Bruce effect

Source: Wikipedia, the free encyclopedia.

The Bruce effect, or pregnancy block,

Hilda M. Bruce,[4] and has primarily been studied in laboratory mice (Mus musculus).[1] In mice, pregnancy can only be terminated prior to embryo implantation, but other species will interrupt even a late-term pregnancy.[5]

The Bruce effect is also observed in

meadow voles,[7] collared lemmings,[8] and it has also been proposed, but not confirmed, in other non-rodent species such as lions[9] and geladas.[10]

Discovery

In an experiment published in 1959, zoologist

castrated or juvenile male mice.[4][11][12] The effect remained when the male mice were kept out of sight or hearing of the females. This suggested that females were distinguishing the males by smell. To test this hypothesis, Bruce and her colleague Alan Parkes recruited perfumers to smell pieces of cloth from the mouse cages. The perfumers could distinguish the smells of different mouse strains.[11]

Mechanisms of action

Detection of pheromones

The

knocked out in females, the presence of an unfamiliar male does not trigger pregnancy disruption.[17]

Recognizing familiar males

Exposure to a male's urinal

noradrenaline will lower the receptivity of the accessory olfactory bulb to these pheromones.[16] The pregnancy disruption will, thus, be averted. This role for noradrenaline has recently been called into question.[15] The hormone oxytocin is also important in this social memory process. Females treated with an oxytocin antagonist are unable to recognize the urinary scent of their mate, and will terminate pregnancy when exposed to any male, known or unknown.[18]

Neuroendocrine pathway

The activation of vomeronasal neuron receptors by male pheromones triggers a complex

corticomedial amygdala, accessory olfactory tract, and stria terminalis.[15] These areas stimulate the hypothalamus to increase the release of dopamine,[15][19] which thus prevents the secretion of prolactin from the anterior pituitary.[3] In the absence of prolactin, an essential hormone for maintaining the corpus luteum, luteolysis takes place.[3] As the corpus luteum can no longer release progesterone, the uterus remains unprimed for embryo implantation, and the pregnancy fails.[19]

Role of estrogens

bloodstream directly via nasal ingestion[13] and travel to the uterus, which has a high density of suitable receptors. Normally, E2 is essential in preparing both the blastocyst and uterus for implantation. However, excessive E2 will prevent implantation from taking place.[20][21] Castrated males are incapable of terminating female pregnancies,[22] except when castrated males are given testosterone.[13] estradiol, a metabolic product of testosterone, is known to disrupt pregnancy in females,[13]
and is present in male urine.

Timing

The incidence of the Bruce effect depends on the timing of pheromone exposure. Post-mating, females experience twice-daily surges of prolactin.[3] Pregnancy is only terminated if exposure to novel male scent coincides with two prolactin surges, one of these occurring in a daylight period.[19]

Evolutionary benefits

In order to have evolved and persisted in the population, the Bruce effect must afford individuals a fitness advantage.[3] The possible advantages of pregnancy block are widely debated.

Males

When given the opportunity, male mice tend to direct their urine in the female's direction.

subordinate
males.

Females

Females can control their likelihood of terminating pregnancy by pursuing or avoiding novel male contact during their most susceptible periods.[26] In this way, females can exert a post-copulatory mate choice, reserving their reproductive resources for the highest-quality male. Certainly, females are more likely to seek proximity to dominant males.[26] In many rodent species, males kill unrelated young; pregnancy block may avoid the wasted investment of gestating offspring likely to be killed at birth.[5][27] The Bruce effect is most common in polygynous rodent species, for which the risk of infanticide is highest.[28]

See also

References

  1. ^
    PMID 6380603
    .
  2. JSTOR 1381067
    .
  3. ^
    ISBN 978-0-387-73944-1. {{cite book}}: |journal= ignored (help
    )
  4. ^
    S2CID 4200823
    .
  5. ^
    S2CID 85020158
    .
  6. S2CID 42871324
    .
  7. PMID 5551417
    .
  8. PMID 7378528
    .
  9. S2CID 84927815
    .
  10. S2CID 34095168
    .
  11. ^ a b MRC National Institute for Medical Research (2014). A Century of Science and Health. MRC National Institute for Medical Research. p. 208.
  12. ISBN 978-0205239399
    .
  13. ^
    PMID 19793839
    .
  14. S2CID 36527505
    .
  15. ^
    S2CID 7946709
    .
  16. ^
    S2CID 4431624
    .
  17. PMID 17947352
    .
  18. PMID 18601710
    .
  19. ^
    PMID 2513390
    .
  20. PMID 11704118
    .
  21. PMID 12601161
    .
  22. PMID 14337805
    .
  23. S2CID 39461569
    .
  24. PMID 7120182
    .
  25. S2CID 44346136
    .
  26. ^
    PMID 19324836
    .
  27. S2CID 85097151
    .
  28. doi:10.1163/156853908X390968
    .

Further reading
Retrieved from "https://en.wikipedia.org/w/index.php?title=Bruce_effect&oldid=1190915175"