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B Holmgren

Publications and source records attributed to B Holmgren.

At least 37 records · Page 2Linked to original sources
PubMed1982

Pre- and post-synaptic dopaminergic receptors involved in apomorphine-induced yawning.

The temporal course of yawning behavior elicited by increasing doses of apomorphine (APO), from 0.01 to 10 mg/kg, was studied experimentally in adult albino rats. In the higher dose range a great prolongation of drug induced yawning latency is observed. This result is explainable by postulating differences in sensitivity of two sets of dopaminergic (DA) receptors: low threshold presynaptic DA receptors which, when activated, disinhibit yawning, and high threshold postsynaptic DA receptors inhibiting yawning. Apomorphine in high doses can entirely suppress physostigmine-elicited yawning.

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↗
PubMed1979

Serotonergic modulation of yawning.

Yawning induced by intraperitoneal (IP) injection of physostigmine (0.15 mgKg-1), in infant or adult rats is potentiated by Lu 10-171 (0.5-10 mgKg-1), a selective serotonin uptake inhibiting drug, which, by itself does not induce yawning. This effect is counteracted by metergoline (5-10 mgKg-1, IP) which blocks serotonin postsynaptic receptors. It is suggested that serotonin may exert a positivie modulating effect on yawning.

Animals↗
PubMed1979

Individual mercury exposure of chloralkali workers and its relation to blood and urinary mercury levels.

On two occasions, chloralkali workers were investigated with regard to personal air mercury exposure, blood mercury and urinary mercury. The first investigation (13 workers, 2 weeks) was made at an exposure above the threshold limit value (64 microgram/m3, range 36--112), the second (16 workers, 8 weeks) at a lower exposure (23 microgram/m3, range 15--43). At the higher level of exposure, good correlations were found between air exposure and blood or urinary mercury for the group, but not for individuals. At the lower level, the correlations were less pronounced for the group. For individuals, the best correlation was found between mean air exposure during one week and blood mercury about half a week later. Other individuals, mainly the least exposed, showed no such correlation. Corresponding correlations were not found for urinary mercury. The urinary excretion rate was determined only for the last few hours of the workday, but the results agree with earlier investigations of 24-h excretion on a group basis. The threshold limit value for mercury in air (50 microgram/m3) corresponds to 150--175 nmol Hg/1 blood (= 30--35 microgram/1) for the group, with large individual variation.

Adult↗
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↗
PubMed1977

Discriminative properties of pentobarbital after repeated noncontingent exposure in gerbils.

Two groups of gerbils were pretreated with pentobarbital (P-barb.) (10 and 20 mg/kg) for 20 days before being subjected to drug discrimination training in a (T-shaped shock-escape maze. The rapidity with which these gerbils acquired the discrimination was compared to that of gerbils that were drug naive until beginning the P-barb.-discrimination training. The acquisition rates of the respective groups did not differ substantially within each dose level (10 and 20 mg/kg), although open-field activity (primarily the rearing scores) differentiated the P-barb.- and vehicle-pretreated animals at both dose levels. The peak effect in rectal temperature, however, was not markedly different after the first and 20th drug exposures, although the temperature effects leveled off earlier during the second recording session. In conclusion, certain parameters (open-field activity) may be changed as a consequence of repeated administrations of P-barb. without a significant parallel loss of the cue or stimulus properties of the drug.

Animals↗
PubMed1977

Cholinergic mechanisms involved in head-shaking of infant rats.

Central cholinergic mechanisms involved in D-amphetamine induced head-shaking (H-S) were explored in 9-day-old albino rats using anticholinergic, anticholinesterase and cholinomimetic drugs. Scopolamine (5 mg/kg, IP) blocks both spontaneous and D-amphetamine induced H-S. Physostigmine (0.10 mg/kg, IP), but not neostigmine, increases D-amphetamine induced H-S up to 400%. Pilocarpine (1-10 mg/kg, IP) per se induces H-S and strongly potentiates the amphetamine H-S effect. Cholinergic--catecholaminergic interactions in the CNS are discussed in relation to the expression of this motor item.

Animals↗
PubMed1977

Circadian variation in an amphetamine induced motor response.

Significant diurnal variation in occurrence and duration of D-amphetamine induced head-shaking were observed in 9-day-old rats. The lowest values were obtained near noon, and the highest around midnight. These variations should be considered if head-shaking is to be used as a quantitative neuropharmacological test.

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↗