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G A van Oortmerssen

Publications and source records attributed to G A van Oortmerssen.

17 recordsLinked to original sources
PubMed1997

No evidence for a Y chromosomal effect on alternative behavioral strategies in mice.

This study takes the first step toward testing a Y chromosomal effect on both aggression and thermoregulatory nest-building behavior in mouse lines either bidirectionally selected for short (SAL) and long (LAL) attack latency or high (HIGH) and low (LOW) nest-building behavior. Using reciprocal crosses between SAL and LAL, and between HIGH and LOW, we found no indications for Y chromosomal effects on thermoregulatory nest-building behavior. As for aggression, we confirmed earlier studies on SAL and LAL, i.e., the origin of the Y chromosome influences attack latency, i.e., aggression. However, we did not find indications for a Y chromosomal effect on aggression in the HIGH and LOW lines. Since aggression and nest-building behavior have been shown to be characteristic parameters of two fundamentally different behavioral strategies, the present data underline the improbability of Y chromosomal genes underlying the genetic architecture of alternative behavioral strategies.

Aggression↗
PubMed1996

Aggression in wild house mice: current state of affairs.

This paper reviews our present state of knowledge of genetic variation in (offensive) aggression in wild house mice. The basic tools in this research were lines bidirectionally selected for attack latency (fast attacking SAL and slow attacking LAL males), descended from a feral population. Using congenic lines for the nonpseudoautosomal region of the Y chromosome (YNPAR), reciprocal crosses between (parental) SAL and LAL, and crosses between parentals and congenics, an autosomally dependent Y chromosomal effect on aggression has been found. Both the pseudoautosomal (YPAK) region and the YNPAR play a role. As for environmental sources of variation, prenatal and postnatal maternal effects are of minor importance for the development of aggression differences. One of the physiological factors by which genetic effects may be mediated is testosterone (T). Besides quantitative aspects, the timing of T release seems crucial. Two important time frames are discussed: the perinatal and pubertal time periods. Finally, neurochemical and neuroanatomical correlates are considered. Differences in neostriatal dopaminergic activity, and sizes of the intra- and infrapyramidal mossy fiber terminal fields, as well as Y chromosomal effects on the latter two, are discussed.

Aggression↗
PubMed1996

Studies on wild house mice. VII. Prenatal maternal environment and aggression.

The effect of the maternal environment on intermale aggression was studied by means of embryo transfer of genetically selected aggressive (SAL) and nonaggressive wild house mice (LAL), and their reciprocal F1's, to standard (NMR1) females. No effect was found on the attack latency scores (ALS), i.e., aggression: all genotypes born and raised under natural conditions showed an ALS similar that of genotypes born and raised by NMR1 females. Since previous studies on wild house mice failed to demonstrate postnatal effects on aggression, and the present results indicate the absence of prenatal maternal environmental effects on aggression, the primacy of genetic over maternal variance in the development of adult intermale aggression in wild house mice is indicated.

Aggression↗
PubMed1995

A comparison between house mouse lines selected for attack latency or nest-building: evidence for a genetic basis of alternative behavioral strategies.

House mouse lines bidirectionally selected for either nest-building behavior or attack latency were tested for both attack latency and nest-building behavior under identical conditions. Male mice selected for high nest-building behavior had shorter attack latencies, i.e., were more aggressive, than those selected for low nest-building behavior and their randomly bred control lines. Conversely, male wild house mice selected for short attack latency showed more nest-building behavior than those selected for long attack latency when tested at 110 days of age. These findings imply a common genetic basis for control of aggression and nesting and support earlier proposals as to how animals may exhibit fundamentally different responses to environmental challenges, either reacting actively to aversive situations (aggressive and high-nesting animals: active copers) or adopting a passive strategy (nonaggressive and low-nesting animals: passive copers).

Aggression↗
PubMed1995

Studies on wild house mice (VIII): Postnatal maternal influences on intermale aggression in reciprocal F1's.

Previous findings have shown a difference in attack latencies, i.e., aggression, between reciprocal F1's of a line selected for short attack latency (SAL) and a line selected for long attack latency (LAL). In the present study, we investigated the influence of postnatal maternal environment on attack latency scores (ALSs). The results show that only the evolution of the ALSs over 3 consecutive days is influenced by crossfostering. Accordingly, we conclude that the postnatal maternal environment affects ALSs only to a small extent.

Aggression↗
PubMed1995

Autosomal and Y chromosomal effects on the stereotyped response to apomorphine in wild house mice.

The behavioral response to apomorphine, a dopamine agonist, was shown to be different between a selection line characterized by Short Attack Latencies (SAL) and a selection line having Long Attack Latencies (LAL) (4). Aggressive SAL mice were more sensitive to apomorphine than nonaggressive LAL males. The aim of this research was to determine whether the stereotyped response to apomorphine is affected by the Y chromosome in the same way as it influences attack latency. For this purpose, F1 reciprocal hybrids as well as congenic lines (SAL.LY and LAL.SY) were used. The major difference between the congenic and parental lines is the nonpairing part of the Y chromosome (non-PAR). Apomorphine was injected subcutaneously at a preselected dose level of 5.0 mg/kg to induce stereotyped behavior manifested in compulsive sniffing, gnawing, and licking. Both the autosomes and the non-PAR Y chromosome affected the response to apomorphine. The effect of the autosomes was in accordance with the aggression data, whereas the effect of the non-PAR Y chromosome was different, and suggests a specific relation between dopamine systems and the non-PAR Y chromosome.

Aggression↗
PubMed1994

Hippocampal mossy fiber distributions in mice selected for aggression.

The sizes of the hippocampal intra- and infrapyramidal mossy fiber terminal fields (IIPMF) of mice from two lines bidirectionally selected for attack latency were measured. Aggressive males possess smaller IIPMF than do non-aggressive ones. We hypothesize that both differences in aggression and sizes of the IIPMF may be mediated by perinatal testosterone.

Aggression↗
PubMed1993

Differential perinatal testosterone secretory capacity of wild house mice testes is related to aggressiveness in adulthood.

Testosterone secretory capacity of testicular Leydig cells was determined in fetal males of an aggressive and a nonaggressive genetic selection line of wild house mice. They were studied at Days 15-18 of gestation and on the first day after birth. A previously described morphometric method was used to quantify 3 beta-hydroxy steroid dehydrogenase (3 beta-HSD)-stained Leydig cells in testicular sections to determine testosterone secretory capacity, which may be considered to reflect circulating plasma testosterone in the fetus. The results of this study show that the testosterone secretory capacity of Leydig cells in the testis changes differentially during intrauterine development in males of the aggressive and nonaggressive selection lines. The peak secretory capacity is reached at Day 17 of gestation for the males of the aggressive selection line, while the peak for the nonaggressive males is reached on the first neonatal day. The larger anogenital distance observed in aggressive males suggests a higher prenatal testosterone level in these males. The importance of the difference in timing of the perinatal 3 beta-HSD peak top individual variation in adult aggressive behavior is discussed.

3-Hydroxysteroid Dehydrogenases↗
PubMed1993

Genetic differences in female house mice in aggressive response to sex steroid hormone treatment.

Male mice, genetically selected for aggression, characterized by short attack latency (SAL) or long attack latency (LAL), differ on several testosterone (T)-related parameters during ontogeny and adult age. The variation in aggressive behavior at adult age may be due to differences in degree of androgenization prenatally. When exposed to T at prenatal, neonatal, and/or adult age, nonlactating females also display intraspecific fighting behavior. In the present study, we investigated in females of the SAL and LAL selection lines, whether the differentiation of aggression involves processes similar to ones seen in males. Therefore, we injected females with testosterone propionate (TP) or vehicle on the day of birth, treated them after ovariectomy at adult age with T, estradiol (E), or vehicle, and tested their aggressive response. We found that neonatally vehicle-treated SAL females show a higher aggressive response to chronic T treatment at adult age than LAL females receiving the same treatment. Females of both selection lines treated with vehicle or E as adults were not aggressive. Neonatal TP treatment did not influence the adult T sensitivity and difference between selection lines in response to T at adult age. However, neonatally TP-treated SAL females showed aggressive behavior when treated with E at adult age, whereas LAL females failed to do so. These results suggest a genetic difference in susceptibility to T and E, which plays a major role prenatally, in organizing the development of sex steroid-dependent neural systems.

Aggression↗
PubMed1992

Differential effects of neonatal testosterone treatment on aggression in two selection lines of mice.

Selection lines of mice, artificially selected for aggression based upon the attack latency score (ALS), were used. In order to determine the relative contribution of neonatal testosterone (T) in the development of aggression, we vary the plasma-T level in males of both selection lines on the day of birth. At 14 weeks the ALS was measured. Neonatal T treatment results in a reduction of aggression in the long attack latency (LAL) line, whereas aggressive behaviour of the short attack latency (SAL) line is not affected. Both selection lines show reduction in testicular weight, although the total amount of T-producing Leydig cells was not affected. Neonatal T may cause a permanent reduction in aggressive behaviour in in the LAL line only, probably due to differential appearance of critical periods. It is suggested that the difference in aggressive behaviour between SAL and LAL selection lines is due to a prenatally determined difference in neonatal T sensitivity of the brain.

Aggression↗
PubMed1991

Heritable variation for aggression as a reflection of individual coping strategies.

Evidence is presented in rodents, that individual differences in aggression reflect heritable, fundamentally different, but equally valuable alternative strategies to cope with environmental demands. Generally, aggressive individuals show an active response to aversive situations. In a social setting, they react with flight or escape when defeated; in non-social situations, they react with active avoidance of controllable shocks and with sustained activity during an uncontrollable task. In contrast, non-aggressive individuals generally adopt a passive strategy. In social and non-social aversive situations, they react with immobility and withdrawal. A main aspect of these two alternative strategies is that individuals with an active strategy easily develop routines (intrinsically determined behaviour), and consequently do not react (properly) to 'minor' changes in their environment, whereas in passively reacting animals it is just the other way around (extrinsically determined behaviour). It has become clear that active and passive behavioural strategies represent two different, but equivalent, coping styles. The coping style of the aggressive males is aimed at the removal of themselves from the source of stress or at removal of the stress source itself (i.e. active manipulation). Non-aggressive individuals seem to aim at the reduction of the emotional impact of the stress (i.e. passive confrontation). The success of both coping styles depends upon the variability or stability of the environment. The fact that aggressive males develop routines may contribute to a fast execution of their anticipatory responses, which is necessary for an effective manipulation of events. However, this is only of advantage in predictable (stable) situations, but is maladaptive (e.g. expressed by the development of stress pathologies) when the animal is confronted with the unexpected (variable situations). The flexible behaviour of non-aggressive individuals, depending strongly upon external stimuli, will be of advantage under changing conditions. Studies on wild house mice living under natural conditions show how active and passive coping functions in nature, and how the two types have been brought about by natural selection.

Adaptation, Psychological↗
PubMed1991

Behavioural differences between artificially selected aggressive and non-aggressive mice: response to apomorphine.

The present study reports a first attempt to unravel the neurochemical background that underlies the difference in behavioural profiles between aggressive and non-aggressive male mice. For this purpose two bidirectionally selected lines for attack latency (SAL and LAL) were used. In pursuit of Cools'9 approach, the susceptibility of individuals of both selection lines to the dopamine agonist apomorphine was measured. The apomorphine was injected subcutaneously at dose levels of 2.5 and 5.0 mg/kg. Apomorphine is considered to stimulate the dopamine receptors in the telencephalon and induces stereotyped behaviour. The responsivity to apomorphine can be rated as a total stereotypy-score. SAL (aggressive) mice showed a significantly greater enhancement of stereotyped behaviour in response to apomorphine than LAL (non-aggressive) mice. In addition, it was demonstrated that this difference is of a quantitative rather than qualitative character. Pharmacokinetic variation between the two lines could be ruled out as cause of the difference. Hence, it was concluded that SAL mice are more sensitive to apomorphine than LAL males, which provides evidence for a difference in the dopaminergic system between the two selection lines. It was suggested that this difference underlies the difference in flexibility in behaviour between aggressive and non-aggressive male mice.

Aggression↗
PubMed1988

Aggression and adaptation to the light-dark cycle: role of intrinsic and extrinsic control.

In wild house mice, the hypothesis that in the organization of behavior the relative contribution of intrinsic factors is more important in aggressive males, while that of extrinsic factors is more important in nonaggressive individuals was confirmed using the circadian rhythmicity of activity. The faster rate of reentrainment and the suppression of activity during a subjective night and during adaptation to the new LD cycle in the nonaggressive males indicate that their circadian rhythmicity of activity is to a large extent determined by the Zeitgeber, an extrinsic factor. The slower reentrainment rate, the lack of response to a subjective night and the normal activity level seen during reentrainment in the aggressive mice suggest strong control by the pacemaker, an intrinsic factor. Tau differences between the aggressive and nonaggressive mice provide some evidence that the pacemaker of nonaggressive males is fairly labile and is easily influenced by external factors, whereas the pacemaker of aggressive animals is rather stable.

Acclimatization↗
PubMed1981

Artificial selection for short and long attack latencies in wild Mus musculus domesticus.

Artificial selection for short and long attack latency levels in wild male Mus musculus over 11 generations was successful for short latencies. The realized heritability of 0.30 is comparable to those found in other selection studies on aggression. In part selection may have been for faster onto-genetic development of short attack latencies. Four attempts to select for longer attack latencies failed because the lines died out immediately or within two generations for unknown reasons. But neither the physical condition of the animals nor their behavior appeared to have been the cause. Female aggressiveness as measured in female-female encounters was not affected by the selection exerted on the males. This suggests that no genetic correlation exists between aggressiveness of males and females, confirming results of P. D. Ebert and J. S. Hyde [(1976). Behav. Genet. 6:291-304] obtained in a selection experiment on aggression using females.

Aggression↗