Dimorphic Behavior
https://auctoresonline.org/article/dimorphic-behavior-and-cognition
Maria Dalamagka
Sexual differences in the
structure and functions of the human brain have been the subject of much
speculation ever since the time of Greek antiquity. Aristotle, designated the
moment at which the male fetus receives its soul at the 40th day of
gestation, whereas the female fetus was supposed to become antimated only six
weeks later, around the 80th day of pregnancy. In the course of 19th
century the interest in the sexual dimorphism of the human brain grew rapidly.
The first studies reported that the male brains were larger and more
asymmetrical than the female brains and that men had relatively more brain
substance in front of the central sulcus than behind (Swaab and Hofman 1984).
The existence of these comparatively minor nad seemingly random morphological
sex differences in the human brain were often used in support of the biological
view of that era, that men were intellectually superior to women nad that white
upperclass people were superior to the other races and lower classes.
Sex differences
in behavior are the result of natural and sexual selection. The dimorphic
classes of behavior described here, courtship, copulatory, and parental
behaviors, reflect both kinds of evolutionary selective pressures. The term dimorphism refers to the existence of two distinct forms within a
single species. The term sexually dimorphic behavior, by extension, implies two
different forms of behavior exhibited by the male and the female. To describe
these behavioral differences between the sexes as sexual dimorphisms does not
violate common usage of the term by the morphological sciences. Among mammalian
forms, both sexes have a pelvis. The difference between the sexes is not in the
presence or absence of a pelvis or pelvic outlet , but in its size, girth , or
other quantitative measure. Countless
examples exist in morphology of sexual dimorphisms based only on quantitative
differences, differences in intensity, or in response of a specific structure
to hormonal stimulation. Current concepts of morphogenesis hold that the genetic sex of all
vertebrates determines whether the embryonic genital ridge develops into a
testis or an ovary. The means of action by which chromosomes direct the
differentiation of the embryonic gonad are unknown; but it is known that the
type of gonad differentiated determines by its secretory products whether male or female secondary
reproductive organs develop. According to the organizational hypothesis
(Phoenix et al., 1959), not only the reproductive organs but also the neural
processes mediating sexual behavior in mammals have the intrinsic tendency to develop
according to a female pattern of body structure and behavior.
Sex steroids can be regarded
as master regulators of sex- specific behaviors ( Morris et al., 2004; Baum,
2003 ). The devel- opmental influence (organizational role) of sex hormones can
lead to enduring effects on brain and behavior. By contrast, in adults sex
steroids elicit reversible changes (activational role) in neural circuits and
behavior. Gonadal hormones bind to distinct nuclear hormone receptors that are
essential for sex- typical displays ( Scordalakes and Rissman, 2003; Raskin et
al., 2009; Kudwa and Rissman, 2003; Wersinger et al., 1997; Juntti et al.,
2010; Ogawa et al., 2000; Lydon et al., 1995 ). These receptors directly
regulate gene expression by binding DNA ( Mangels- dorf et al., 1995 ), and
they can initiate nontranscriptional signaling via mechanisms such as
interactions with intracellular kinases and transmembrane receptors ( Foradori
et al., 2008; Lishko et al., 2011; Micevych and Dominguez, 2009; Revankar et
al., 2005; Vasudevan and Pfaff, 2008; McDevitt et al., 2008 ). Sex hormones or
their metabolites can also bind to neurotrans- mitter receptors to gate their
activity (Henderson, 2007). Such nontranscriptional signaling can control
neural function at time scales that allow real time modulation of behavior.
Prior work has identified
genes downstream of sex hormones that regulate sexually dimorphic behaviors ( Kayasuga
et al., 2007; Wersinger et al., 2002; Nelson et al., 1995; Winslow and Insel,
2002 ). The relative paucity of such genes is in contrast to the diversity of these
behaviors, and suggests that the underlying neural circuits may be regulated
largely by nontranscriptional hormone signaling.
Sexually dimorphic influences
on human cognition and behaviour may affect the phenotypic expression of ‘disorders’
and ‘traits’. ‘Disorders’ are sporadic/heritable abnormalities due to
non-functional or otherwise mutated genes. ‘Traits’ represent normal variation
in sexually dimorphic characteristics. X-linked disorders, such as fragile X
syndrome or Rett syndrome, are sexually dimorphic in their expression but they represent
extreme cases – dysfunction of a critical gene, even though expression of that
gene might be neither dominant nor recessive in the conventional Mendelian
sense. X-linked behavioural traits, quantitative variants, include male
aggression and parental behaviour. Sexually
dimorphic cognitive traits include spatial orientation; in rodents, male spatial
learning advantages observed in the radial or water maze are caused by
male–female differences in strategy selection. Females (rats and humans)
navigate preferentially using landmarks, but males rely on a broader set of
spatial representations. These traits are probably influenced by a Y-linked
locus , although an X-linked locus may play a contributory role . During
evolution, could X-linked genes for specific cognitive abilities, and a female
preference for males who demonstrate those traits, have become closely linked, and
hence jointly inherited ? Owing to the obligatory expression of all X-linked
genes in males, any X-linked trait that is advantageous to males (or to
females) would spread rapidly in the population. If higher cognitive abilities
were a critical step in our own evolution, it makes sense that you might find
those functions on the X-chromosome.
Studies on human
facial sexual dimorphism have yielded intriguing insights into perceptions of other
characteristics, such as attractiveness or
trustworthiness, based on facial masculinity or
femininity. Specifically, by manipulating the degree of sexually dimorphic
facial traits in computerized faces, scientists have been able to study what
judgmental differences arise as a result of physical alterations. What is
significant about these findings is their evolutionary implications, in
particular the facial cues that trigger innate judgments in reaction to a
masculine or feminine face. Multiple studies have confirmed the correlations
between sexually dimorphic faces and ratings of attractiveness (Smith et al.
2008; Lee et al. 1998; Welling et al. 2008), and many psychologists theorize
that such judgments are evolutionarily based. Sexual selection in humans is
largely based upon facial cues and their reflection of an individual’s
reproductive quality. In a recent study, Little et al. (2008) found that
symmetry and sexual dimorphism in faces are both judged as more attractive to
the opposite sex, leading the researchers to conclude that both qualities are
reflective of biological quality, and that such judgments are likely to be the
result of sexual selective pressures and mate choice preferences. Much research
has been conducted on external judgments of personality as they relate to
facial asymmetry and neuroticism (Stackelford & Larsen, 1997), facial
symmetry and personality (Fink et al., 2006), facial attractiveness and
narcissism (Holtzman and Strube, 2009) and judgment accuracy differences
between the sexes (Penton-Voak et al, 2006).
References
Akesson, T.R., Mantyh, P.W., Mantyh, C.R., Matt,
D.W., and Micevych, P.E. (1987). Estrous cyclicity of 125I-cholecystokinin
octapeptide binding in the ventromedial hypothalamic nucleus. Evidence for
downmodulation by estrogen. Neuroendocrinology 45 , 257–262.
Arnold, A.P., Rissman, E.F., andDe Vries, G.J.
(2003). Two perspectivesonthe origin of sex differences in the brain. Ann. N Y
Acad. Sci. 1007 , 176–188.
Baum, M.J. (2003). Activational and
organizational effects of estradiol on male behavioral neuroendocrine function.
Scand. J. Psychol. 44 , 213–220.
Bendesky, A., Tsunozaki, M., Rockman, M.V.,
Kruglyak, L., and Bargmann, C.I. (2011). Catecholamine receptor polymorphisms
affect decision-making in C. elegans. Nature. Available at:
http://www.ncbi.nlm.nih.gov/pubmed/ 21412235
[Accessed April 17, 2011].
Blaustein, J.D. (2008). Neuroendocrine
regulation of feminine sexual behavior: lessons from rodent models and thoughts
about humans. Annu. Rev. Psychol. 59 , 93–118.
de Bono, M., and Bargmann, C.I. (1998). Natural
variation in a neuropeptide Y receptor homolog modifies social behavior and
food response in C. elegans. Cell 94 , 679–689.
Cahill, L. (2006). Why sex matters for
neuroscience. Nat. Rev. Neurosci. 7 , 477–484.
Canteras, N.S., Simerly, R.B., and Swanson, L.W.
(1995). Organization of projections from the medial nucleus of the amygdala: a
PHAL study in the rat. J. Comp. Neurol. 360 , 213–245.
Carroll, J.S., Meyer, C.A., Song, J., Li, W.,
Geistlinger, T.R., Eeckhoute, J., Brodsky, A.S., Keeton, E.K., Fertuck, K.C.,
Hall, G.F., et al. (2006). Genome- wide analysis of estrogen receptor binding
sites. Nat. Genet. 38 , 1289–1297.
Clodfelter, K.H., Holloway, M.G., Hodor, P.,
Park, S.-H., Ray, W.J., and Waxman, D.J. (2006). Sex-dependent liver gene
expression is extensive and largely dependent upon signal transducer and
activator of transcription 5b (STAT5b): STAT5b-dependent activation of male
genes and repression of female genes revealed by microarray analysis. Mol.
Endocrinol, 20 , 1333– 1351.
Cooke, B.M. (2006). Steroid-dependent plasticity
in the medial amygdala. Neuroscience
138 , 997–1005
Cooke, B., Hegstrom, C.D., Villeneuve, L.S., and
Breedlove, S.M. (1998). Sexual differentiation of the vertebrate brain:
principles and mechanisms. Front. Neuroendocrinol. 19 , 323–362.
Dugger,B.N.,Morris,J.A.,
Jordan,C.L.,andBreedlove,S.M.(2007).Androgen receptors are required for full
masculinization of the ventromedial hypothal- amus (VMH) in rats. Horm. Behav.
51 , 195–201.
Dulac, C., and Wagner, S. (2006). Genetic
analysis of brain circuits underlying pheromone signaling. Annu. Rev. Genet. 40
, 449–467.
Enoch, M.-A., Hodgkinson, C.A., Yuan, Q.,
Albaugh, B., Virkkunen, M., and Goldman, D. (2009). GABRG1 and GABRA2 as
independent predictors for alcoholism in two populations.
Neuropsychopharmacology 34 , 1245–1254.
Foradori, C.D., Weiser, M.J., and Handa, R.J.
(2008). Non-genomic actions of androgens. Front. Neuroendocrinol. 29 , 169–181
Gagnidze, K., Pfaff, D.W., and Mong, J.A.
(2010). Gene expression in neuroen- docrine cells during the critical period
for sexual differentiation of the brain. Prog. Brain Res. 186 , 97–111.
Garcia, L.R., Mehta, P., and Sternberg, P.W.
(2001). Regulation of distinct muscle behaviors controls the C. elegans male’s
copulatory spicules during mating. Cell 107 , 777–788.
Henderson, L.P. (2007). Steroid modulation of
GABAA receptor-mediated transmission in
the hypothalamus: effects on reproductive function. Neuro- pharmacology 52 ,
1439–1453
Barrett, L. F., & Pietromonaco, P. R. (1997).
Accuracy of the five–factor model in predicting perceptions of daily
social interactions. Personality and Social Psychology Bulletin,
Volume 23, 1173–1187.
Bronstad, M., Langlois, J., Russell, R (2008).
Computational models of facial attractiveness judgments. Perception,
Volume 37, 126-142.
Carré, J., McCormick, C., Mondloch, C. (2009). Facial
Structure Is a Reliable Cue of Aggressive Behavior. Psychological Science,
Volume 20, 1194-1198.
Fink, B., Neave N., Manning J., Grammer K. (2006).
Facial symmetry and judgements of attractiveness, health and personality.
Personality and Individual Differences, Volume 41, 491-499.
Fink, B., Neave N., Manning J., Grammer K. (2005).
Facial symmetry and the ‘big-five’ personality factors. Personality and
Individual Differences, Volume 39, 523-529.
Holtzman, N.S., Strube, M.J. (2009). Holtzman, N.S.,
Strube, M.J., Narcissism and Attractiveness, Journal of Research in
Personality, doi: 10.1016/j.jrp.2009.10.004.
Noor, F., Evans, D.C. (2003). The effect of facial
symmetry on perceptions of personality and attractiveness. Journal of
Research in Personality, Volume 37, 339–347.
Penton-Voak, I.S., Pound, N., Little, A.C., &
Perrett, D.I. (2006). Personality judgments from natural and composite facial
images: More evidence for a “kernel of truth” in social perception. Social
Cognition, Volume 24, 490-524.
Smith, F., Jones, B., DeBruine, L., Little, A. (2008).
Interactions between masculinity–femininity and apparent health in face
preferences. Behavioral Ecology, Volume 20, 441-445.
Watson, D. (1989). Strangers’ ratings of the five
robust personality factors: Evidence of a surprising convergence with
self-report. Journal of Personality and Social Psychology, 57,
120-128.
Khaitovich P, Hellmann I, Enard W, Nowick K,
Leinweber M, Franz H, Weiss G, Lachmann M & Paabo S. Parallel patterns of
evolution in the genomes and transcriptomes of humans and chimpanzees.
Science 2005 309 1850–1854.
Preuss
TM, Caceres M, Oldham MC & Geschwind DH. Human brain evolution: insights
from microarrays. NatureReviewsGenetics 2004 5 850–860.
Hurst LD.
Evolutionary genomics. Sex and the X. Nature 2001 411 149–150.
Caceres
M, Lachuer J, Zapala MA, Redmond JC, Kudo L, Geschwind DH, Lockhart DJ, Preuss
TM & Barlow C. Elevated gene expression levels distinguish human from
non-human primate brains. PNAS
2003 100 13030–13035.
Gu J
& Gu X. Further statistical analysis for genome-wide expression evolution
in primate brain/liver/fibroblast tissues. Human Genomics 2004 1 247–254.
Dorus S, Vallender EJ, Evans PD, Anderson JR,
Gilbert SL, Mahowald M, Wyckoff GJ, Malcom CM & Lahn BT. Accelerated
evolution of nervous system genes in the origin of Homo sapiens. Cell
2004 119 1027–1040.
Check E. Genetics: the X factor. Nature 2005 434
266–267.
Khil PP & Camerini-Otero RD. Molecular
features and functional constraints in the evolution of the mammalian X
chromosome. Critical Reviews in Biochemistry and Molecular Biology 2005
40 313–330.
Charlesworth D & Charlesworth B. Sex
chromosomes: evolution of the weird and wonderful. Current Biology 2005 15
R129–R131.
Arnold AP. Sex chromosomes and brain gender.
Nature Reviews Neuroscience 2004 5 701–708.
Dobyns
WB, Filauro A, Tomson BN, Chan AS, Ho AW, Ting NT, Oosterwijk JC & Ober C.
Inheritance of most X-linked traits is not dominant or recessive, just
X-linked. American Journal of Medical Genetics. Part A 2004 129 136–143
Jonasson Z. Meta-analysis of sex differences in
rodent models of learning and memory: a review of behavioral and biological
data. Neuroscience and Biobehavioral Reviews 2005 28 811–825.
Stavnezer
AJ, McDowell CS, Hyde LA, Bimonte HA, Balogh SA, Hoplight BJ & Denenberg
VH. Spatial ability of XY sex-reversed female mice. Behavioural Brain Research
2000 112 135–143.
Ross J,
Roeltgen D & Zinn A. Cognition and the sex chromosomes: studies in Turner
syndrome.
Hormone Research 2006 65 47–56.
Zechner U, Wilda M, Kehrer-Sawatzki H, Vogel W,
Fundele R & Hameister H. A high density of X-linked genes for general
cognitive ability: a run-away process shaping human evolution? Trends in Genetics 2001 17 697–701.
.
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