Sexual hormones produced differ from male to female.

Sexual dimorphism, comparing
behaviours and hormones in male and females.



Sexual dimorphism is seen in many species across the
whole animal kingdom, but this is more than just the size, appearance and
sexual organs of animals. It also involves the behaviour of the species,
hormones produced, rates of growth, blood formation, metabolism and endocrine
activity (GLUCKSMANN, 1974). This paper will be dwelling deeper into
behaviours which may occur in animals and how they differ from the other sex. This
will also consider the paternal behaviours which happen between species and if
hormones produced differ from male to female. Papers have shown that the age
range of species will influence hormones which are produced and behaviours
which can be performed. Over time evolution has played a part in the
development of sexual dimorphism of male and female traits (Plavcan, 2001),
this could be another possibility of the differentiation in the animal kingdom.
Sexual dimorphism is thought to generally be caused by sexual selection (Ralls, 1977) but
other factors can also affect this such as organizational effects and
activational effect (Beatty, 1979) which shall be discussed more in depth.


and Activational effect

The brain and behaviour are affected by the actions of
the sex steroids, these are traditionally known as organizational and
activational effect (ARNOLD, 1985). Organizational effects are permanent and occur in early
development (ARNOLD, 1985) and preliminary structures start to form reproductive
organs, for the female ‘Mullerian ducts’ and for the male ‘Wolffian ducts’. When
in the development stage all embryos have both ‘ducts’ this is called bipotential
(, 2018). If no hormones are secreted, then the Wolffian ducts
degenerate and the Mullerian ducts start to form as the female reproductive
organs in mammals. If anti-Mullerian hormones (AMH) and testosterone are released,
then the Mullerian ducts degenerate and the Wolffian ducts start to form into
the male reproductive organs. Defeminization and masculinization are needed if
the zygote is to complete the normal development of the male brain (Baum, 1979).
Exposure from    testicular androgens
cause these to processes to happen (Baum, 1979). Activational effects such as
the loss of capacity for estradiol and progesterone to induce female sex
behavior are lost, then this is known as defeminization (SCHWARZ and MCCARTHY,
2008). Masculinization is the development of sex changes and the organizational
of neural substrate to express male sexual behavior (SCHWARZ and MCCARTHY,

Activational effects occur throughout life and are learnt behaviors and
thought to be called this because this because they activate neural pathways
which are already existing (ARNOLD, 1985). An
example of this is seen in the female guinea pig, when they are exposed
testosterone propionate their behavior will start to defeminize and will start
to show more masculine behaviours, whilst if a genetic male is deprived
throughout its perinatal life from androgens then they will be permanently
feminized and demasculinized during adulthood (ARNOLD, 1985).






Sex determination is different across the whole animal
kingdom, the sex determination is dependent on a series of molecular events
which cause the bipotential gonad to form into an ovary or into the testes (Öçal,
2011). In mammal’s females have two X chromosomes and the male has a X and Y
chromosome, the sperm carries the sex chromosome which determines the sex of
the offspring. Testes are formed during the sixth week of gestation if a male
was to be determined, the sex-determining region Y (SRY) initiates this by down
streaming the regulation of sex-determining factors (Öçal, 2011). This SRY gene
is located in the Y chromosome. After its release, SOX-9 gene is activated and
is upregulated by the developing testis (Öçal, 2011). SOX-9 is essential for
the further development of the testes as it up-regulates other genes such as
PGD2 and FGF9, this then allows SOX-9 to maintain being expressed causing to a
feed-forward loop in the XY gonads (Öçal, 2011). Next AMH is released this
causes the Mullerian ducts to degenerate, AMH is produced by Sertoli cells and
androgens from the Leydig cells (Öçal, 2011). An insulin like factor (INSL3) is
used to descend the testes to the scrotum (Öçal, 2011). The production of
androgens is essential for the development to masculinize the mammals brain and

Females have different factors in which ovarian
differentiation, when the embryo has not been exposed to the SRY gene the
support cell differentiate as granulosa cells, this then starts the ovarian
pathway (Öçal, 2011). For the ovarian development a precise amount of DAX1 gene
must be expressed. If over expression of this gene happens this antagonises the
testes and stops them from forming. (Öçal, 2011). Ovarian development, maintenance
and regulation of the Mullerian ducts is a major role in which is played by the
gene WNT4, this signals down the pathways to keep these roles making sure the
ovaries are being developed, if this gene was absent then testes would start to
form (Öçal, 2011). The fallopian tubes, uterus and the upper 2/3’s of the vagina
rises due to the Mullerian ducts (Öçal, 2011), after this the development
carries on further. The genital tubercle forms in to the clitoris, the labia
majora starts to form from the labio-scrotal folding and the urethral begins to
fold a becomes the labia minora (Öçal, 2011).


behaviours and hormones used

Sex is sexually dimorphic, and a variety of behaviours
can be seen over throughout many species. The hypothalamic-pituitary-gonadal
(HPG) this refers to the hypothalamus, pituitary gland and the gonadal glands, each
one of these glands are within the endocrine system. The HPG axis helps to
promote and maintain reproduction (Yonker et al., 2011) by releasing hormones
for the male and the female. In the male rat during puberty the HPG becomes hyper
activated, this causes more frequent releases of luteinising hormone (LH) causing
large amounts of testosterone to be released (Ivell, Heng and Anand-Ivell,









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steroids on brain and behavior: A reanalysis. Hormones and Behavior,
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Baum, M. (1979). Differentiation of coital behavior in mammals: A
comparative analysis. Neuroscience & Biobehavioral Reviews,
3(4), pp.265-284.

Beatty, W. (1979). Gonadal hormones and sex differences in
nonreproductive behaviors in rodents: Organizational and activational
influences. Hormones and Behavior, 12(2), pp.112-163.

Reviews, 49(4), pp.423-475.

Ivell, R., Heng, K. and Anand-Ivell, R. (2014). Insulin-Like Factor 3
and the HPG Axis in the Male. Frontiers in Endocrinology, 5.

Öçal, G. (2011). Current Concepts in Disorders of Sexual
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3(3), pp.105-114.

Plavcan, J. (2001). Sexual dimorphism in primate evolution. American
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Ralls, K. (1977). Sexual Dimorphism in Mammals: Avian Models and
Unanswered Questions. The American Naturalist, 111(981),

SCHWARZ, J. and MCCARTHY, M. (2008). The role of neonatal NMDA receptor
activation in defeminization and masculinization of sex behavior in the
rat. Hormones and Behavior, 54(5), pp.662-668. (2018). Sex Determination and Differentiation |
SexInfo Online. online Available at:
Accessed 11 Jan. 2018.

Yonker, J., Chang, V., Roetker, N., Hauser, T., Hauser, R. and Atwood,
C. (2011). Hypothalamic–pituitary–gonadal axis homeostasis predicts
longevity. AGE, 35(1), pp.129-138.


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