download.jpgbrain-scan.jpgimages (1).jpg
Behaviour and aggression in developing brains

Article: Arrested Developmenthttp://www.nature.com/news/science-in-court-arrested-development-1.10456

Group Members
Alexei Brown - z3415162
Michelle Qiu - z3416120
Matthew Lippa – z3373725
Neal Bromfield - z3415498


1. Introduction

Teenage development used to be understood as being simply somewhere between children and adults. Hormones, overprotective parents and the need for independence were all thought to be the cause of the differences in behaviour. Thanks to state of the art research methods such as magnetic resonance imaging, it is becoming evident that the teenage brain operates entirely differently to that of an adult.

Lizzie Buchen’s article Science in Court: Arrested Development, featured in the journal Nature, analyses the contemporary research on brain development and the impact it has on the sentencing of juveniles in the United States. The article examines the conflict between the criminal justice system and modern scientific understanding of brain development.
Neuroscience is currently being used as evidence of the immaturity of adolescent brains in juvenile courts, but perhaps the court system should be weary of the malleability of scientific understanding. Can we understand juvenile cases that question the intent of the accused by understanding the nature of the developing brain? There has been much behavioural research that demonstrates that adolescents are more impulsive, less responsible and take greater risks than adults. However, skeptics point out that while our understanding of structural changes in the developing brain increases it does not change the type of punishments are that appropriate nor the severity of the crime.

Our research examines the extent to which brain development impacts teenage maturity and aggression. The neurobiology of the adolescent brain will be explored first, followed by the impact of on behaviour.
teen-brainx-large.jpg
Fig 1. By Gary Olsen, Dubuque Community School District


Recent neuroimaging research has shown that much growth and change occurs during adolescence (Johnson, Blum, & Giedd, 2009). The frontal lobes,
responsible for executive functions such as: impulse control, planning, and attention, are one of the last areas of the brain to mature (Johnson et al., 2009). Poor executive functioning can impair judgement and decision-making.

Chemical components, such as neurotransmitters and hormones, can play a large role in affecting behaviours such as aggression. Noradrenaline and low levels of serotonin can affect aggression and impulsiveness in the developing brain. Hormonal neuropeptides oxytocin and vasopressin also play essential roles in regulating behaviours such as aggression. Finally, there will be a critical analysis of the use of neuroscience in the juvenile court system.



2. Neuroscientific Context


2.1 Adolescent brain


There has been a large amount of research that establishes that there is much growth and change in the brain during adolescence. This research has been conducted using imaging technologies such as functional and structural magnetic resonance imaging (fMRI and sMRI) (Johnson et al., 2009). During adolescence, cortical brain areas thicken as neural connections grow, and myelin - fatty cell material - wraps around neural connections (Johnson et al., 2009). Simultaneously, connections that are seldom used are pruned away. MRI data shows that grey matter increases into the early teens and then decreases throughout life. The volume of white matter, which reflect myelination of axons, increases during puberty (McAnarney, 2008). Myelination and pruning enhance the brain’s ability to transfer information to different areas in an effective way.

teen-white-matter_300.gif
Fig. 2 Graph showing strength of connections across ages

Teenage brains are built to seek out thrills, skills, and new experiences. They are highly responsive to rewards and emotions when making decisions. The reason for this is because the nucleus accumbens, which develops early, seeks pleasure and rewards. This accounts for exaggerated sensitivity to rewards, and also applies to taking away rewards eg. restricting time on the computer and internet or grounding. Early development of this area is advantageous as it is a crucial period for learning in adolescence. While the back of the brain becomes quite strong, the prefrontal cortex at the front of the brain needs further development. Emotional maturity also develops by way of growth of neural connections between the amygdala (the emotional centre of the brain) and frontal lobes (Johnson et al., 2009). Several researchers have professed that a gap in maturation between the socio-emotional part of the brain, which develops early in adolescence, and the cognitive control system, which develops in late adolescence, may help to explain risk-taking behaviour in juveniles (Johnson et al., 2009).





2.2 Pre-frontal cortex

The pre-frontal cortex is the area behind the forehead which is part of the frontal lobe. It regulates behaviour and emotions and is the last part of the brain to complete development.

Why is the pre-frontal cortex important?
prefronta;.jpg
Fig.3

  • Personality expression
  • Decision making and predictive cognition
  • Moderating social behaviour
  • Impulse control
  • Judgement and reasoning

In figure 3, the difference between a normal individual's MRI in comparison to a sample murderer's is evident in a significant lack of activation in the pre-frontal cortex.
It turns out the connection between the frontal lobe and the rest of the brain is not as strong. This is because teenagers do not have the same amount of myelin that adult brains have. Recent studies have shown that neural insulation isn't complete until mid 20s.
Some criminals do show an activation in the pre-frontal cortex but lack it in the amygdala.


2.3 Amygdala

b1.jpg
Fig.4.2 Teens rely on the amygdala
b2.jpg
Fig.4.1 Adults rely more on the frontal cortex

Reactions, rather than rational thought, emerge from the amygdala. Neural connections between the amygdala and the frontal lobe become denser as we approach adulthood, accounting for emotional maturity.
When processing emotions, teenagers rely on the amygdala shown in figure 4.2, while adults rely more on the frontal cortex shown in figure 4.1.
When we see fully functioning pre-frontal cortex in criminals there is usually a lack of activation in the amygdala. Psychopaths lack emotion, empathy, remorse, guilt.

The amygdala is involved in emotional regulation, especially of fear and aggression. Damage to the amygdala has been linked to emotional and social disturbances. There have been cases such as in that of Charles Whitman where effects on the amygdala have resulted in very serious behavioural and social malfunction. Stimulation of the amygdala in hamsters has increased aggressive responses (Potegal et al., 1996). Several experiments carried out on the hamsters support the claim that the amygdala is a component in the aggression pathway. In primates however compared to other animals the function of the amygdala in mediating aggressive response is believed to be more affected by the context of the situation. It is less clear in primates as lesions to the amygdala lead to increases in both socially altruistic responses or aggression (Amaral et al, 2006).


3. Neurobiology of Aggression


There are multiple pathways within the neocortical and subcortical structures of the brain which are highly involved in the regulation of aggressive behaviour. Critical areas in mammals in controlling the expression of aggression are found within the hypothalamus and certain areas of the mid brain (Hermans et al., 1983). The exact pathways involved in controlling aggressive behaviour may vary depending on the trigger and the intention.

The hypothalamus and periaqueductal gray of the midbrain, are areas which control the autonomic and behavioural components of aggression in most mammals studied. The role of the hypothalamus with aggressive behavioural responses can be observed by interacting with the hypothalamus with electronic stimulation, aggressive behaviour reactions can be produced. The receptors that mediate this in the hypothalamus determining aggression levels are based on interactions of both serotonin and vasopressin (Delville et al., 1997). These vital areas have direct connections with other structures such as the amygdala and the prefrontal cortex that are important in the formation of an aggressive response. Certain neurotransmitters also have various effects on aggression depending on the pathway and other factors.

The pathway of aggression can be widely varied due to what is intended and what it is responding to. The role of the amygdala and pre-frontal cortex play a big role here.

3.1 Serotonin

Serotonin deficits are believed to be linked to increased instances of aggression, studies in mice have shown that serotonin sets the threshold for aggression (Audero et al, 2013).
Low levels of serotonin may also have other effect on other neurochemical systems such as the reward pathway further affecting an aggressive response. The effects of low level serotonin on aggression seem particularly apparent in the pre-frontal cortex (Caramaschi et al 2008). Mice with a knockout 5-HT1b recoptors are said to have an aggressive phenotype indicating in part the role in part of the interaction of serotonin and aggressive behaviour. Serotonin deficiency can thus be considered a trigger for adrenaline.

external image Dopamine_and_serotonin_pathways.gif

3.2 Noradrenaline

Noradrenaline or norepiniephrine can also influence aggression responses indirectly via hormonal pathways and directly acting on the central nervous system and the brain itself. Studies have found that "deficiency in monoamine oxidase A (MAOA), an enzyme that degrades serotonin and norepinephrine, has recently been shown to be associated with aggressive behaviour" (Cases et al 1996).

3.3 GABA

GABA is thought to tonically inhibit aggressive behaviour. This is by acting on the GABAA receptors. Levels of GABA are inversely correlated with aggression. However GABA agonists at low doses increase aggression and at high doses decrease aggression so it is a bitionic effect. GABA and serotonin have been used in studies exploring ways to reduce aggresive responses " GABAergic and serotonergic systems and have high efficacy and selectivity to reduce excessive levels of aggressive and violent behaviors without side-effects" (Rosa et al).

3.4 Dopamine

Dopamine inhibits maternal aggression. In the ventral tegmental area of the brain lesions of dopamine neurons results in increased instances of maternal aggression. It plays a role with serotonin in the regulation of aggression and in other complimentary pathways.

3.5 Testosterone

Testosterone has in some species shown to increase aggression but it is not all that clear. High testosterone levels are not always correlated with an increase in aggression in mammals. Studies done on hamsters showed that in female hamsters high testosterone and aggression are not correlated, nor in male hamsters who are not in breeding condition, the aggression role of testosterone is also sometimes not apparent in situations where androgen receptors have been changed. However testosterone is linked strongly to aggression and is highly relevant in regards to the article. At an adolescent stage higher levels of testosterone are present and while high levels of testosterone are not necessarily correlated for aggressive behaviour it is fundamental for its expression. Testosterone facilitates aggression by modulating vasopressin receptors in the hypothalamus. (Delville et al 1996)

In mice testosterone is required in development and adulthood for aggressive behaviour to be properly present. Females with high amounts of testosterone at birth in mice will display enhanced aggressive behaviour as adults.

3.6 Vasopressin

Vasopressin has been implicated in male-typical social behaviours including aggression. The receptor types for vasopressin are V1aR and V2R which is in the periphery but what we are interested in is V1bR.
Mice with knock out V1bR receptors have shown greatly inhibited aggression behaviour and the frequency of fights with intruder mice also severely reduced. However despite the reduction in aggression the mice with the V1bR KO suffered in the most meagre ability for social recognition and failed to have normal social preferences and were less motivated (Wersinger et al 2002).

3.7 Oxytocin

Oxytocin has roles in regulating bonds with others and offspring, it is active also in pathways regarding protective aggression (Heinrichs et al, 2008). Oxytocin in the central amygdala of hamsters has been shown also to increase maternal aggression.


In an adolescent brain many changes take place impacting on these neurotransmitters and hormones greatly affecting in some cases the aptitude of aggressive behaviour. Serotonin as mention above is a vital controlling aggression and deficits lead to an increase in aggressive behaviour. This is a highly relevant point in regards to adolescents as Serotonin is found to be
be up to 4 times lower in the anterior cingulate cortex in an adolescents brain compared to children and adult (Teicher et al 1999).

In adolescents it seems that many hormones and neurotransmitters are affected simultaneously in a way that greatly promotes aggression in a sense. Apart from serotonin the other great accomplice to an aggressive brain here is testosterone which is at the highest amount in a human lifetime in the adolescent phase.

By understanding the neurotransmitters and the neural mechanisms resulting in aggression we can better understand why this affects adolescents so severely.

(See Appendix III for further reading)


4. Critical Analysis

download (1).jpg

Behaviour in adolescence is a function of multiple influences including, but not limited to, experience, parenting, socio-economic status, nutrition, culture, psychological wellbeing and social interaction. Contemporary efforts to pinpoint the causes of aggression in the decision making process of some adolescents have had limited results.

Only once the underlying mechanisms of the development of criminals are understood can we hope to prevent and decrease criminal behaviour. The opportunity to innovate methods of intervention that reinforce positive development in adolescents seems more plausible as the research continues.

The desire to provide young adults with the tools not only to survive, but to thrive, in development is driving both the research and the discussion of adolescent brain development. At the forefront of this discussion are two unanswered questions. What causes adolescents to become criminals; and can we detect criminal dispositions early on? Science In Court: Arrested Development addresses both these questions directly, early on and in light of the criminal justice system.

The article argues that as development of the adolescent brain continues throughout the teenage years into the early 20’s, the justice system should prioritize rehabilitation over punishment for young adults. It bases this argument in myelination, synaptic pruning, and overall neurological changes. Previously, both myelination and synaptic pruning were thought to have been completed before the onset of adolescence. Myelination, as stated in the article “speed[s] up signal transmission in brain cells, particularly between brain regions”. The article then notes that diffusion tension imaging shows myelination occurring throughout early adult hood. Science In Court: Arrested Development is lacking in the demonstration of the connection between myelination and criminal behaviour. There is no citation to verify that the process of myelination leads to a predisposition to criminal activity, nor that it increases the efficacy of rehabilitation.

Similarly, “Structural magnetic resonance imaging (MRI) shows that [synaptic] pruning goes on into early adulthood”. However, it fails to thoroughly establish a well-demonstrated connection between synaptic pruning and criminal activity nor the effect of synaptic pruning and rehabilitation.

The final reference to neurobiological mechanisms is that “ongoing development affects activity levels in different parts of the brain”. The development of “functional MRI (fMRI), which reveals activity in the brain” has shown that significant changes to the developing brain of a young adult “occur in brain systems associated with impulse control, resisting immediate rewards and emotional processing”.

Whilst more nebulous than the other references, the article is able to cite both, the papers in which the changes have been seen, and the link between the neural mechanism and changes in behavior. It also clearly states that the changes in behaviors effected are strongly related to the decision making process that is relevant to criminal activity. Over active reward systems and the limited activity of the prefrontal cortex are well discussed and sources. A clear link between the activity of these components and risk taking behaviour is established and a strong case is made for prioritising rehabilitation over penalising. There is also an adequate discussion of the opinion of contemporary researchers directly involved.

This article does not stand up to the highest degree of scrutiny, but it does satisfy this critical analysis. The article discusses effects of developments in modern neuro-scientific research on the criminal justice system and society as a whole. Science In Court: Arrested development is well aware of the divergence between the large implications of this research and the nature of the research itself. The conflict between scientific research and the law making process makes up the majority of the article. The grey and un-biased nature of scientific research is clearly established. The black and while ambitions of the legal system making process is faithfully conflicted with the research presented.

This article was published in the journal Nature and it safely meets the standard of the journal. The article is well suited to its audience: the moderately educated and affluent readers and the structure and language reflects this. The science referenced is not intense enough to require background reading, yet it is explained at a detail that enhanced the overall validity of the article.

This article successfully exhibits the limitation of the research while triumphantly presenting the promise the science provides. This article intends to invigorate debate and neither exploits nor misrepresents the science it references. This article was chosen for its high quality and masterful delivery of information.


5. Appendices


5.1 Appendix I


We chose the topic in our first meeting by brainstorming. An initial idea was to find an article about the effect of neurotransmitters on behaviour. One of our group members suggested Science In Court: Arrested Development as they had already downloaded and read the article. All group members were very interested in the topic and agreed that it was a worthy, diverse and interesting topic to research for the project.

The article comes from Nature, a well known and respected journal. Furthermore, we felt that the topic of the article was relevant to a contemporary audience as it was published recently in 2012, and covered various scientific, legal and ethical issues in modern society. The article had many links to topics studied in the course including neuroanatomy, neurotransmitters and neuroimaging techniques. Information used in the report was gathered from other reputable and relevant scientific journals and websites.


5.2 Appendix II


Reviewers provided positive comments and constructive feedback. Strong points included the good choice of topic, the fact that the article was interesting, and detailed criticism of the article. Weak points included the fact that grammatical errors affected readability, that not enough references were used to backup arguments, and that the appendix and references list needed revision. These issues were addressed in a group meeting. Team members discussed the areas needed for improvement and each person was allocated a different role and area of the project to improve and revise.


5.3 Appendix III


Further reading

Xie, H (2011). "Developmental trajectories of aggression from late childhood through adolescence: similarities and differences across gender". Aggressive Behavior 37 (5): 387–404.
Keeler, L.A (2007). "The differences in sport aggression, life aggression, and life assertion among adult male and female collision, contact, and non-contact sport athletes". Journal of Sport Behavior 30 (1): 57–76.

https://neurowiki2012.wikispaces.com/The+Teenage+Brain#21

5.4 Appendix IV


Related articles









6. References



Amaral, D.G.; Bauman, M.D.; Lavenex, P.; Mason, W.A.; Toscano, J.E. (2006). "The Expression of Social Dominance Following Neonatal Lesions of the Amygdala or Hippocampus in Rhesus Monkeys (Macaca Mulatta)". Behavioral Neuroscience 120 (4): 749–760.


Audero, E; Mlinar, B; Baccini, G; Skachokova, ZK; Corradetti, R; Gross C (2013) "Suppression of Serotonin Neuron Firing Increases Aggression in Mice." The Journal of Neuroscience, 33(20): 8678-8688; doi: 10.1523/


Caramaschi, D; De Boer, SF; De Vries, H; Koolhaas, JM (2008). "Development of violence in mice through repeated victory along with changes in prefrontal cortex neurochemistry". Behavioural Brain Research 189 (2): 263–72.


Cases O., Lebrand C., Giros B., Vitalis T., De Maeyer E., Caron M. G., et al. (1998). Plasma membrane transporters of serotonin, dopamine, and norepinephrine mediate serotonin accumulation in atypical locations in the developing brain of monoamine oxidase A knock-outs. J. Neurosci. 18, 6914–6927.


Delville, Y; Mansour KM; Ferris, CF (1996) " Testosterone facilitates aggression by modulating vasopressin receptors in the hypothalamus" Physiology & Behavior, Volume 60, Issue 1, pp25–29


Delville, Yvon; Ferris, Craig F.; Fuler, Ray W.; Koppel, Gary; Richard, RW; Jr, H. Melloni; Perry, Kenneth W. (1997). "Vasopressin/Serotonin Interactions in the Anterior Hypothalamus Control Aggressive Behavior in Golden Hamsters". The Journal of Neuroscience 17 (11): 4331–4340.


Edmonds, Molly. (2008). Are teenage brains really different from adult brains?. Retrieved from http://science.howstuffworks.com/life/teenage-brain.htm


Heinrichs, M; Domes, G (2008). "Neuropeptides and social behaviour: effects of oxytocin and vasopressin in humans". Progress in brain research. Progress in Brain Research 170: 337–50.


Hermans, J.; Kruk, M.R.; Lohman, A.H.; Meelis, W.; Mos, J.; Mostert, P.G.; Van Der, Poel (1983). "Discriminant Analysis of the Localization of Aggression-Inducing Electrode Placements in the Hypothalamus of Male Rats". Brain Research 260 (1): 61–79. http://www.sciencedirect.com/science/article/pii/0006899383907643


Jayson, S (2007). Expert: Risky teen behavior is all in the brain. USA Today. Retrieved from http://usatoday30.usatoday.com/news/health/2007-04-04-teen-brain_N.htm


Johnson, S. B., Blum, R. W., & Giedd, J. N. (2009). Adolescent Maturity and the Brain: The Promise and Pitfalls of Neuroscience Research in Adolescent Health Policy. Journal of Adolescent Health, 45(3), 216-221. doi: http://dx.doi.org/10.1016/j.jadohealth.2009.05.016


Knox, R (2010). The Teen Brain: It's Just Not Grown Up Yet. NPR: National Public Radio. Retrieved from http://www.npr.org/templates/story/story.php?storyId=124119468


McAnarney, E. R. (2008). Adolescent Brain Development: Forging New Links? Journal of Adolescent Health, 42(4), 321-323. doi: http://dx.doi.org/10.1016/j.jadohealth.2007.10.012


Moskowitz, C (2011). Ciminal Minds Are Different From Yours, Brain Scans Reveal. Livescience. Retrieved from http://www.livescience.com/13083-criminals-brain-neuroscience-ethics.html


Potegal, M; Ferris, CF; Herbert, M; Meyerhoff, J; Skaredoff, L (1996). "Attack Priming In Female Syrian Golden Hamsters is Associated with a c-fos-coupled Process within the Corticomedial Amygdala". Neuroscience 75 (3): 869–880. http://www.sciencedirect.com/science/article/pii/0306452296002369


Rosa M.M; de Almeida; Ferrari, PF; Parmigiani, S; Miczek, KA (2005) "Escalated aggressive behavior: Dopamine, serotonin and GABA" European Journal of Pharmacology, (526) 51–64


Spinks, S (2002). One Reason Teens Respond Differently to the World: Immature Brain Circuitry. Frontline. Retrieved from http://www.pbs.org/wgbh/pages/frontline/shows/teenbrain/work/onereason.html

Teicher, M.H. & Andersen, S.L. Limbic serotonin turnover plunges during puberty. Poster at Meeting of the Society for Neuroscience, (1999).

Wersinger, SR; Ginns, EI; O'Carroll, AM; Lolait, SJ; Young, WS (2002) " Vasopressin V1b receptor knockout reduces aggressive behavior in male mice." Mol Psychiatry. 7(9):975-84.


Planning

Division of Labour
Matthew – Introduction, Appendix, Neuroscientific Context, Adolescent Brain

Michelle – Neuroscientific context – Adolescent Brain, Amygdala, Prefrontal cortex; graphics (including figures, diagrams, photographs, etc)

Alexei – Neurobiology of Aggression; outlines how transmitters act on developing brain (reference hormones, ie relation of neurotransmitters and development)

Neal – Critical Analysis

All group members to edit and provide references

Deadlines
Project Draft ready by 2 September for 9 September 10am
Review Comments due by 16 September 10am
Final Project ready for 23 September

Minutes
Meetings: Minutes of 1st meeting
Planning: August 9 2013, second meeting on 19 September (see Draft Discussion forum for notes)

Editing: from 16 to 23 September

Team photo

team photo.jpg

Amaral, D.G.; Bauman, M.D.; Lavenex, P.; Mason, W.A.; Toscano, J.E. (2006). "The Expression of Social Dominance Following Neonatal Lesions of the Amygdala or Hippocampus in Rhesus Monkeys (Macaca Mulatta)". Behavioral Neuroscience 120 (4): 749–760.
Audero, E; Mlinar, B; Baccini, G; Skachokova, ZK; Corradetti, R; Gross C (2013) "Suppression of Serotonin Neuron Firing Increases Aggression in Mice." The Journal of Neuroscience, 33(20): 8678-8688; doi: 10.1523/
Caramaschi, D; De Boer, SF; De Vries, H; Koolhaas, JM (2008). "Development of violence in mice through repeated victory along with changes in prefrontal cortex neurochemistry". Behavioural Brain Research 189 (2): 263–72.
Cases O., Lebrand C., Giros B., Vitalis T., De Maeyer E., Caron M. G., et al. (1998). Plasma membrane transporters of serotonin, dopamine, and norepinephrine mediate serotonin accumulation in atypical locations in the developing brain of monoamine oxidase A knock-outs. J. Neurosci. 18, 6914–6927.
Delville, Y; Mansour KM; Ferris, CF (1996) " Testosterone facilitates aggression by modulating vasopressin receptors in the hypothalamus" Physiology & Behavior, Volume 60, Issue 1, pp25–29
Delville, Yvon; Ferris, Craig F.; Fuler, Ray W.; Koppel, Gary; Richard, RW; Jr, H. Melloni; Perry, Kenneth W. (1997). "Vasopressin/Serotonin Interactions in the Anterior Hypothalamus Control Aggressive Behavior in Golden Hamsters". The Journal of Neuroscience 17 (11): 4331–4340.
Edmonds, Molly. (2008). Are teenage brains really different from adult brains?. Retrieved from http://science.howstuffworks.com/life/teenage-brain.htm
Heinrichs, M; Domes, G (2008). "Neuropeptides and social behaviour: effects of oxytocin and vasopressin in humans". Progress in brain research. Progress in Brain Research 170: 337–50.
Hermans, J.; Kruk, M.R.; Lohman, A.H.; Meelis, W.; Mos, J.; Mostert, P.G.; Van Der, Poel (1983). "Discriminant Analysis of the Localization of Aggression-Inducing Electrode Placements in the Hypothalamus of Male Rats". Brain Research 260 (1): 61–79. http://www.sciencedirect.com/science/article/pii/0006899383907643
Jayson, S (2007). Expert: Risky teen behavior is all in the brain. USA Today. Retrieved from http://usatoday30.usatoday.com/news/health/2007-04-04-teen-brain_N.htm
Johnson, S. B., Blum, R. W., & Giedd, J. N. (2009). Adolescent Maturity and the Brain: The Promise and Pitfalls of Neuroscience Research in Adolescent Health Policy. Journal of Adolescent Health, 45(3), 216-221. doi: http://dx.doi.org/10.1016/j.jadohealth.2009.05.016
Knox, R (2010). The Teen Brain: It's Just Not Grown Up Yet. NPR: National Public Radio. Retrieved from http://www.npr.org/templates/story/story.php?storyId=124119468
McAnarney, E. R. (2008). Adolescent Brain Development: Forging New Links? Journal of Adolescent Health, 42(4), 321-323. doi: http://dx.doi.org/10.1016/j.jadohealth.2007.10.012
Moskowitz, C (2011). Ciminal Minds Are Different From Yours, Brain Scans Reveal. Livescience. Retrieved from http://www.livescience.com/13083-criminals-brain-neuroscience-ethics.html
Potegal, M; Ferris, CF; Herbert, M; Meyerhoff, J; Skaredoff, L (1996). "Attack Priming In Female Syrian Golden Hamsters is Associated with a c-fos-coupled Process within the Corticomedial Amygdala". Neuroscience 75 (3): 869–880. http://www.sciencedirect.com/science/article/pii/0306452296002369
Rosa M.M; de Almeida; Ferrari, PF; Parmigiani, S; Miczek, KA (2005) "Escalated aggressive behavior: Dopamine, serotonin and GABA" European Journal of Pharmacology, (526) 51–64
Spinks, S (2002). One Reason Teens Respond Differently to the World: Immature Brain Circuitry. Frontline. Retrieved from http://www.pbs.org/wgbh/pages/frontline/shows/teenbrain/work/onereason.html
Wersinger, SR; Ginns, EI; O'Carroll, AM; Lolait, SJ; Young, WS (2002) " Vasopressin V1b receptor knockout reduces aggressive behavior in male mice." Mol Psychiatry. 7(9):975-84.