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R Urbá-Holmgren

Publications and source records attributed to R Urbá-Holmgren.

17 recordsLinked to original sources
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↗
PubMed1992

Age-dependent changes in serotonergic modulation of yawning in the rat.

Serotonin (5-HT) effects on physostigmine (PHY)-induced yawning were studied in LY Sprague-Dawley rats by injecting Lu 10 171 (citalopram), a specific 5-HT uptake blocker, and two antagonists--methiothepine and ritanserin--which differ slightly in the selectivity of their actions on different 5-HT receptor subtypes. Infant and young rats show significant increases in PHY-induced yawning when preinjected with citalopram (5-10 mg/kg). Two-month-old animals show this effect only with 10 mg/kg. With adult animals (3-5 months old), the effect is the opposite: Yawning decreases. The facilitory effect in infant and young rats was counteracted by methiothepine but not by ritanserin, suggesting that it is mediated through 5-HT1A or 5-HT1B receptor subtypes. The inhibitory effect of citalopram in adult rats was unmodified by the two antagonists used, leaving open the possibility that it is mediated by 5-HT3 receptors.

Aging↗
PubMed1991

Sleep and EEG disturbances in a rat neurological mutant (taiep) with immobility episodes: a model of narcolepsy-cataplexy.

The electroencephalographic sleep patterns recorded during short periods of time (3 h) of a neurological mutant rat (taiep) were studied. This rat exhibits, among other signs, immobility episodes that are similar to those observed in narcolepsy-cataplexy. We describe findings of long term (6 months) electroencephalographic studies done in 9 mutant and 5 control rats. The mutant rats present electroencephalographic and behavioral disorders consisting of: (a) bursts of cortical waxing and waning waves occurring during the drowsy state; in some animals this activity represents up to 25% of the total drowsiness time; (b) shortened sleep time; (c) fragmented paradoxical sleep; (d) immobility episodes when the animals are subjected to an emotional excitement; and (e) electrographic activity of paradoxical sleep without atonia during the immobility episodes. These findings show that the taiep mutant shows several aspects of narcolepsy-cataplexy and it may represent an experimental model for the study of this pathology.

Animals↗
PubMed1990

Genotypic dependency of spontaneous yawning frequency in the rat.

By inbreeding we have obtained two sublines of Sprague-Dawley rats which differ significantly in spontaneous mean yawning frequency (MYF). In generation F21 of the high-yawning (HY) subline MYF was 21.5 yawns/h (y/h) in males and 1.95 y/h in females, at the age of 2 months. In the low-yawning (LY) subline, in generation F16 the MYF was 0.9 y/h in males and only 0.5 y/h in females. During the first 15 days there are no differences in yawning frequency between HY and LY rats. Thereafter yawning increases with age, more steeply in the HY subline. The results of reciprocal crosses between both sublines indicate that the LY character is partially dominant over the HY one.

Age Factors↗
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↗
PubMed1989

Sprague Dawley rat mutant with tremor, ataxia, tonic immobility episodes, epilepsy and paralysis.

A spontaneous neurological mutation was detected in a colony of Sprague Dawley rats. The animals developed a progressive neurological syndrome characterized by tremor (which appeared at the age of 1 month), ataxia (at 4 months), immobility episodes (after 5-6 months), audiogenic seizures and hindlimb paralysis (after 10 months). Cross breeding experiments indicate that this is an autosomal recessive mutation, which we have named taiep subline.

Animals↗
PubMed1985

Association of spontaneous and dopaminergic-induced yawning and penile erections in the rat.

In a Sprague-Dawley-derived line of rats, selectively bred to establish a high incidence of spontaneous yawning behavior, the simultaneous and systematic monitoring of yawning and penile erections, during observation periods of one hour, demonstrates a linear correlation between these two behavioral patterns. Dose-effect curves of yawning and penile erections elicited by apomorphine and bromocriptine, and their inhibition by metoclopramide are quite similar. These results strongly suggest that yawning and penile erection are subject to some common regulating and modulating mechanisms, one of which seems to involve dopaminergic pathways.

Animals↗
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↗
PubMed1980

Sex hormone influences on yawning behavior.

Young male albino rats yawn significantly more than females or castrated males when injected with physostigmine (0.10 mg/kg). Treatment with testosterone (100 micrograms daily) during seven days restores cholinomimetically induced yawning in castrated males, and increases yawning in normal and androgenized females. Treatment with estradiol (200 micrograms daily) during one week does not modify physostigmine induced yawning behavior in castrated males nor in androgenized females.

Animals↗
PubMed1978

Blockade of both pilocarpine and amphetamine-induced head-shaking with dopamine receptor antagonists.

The range of central dopaminergic mechanisms involved in both d-amphetamine- and pilocarpine-induced head-shaking was studied in 7--9 days old rats by means of two DA antagonists: pimozide and spiroperidol. Both blocking agents exert their effects on H--S following dose-response curves which are similar, whatever the drug used to evoke head-shaking. A complete blocking effect on H--S is reached with pimozide at a dose of 2 mg kg-1; with spiroperidol at 0.1 mg kg-1 (for pilocarpine-induced H--S) and at 0.2 mg kg-1 (for H--S evoked by d-amphetamine). These results, together with those previously reported, suggest that dopaminergic and cholinergic facilitatory influences on H--S seem to be organized in series.

Animals↗
PubMed1978

Ontogeny of two cholinergically mediated central effects: stereotyped yawning and potentiation of head-shaking.

The ontogenetic course of two cholinergically mediated central neuropharmacological effects, yawning and potentiation of head-shaking induced by D-amphetamine (5 mg/kg), was explored in developing rats. Physostigmine (0.1 mg/kg) and pilocarpine (4 mg/kg) evoke stereotyped yawning in neonatal rats, the effect declining in the middle of the second week of life. Both cholinomimetic drugs strongly potentiate amphetamine induced head-shaking between the 4th and 10th postnatal days. Pilocarpine per se is capable of inducing head-shaking, in the absence of amphetamine, in rats from 8 to 12 days. Infant rat yawning and head-shaking are blocked by scopolamine (5 mg/kg). Nicotine (0.1 mg/kg) potentiates head-shaking but inhibits yawning. Yawning is also depressed by D-amphetamine. The early maturation of these cholinergic effects is discussed in comparison to the later maturation of several forebrain cholinergic systems.

Animals↗
PubMed1976

Spontaneous and amphetamine induced head-shaking in infant rats.

A variable proportion of albino rats 6-11 days old exhibit spontaneous and infrequent rotatory head-shaking episodes. This motor pattern is slightly anticipated and significantly increased in occurrence and duration by the administration of D-amphetamine (5 mg/Kg), with a maximal effect of the drug on the 9th day. The rate of amphetamine induced rhythmic head oscillations increases with age from below 5 cps on the 5th day to about 9 cps on the 10th day. The results are discussed in relation to maturation of both the underlying catecholaminergic pathways, activated by D-amphetamine, and the stretch reflex systems of the head and neck muscles participating in the rhythmic activity. Emphasis is placed on the difference between head-shaking and stereotyped activity.

Aging↗
PubMed1976

Relative role of catecholamines in head-shaking of infant rats.

The relative contribution of catecholaminergic mechanisms in head-shaking (H-S) of infant rats was explored by comparing the H-S inducing effects of apomorphine and amphetamine in rats from 4-14 days old, and the blocking effect of neuroleptic drugs (chlorpromazine and haloperidol) and more specific alpha- and beta-adrenergic receptor antagonists (phenoxybenzamine and propranolol), on amphetamine induced head-shaking. As apomorphine, but not amphetamine, may induce H-S in four-day-old rats, and the latter drug potentiates apomorphine induced H-S, even in days in which, if injected alone it has no effect, it is suggested that both dopaminergic and noradrenergic mechanisms are involved in H-S, thus differentiating this motor item from other motor patterns included in stereotyped behaviour. This suggestion is further supported by the demonstration that while D-amphetamine induced H-S is blocked by phenoxybenzamine, other stereotyped motor patterns continue unimpaired.

Animals↗