assignment # 04 - review of the paper "Testosterone and aggression in Birds"

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This blog was designed as an assignment for the

BIOL 4550 course at Memorial University of Newfoundland

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A review of the paper "Testosterone and Aggression in birds"

by John C. Wingfield, Grerogy F. Ball, Alfred M. Duffy Jr, Robert E Hegner and Marilyn Ramenofsky.

this paper can be found at:  

http://www.jstor.org/stable/pdfplus/27854889.pdf?acceptTC=true

 

 

 

Summary


This paper is a review of other currently published papers. By using radioimmunoassay, the described researchers are able to investigate plasma testosterone levels in birds in both field (“free-living”) and laboratory settings.

 

This paper discusses testosterone’s effects (both organizational and activational) in various species of birds.  The paper also describes the "challenge hypothesis", in which the correlation between elevated testosterone levels and aggression are only seen during periods of heightened interactions between males (for example during breeding season).

 This paper establishes that testosterone is involved in aggression, by summarizing other papers which have used castrated, non castrated and testosterone-injected birds.  When the testes/elevated testosterone levels are present, increased frequency and intensity of aggression and sexual behaviours (singing, threat postures & fights) can be seen.  The paper then continues to indicate that a hierarchy can be established, after which habituation occurs in order to avoid costly fighting between neighbouring birds. This habituation is signified by a constant level of testosterone (no more elevated levels of testosterone upon encountering this neighbour.  While an injection of testosterone will increase aggression, the established social hierarchies generally do not change.

 

This paper indicates that both visual and auditory stimuli are needed together in order to elevate the testosterone levels in birds. One experiment was to use a male decoy bird (& a recorded bird song) to stimulate an intrusion onto a territory. Males who were exposed to the decoy had higher levels of testosterone than the birds who weren't exposed to the decoy, but only after 10 minutes. It was also shown that the neighbours of the fighting birds had a constant level of testosterone; preventing a 'ripple effect', in which all the birds of a population would have a surge in testosterone (and decreases in parental care).

The paper also mentions that levels of aggression can be influenced by: the species, social context, demographics and environmental influences. Some environmental influences include the lenght of the day (long days lead to increased testosterone), territory boundaries and challenging males (which lead to the challenge hypothesis). 

The usual trend that is observed is that LH and testosterone rises in spring, remains elevated throughout the breeding season and decreases after the breeding season.  Different reproductive strategies will have different levels of testosterone.  Monogamous males have high levels of testosterone for short periods; during territory establishment and sometimes during egg laying phase (mate guarding).   Meanwhile polygamous males have elevated levels of testosterone for longer periods of time, because they need to fight males for multiple females.  When a male bird needs to guard its mate/territory/resources from other male birds, an elevated level of plasma testosterone can be observed. However if there are plentiful resources and females, there will be less competition and low levels of plasma testosterone can be observed.

 

 

Paper critiques

The figures were very good in illustrating some of the points of the paper. For example figure 4 helps to illustrate the different changes in the levels of plasma testosterone that are present in each reproductive strategy.  While figure 3 helps to illustrate the importance of taking measurements of each phase of reproduction as opposed to just averaging the data across the entire year.

However, the figures and tables given do not have any recorded significance value associated with the data; we are eant to assume that the proper statistical tests were performed and that the data is significant.  Also on figures 4 and 5, there are no scale given for the plasma testosterone levels.

 


Possible future experiments

Will birds (with no prior hierachies), who are injected with various levels of testosterone, form hierachies in which their status is correlated to the amount of testosterone that was injected?

In order to investigate this experiment, the researchers could observe birds and calculate a baseline aggression for each bird in each group.  They could then take a bird from each group that had the same aggression rating and inject varying amounts of testosterone and place them into a neutral area.  A few weeks later, the researchers could calculate baseline aggressions again to see if hierarchies formed in relation with the amounts of testosterone that were initially injected.

 

References

 

 

 

Wingfield, J. C., Ball, G. F., Jr., A. M. D., Hegner, R. E., & Ramenofsky, M. (1987). Testosterone and aggression in birds. American Scientist, 75(6), pp. 602-608. Retrieved from http://www.jstor.org/stable/27854889

Assignment # 03 - Testosterone function

Testosterone can be found in both males and females.  Testosterone plays an important role during fetal development, puberty and throughout the adult life.  A lack of testosterone in either sex is referred to as “hypogonadism”.

Function & the effects of Hypogonadism

Development

During fetal development, testosterone masculines the brain (by changing into estrogen & crossing the Blood brain barrier) and develops male characteristics of the brain [Mainwarring, 1977].  Hypogonadism during this phase would result in mental retardation, underdeveloped male genitals, or development of female genitalia [Mayo clinic].

Puberty

During puberty testosterone is responsible for increasing muscle mass, adipose tissue, body hair, development of breast tissue (in women), and growth of male genitalia [Mayo clinic].

Hypogonadism can lead to delayed or absent puberty (delayed, underdeveloped or absence of the aforementioned effects of testosterone).

  

Adulthood

during adulthood testosterone is responsible for  Well-being, aggression, cognitive function, bone mineral density and sexual libido in men and women.

 

In women 

Testosterone is involved with greater well-being and with reduced anxiety/depression, puberty and is an important component of female sexuality [Davis, 2001].  In women, testosterone deficiency is characterized by fatigue, and decreases in: motivation, libido, well-being and available “free” Testosterone.  Orally administered estrogen (the pill) can decrease free testosterone by creating more SHBG to bind to the testosterone [Davis, 2001].Hypogonadism in women is less studied, but can be seen after a hysterectomy, injection of exogenous estrogen or during menopause [Davis, 2001].  Testosterone replacement therapy is under investigation for women (methyltestosterone can be prescribed in the United States) [Davis, 2001]. 

In men 

Testosterone is involved with fetal development, mood, aggression, cognitive function, bone mineral density and sexual libido [Howell, 2001].  Hypogonadism in men can result in erectile dysfunction, infertility, fatigue, development of breast tissue, decrease in body hair, bone mass, libido and muscle mass [mayo clinic].  Treatment includes androgen replacement (oral testosterone, intramuscular injections, subcutaneous implants and transdermal therapy) [Howell, 2001].

Hypogonadism

 

Decreased testosterone can cause: 

Lack of libido

Infertilty

Late/absent puberty

Lack of energy

Depression 

Mood swings

 

Treatment can include:

 Hormone replacement therapy

exercise

dietary changes

stress reduction

 

 

Types of Hypogonadism: 

Primary hypogonadism  = Congenital  testicular dysfunction

Develomental problems while still in the womb can cause problems with testosterone production in the testes.  Because the hypothalamus and pituitary are functioning properly, there will be elevated levels of LH & FSH, but still no testosterone production.

Can be due to:

FSH and LH receptor mutations

Cryptorchidism

Myotonic dystrophy

Klinefelter's syndrome: A male who has an extra X chromosome. The most common genotype is XXY.  There will be a problem with testosterone production by the testes.

 

Secondary hypogonadism =  Aquired  hypothalamic-pituitary dysfunction

The hypothalamus and pituitary are not functioning correctly.  Low levels of LH & FSH will cause no signal to the testes to produce the testosterone.  

Can be due to:

-aging (called "andropause" in men).

-pituitary tumours

-ingestion of drugs

-head trauma

 

References

Davis, S. (2001) Testosterone deficiency in women. The Journal of reproductive medicine. Vol 46. Pg 291-296

Howell, S (2001) Testosterone deficiency and replacement. Hormone research, vol 56, pg 86

  

Mainwaring, W.I.P (1977) The Mechanism of Action of Androgens.  Springer-Verlag New York Inc. pg.32-41

Websites

 

Mayo clinic (2010) Mayo Foundation for Medical Education and Research (MFMER). found at www.mayoclinic.com

(2006) Cecil Texbook of Medicine found at: http://enotes.tripod.com/hypogonadism.htm