawning response to placebo and four doses of Apo HC1 (3.5, 5.0, 7.0, and 10.5 ug/kg sc) was evaluated in five normal men using a polygraphic technique. The yawning response was also assessed in normal young (less than 30 yrs; N = 16) and elderly (greater than 60 yrs; N = 12) volunteers. 8. Under experimental conditions of study, placebo induced spontaneous yawning. This was antagonized by 3.5 and 5.0 ug/kg Apo HC1 but increased by 7.0 ug/kg Apo HC1. These observations are compatible with the view that Apo HC1 in doses of 3.5-5.0 ug/kg stimulates presynaptic DA receptors whereas 7.0 ug/kg stimulates postsynaptic DA receptors. 9. Spontaneous and Apo-induced yawning were significantly decreased in the elderly which suggests that D2 receptor function declines with normal aging.

Adult↗
PubMed1990

Role of calcium in the expression of ACTH-induced stretching, yawning and penile erection.

The effect of omega-conotoxin GVIA, a potent and selective inhibitor of N-type calcium channels and of the organic calcium channel inhibitors nimodipine, verapamil and flunarizine, on stretching, yawning and penile erection induced by ACTH 1-24 was studied in male rats. omega-Conotoxin (1-10 ng ICV 15 min before ACTH, 10 micrograms ICV), but not carboxymethylated omega-conotoxin, induced a dose-dependent prevention of all ACTH effects. In contrast, organic calcium channel inhibitors (20 mg/kg IP 30-60 min before ACTH) failed to modify ACTH-induced stretching and yawning but induced a 25% decrease in the number of penile erection episodes induced by the peptide, and prevented, like ICV omega-conotoxin, oxytocin- and apomorphine-induced yawning and penile erection. When injected in the paraventricular nucleus of the hypothalamus, omega-conotoxin prevented the above behavioral responses induced by apomorphine and oxytocin but not by ACTH 1-24. The present results suggest that ACTH induces stretching, yawning and penile erection by mobilizing calcium through central omega-conotoxin-sensitive calcium channels in brain sites different from those sensitive to oxytocin and apomorphine.

Animals↗
PubMed2004

Adrenalectomy and dexamethasone replacement on yawning behavior.

Yawning, a phylogenetic behavior, present in reptiles, birds and mammals, has been studied for several decades, but to date its physiological function is still unknown. The role of stress as well as several peptides and the hypothalamus has been studied in relation to its regulation. To date however, no studies has been carried out to determine the role of the adrenal glands. Therefore, yawning behavior was studied in adrenalectomized rats, who then received dexamethasone replacement. The results show that rats whose adrenal glands were removed stopped both spontaneous and apomorphine-induced yawning, while dexamethasone reverted this effect. The results are discussed in terms of the possible role of corticosterone on yawning behavior.

Adrenal Glands↗
PubMed1997

N-methyl-D-aspartic acid-induced penile erection and yawning: role of hypothalamic paraventricular nitric oxide.

A dose of N-methyl-D-aspartic acid (NMDA, 50 ng) that induces penile erection and yawning when injected into the paraventricular nucleus of the hypothalamus, increased the concentration of NO2- from 1.10 +/- 0.28 microM to 7.32 +/- 1.12 microM and of NO3 from 4.96 +/- 0.69 microM to 10.5 +/- 1.61 microM in the paraventricular dialysate obtained from male rats by in vivo microdialysis. NO2- concentration was not increased by (+/-)-alpha-(amino)-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA, 100 ng) or by trans-(+/-)-1-amino-1,3-cyclopentanedicarboxylic acid (ACPD) (100 ng), which were unable to induce these behavioral responses. N-Methyl-D-aspartic acid effect on NO2- concentration, penile erection and yawning was prevented by dizolcipine (MK-801) (10-100 ng) or by the nitric oxide synthase inhibitor N(G)-nitro-L-arginine methyl ester (20 microg), but not by the oxytocin receptor antagonist [d(CH2)5,Tyr(Me)2,Orn8]vasotocin (100 ng), or by the guanylate cyclase inhibitor methylene blue (20 microg) given in the paraventricular nucleus 15 min before N-methyl-D-aspartic acid or by the dopamine receptor antagonist haloperidol (0.5 mg/kg) given intraperitoneally 30 min before N-methyl-D-aspartic acid. In contrast, the nitric oxide scavenger hemoglobin (20 microg) given in the paraventricular nucleus prevented N-methyl-D-aspartic acid-induced NO2- concentration increase, but was unable to prevent penile erection and yawning. The results suggest that N-methyl-D-aspartic acid induces penile erection and yawning by increasing nitric oxide synthase activity in the paraventricular nucleus of the hypothalamus, possibly in the cell bodies of oxytocinergic neurons projecting to extra-hypothalamic brain areas and mediating these behavioral responses.

Animals↗