Fetal yawning activity in normal and high-risk fetuses: a preliminary observation.
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OBJECTIVE: To study yawning activity in healthy fetuses and in fetuses at high risk. METHODS: Yawning activity was studied in 16 healthy and 22 high-risk fetuses. Studies were performed in the postprandial state at 09.00 and 12.00 in a quiet room with the woman in the lateral recumbent position. All ultrasound examinations were performed using a 3.5-MHz Acuson 128 PX curvilinear probe. Fetal lips, mouth, tongue, pharynx, larynx, trachea and esophagus were surveyed in serial coronal and sagittal planes. All fetal mouthing movements were analyzed by a review of the videotape in slow motion. RESULTS: In both normal and high-risk fetuses, yawning was represented by isolated mouthing movements and consisted of slow opening of the mouth with simultaneous downward movements of the tongue. This phase occupied 50-75% of the yawning cycle. After reaching its maximum opening, the mouth remained wide open for 2-8 s and returned to its resting position within seconds. Growth-restricted fetuses demonstrated yawning patterns consisting of isolated yawns similar to those seen in healthy fetuses. Unusual bursts of fetal yawning activity were recorded in anemic fetuses. CONCLUSION: Yawning activity in anemic fetuses may represent a compensatory process to increase venous return to the heart. (
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Investigation of stretching behaviour induced by the selective 5-HT6 receptor antagonist, Ro 04-6790, in rats.
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1. The present study examined the effects of the selective 5-HT6 receptor antagonist 4-amino-N-(2, 6 bis-methylamino-pyrimidin-4-yl)-benzene sulphonamide (Ro 04-6790) on locomotor activity and unconditioned behaviour in male Sprague Dawley rats (230-300 g). 2. In non-quantified behavioural observations, animals treated with Ro 04-6790 (3, 10 or 30 mg kg(-1), i.p) showed no overt behavioural signs except a dose-dependent reduction in locomotor activity and a behavioural syndrome of stretching, yawning and chewing. The latter behaviour was most pronounced between 30 and 90 min following the administration of Ro 04-6790. 3. Detailed analysis of the stretching and yawning behaviour showed that Ro 04-6790 (3, 10 or 30 mg kg(-1), i.p.) dose-dependently induced stretching. The number of stretches observed following treatment with either Ro 04-6790 (10 mg kg(-1) i.p.) or Ro-04-6790 (30 mg kg(-1), i.p.) was significantly greater than that observed in saline-treated rats. The yawning behaviour, however, was not dose-dependent nor was the number of yawns in any of the drug treated groups significantly greater than in those treated with saline. 4. Pretreatment (30 min) with the non-selective muscarinic antagonists scopolamine (0.1, 0.3 or 1 mg kg(-1), i.p.) and atropine (0.3, 1 or 3 mg kg(-1), s.c.) but not methylatropine (1, 3 or 10 mg kg(-1), s.c) significantly inhibited stretching induced by Ro 04-6790 (30 mg kg(-1), i.p.). 5. The dopamine D2-like receptor antagonist, haloperidol (0.03, 0.1 or 0.3 mg kg(-1), s.c.) given at the same time as Ro 04-6790 (30 mg kg(-1), i.p.) had no effect on the stretching induced by the 5-HT6 antagonist. 6. These data suggest that systemic injection of the 5-HT6 antagonist, Ro 04-6790, produces a stretching behaviour that appears to be mediated by an increase in cholinergic neurotransmission in the CNS and which could be a useful functional correlate for 5-HT6 receptor blockade. There is no evidence for dopamine D2-like receptor involvement in this behaviour. (
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Yawning: role of hypothalamic paraventricular nitric oxide.
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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. (
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Water-soluble antioxidants in human tears: effect of the collection method.
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PURPOSE: To resolve differences in published data on tear antioxidant levels by comparing the concentration of water-soluble antioxidants in human reflex tears collected by capillary tube and by the Schirmer strip collection method and in basal and reflex tears collected using the Schirmer strip method. METHODS: Yawn-induced reflex tears (collected simultaneously by capillary tubes and by Schirmer strips) and basal tears (by Schirmer strips and using local anesthetic) were collected from 12 healthy subjects. Tear cysteine, ascorbate, glutathione, urate, and tyrosine were measured by high-performance liquid chromatography within a few minutes of collection. RESULTS: Cysteine, ascorbate, glutathione, and tyrosine were 5 to 10 times higher (P < 0.01) in both reflex and basal tears collected by Schirmer strip compared with reflex tears collected by capillary tube from the same subject. Urate levels were slightly but nonsignificantly higher in Schirmer strip samples (P > 0.05). CONCLUSIONS: The conflict in published data on tear antioxidants is caused by differences in collection methods. With the exception of urate, antioxidants accumulate to very high levels in corneal cells. Spuriously high antioxidant levels in tears collected using Schirmer strips, therefore, are most probably caused by contamination with intracellular constituents. The capillary tube collection method is proposed as the method of choice for reflex tear collection for biochemical studies. This less-invasive method facilitates the evaluation of tear antioxidant levels as a biomonitoring tool for corneal health. Although moderately increased antioxidant levels may be beneficial, the authors hypothesize that marked increases may indicate damage to the ocular surface. (
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Amphetamine-induced enhancement of neostriatal in vivo microdialysate dopamine content in rats, quinpirole-primed as neonates.
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Amphetamine (AMPH)-induced sensitization of central dopamine (DA) receptors, produced by repeated AMPH treatments, is associated with increased AMPH-induced DA release in the rat forebrain. However, for DA receptor sensitization produced by repeated DA receptor agonist treatments, the effects on forebrain DA release are not known. The objective of our study was to determine this. DA receptor sensitization was produced by administering the DA D2 agonist quinpirole (50 microg/kg/day) to rats, from the 1st to 11th days after birth - a process known as 'priming'. When these rats were tested at 3 months, DA receptor sensitization was manifested as increased quinpirole-induced yawning. We also found that AMPH (1.0 mg/kg, ip) acutely induced a 5-fold greater increase in DA content in the neostriatal in vivo microdialysate of these quinpirole-primed rats (vs. controls), accompanied by a reduction in dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) levels in the microdialysate. Conversely, an acute injection of quinpirole x HCl (100 microg/kg, ip) reduced the microdialysate contents of DA, DOPAC and HVA to comparable levels in quinpirole-primed and control rats. Therefore, we can conclude that long-lived DA receptor sensitization, produced by repeated DA D2 agonist treatments in ontogeny, is associated with enhanced AMPH-induced DA release in the neostriatum in adulthood, but is not accompanied by evident alteration in quinpirole-induced DA release. (
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An assessment of the effects of serotonin 6 (5-HT6) receptor antagonists in rodent models of learning.
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Antagonists of serotonin 6 (5-HT6) receptors have been reported to enhance cognition in animal models of learning, although this finding has not been universal. We have assessed the therapeutic potential of the specific 5-HT6 receptor antagonists 4-amino-N-(2,6-bis-methylamino-pyrimidin-4-yl)-benzenesulfonamide (Ro 04-6790) and 5-chloro-N-(4-methoxy-3-piperazin-1-yl-phenyl)-3-methyl-2-benzothiophenesulfonami de (SB-271046) in rodent models of cognitive function. Although mice express the 5-HT6 receptor and the function of this receptor has been investigated in mice, all reports of activity with 5-HT6 receptor antagonists have used rat models. In the present study, receptor binding revealed that the pharmacological properties of the mouse receptor are different from the rat and human receptor: Ro 04-6790 does not bind to the mouse 5-HT6 receptor, so all in vivo testing included in the present report was conducted in rats. We replicated previous reports that 5-HT6 receptor antagonists produce a stretching syndrome previously shown to be mediated through cholinergic mechanisms, but Ro 04-6790 and SB-271046 failed to attenuate scopolamine-induced deficits in a test of contextual fear conditioning. We also failed to replicate the significant effects reported previously in both an autoshaping task and in a version of the Morris water maze. The results of our experiments are not consistent with previous reports that suggested that 5-HT6 antagonists might have therapeutic potential for cognitive disorders. (
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Inhibitory effect of morphine on yawning induced by cholinoceptor and dopamine D2 receptor activation in rats.
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1. Bromocriptine (2, 4 and 8 mg kg-1, i.p.), physostigmine (0.05, 0.1 and 0.2 mg kg-1, i.p.) and pilocarpine (1, 3 and 5 mg kg-1, i.p.) induced dose-dependent yawning in rats. 2. These responses were reduced in a dose-dependent manner by pretreatment with morphine. 3. The inhibitory effect of morphine was reversed by naloxone. 4. Naloxone alone induced slight but significant yawning. 5. The present results suggest that morphine inhibits yawning in rats at an opiate receptor downstream from the sites at which cholinoceptor and dopamine D2 activation induce yawning. The anatomical location of these sites remains to be established. (
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Contagious yawning in chimpanzees.
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Six adult female chimpanzees were shown video scenes of chimpanzees repeatedly yawning or of chimpanzees showing open-mouth facial expressions that were not yawns. Two out of the six females showed significantly higher frequencies of yawning in response to yawn videos; no chimpanzees showed the inverse. Three infant chimpanzees that accompanied their mothers did not yawn at all. These data are highly reminiscent of the contagious yawning effects reported for humans. Contagious yawning is thought to be based on the capacity for empathy. Contagious yawning in chimpanzees provides further evidence that these apes may possess advanced self-awareness and empathic abilities. (
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