Problem 2: Biological explanations Flashcards

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1
Q

How do personal capabilities and predispositions influence a person?

A

They affect how the environment influences the shaping of behavior and, reciprocally, how the behavior can modify biological tendencies.

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2
Q

Describe two general trajectories of criminality in youth

A

The first trajectory is the adolescent-limited, which represents the majority of youths who will engage in delinquent activities at
some point during adolescence but desist in early adulthood.

The second trajectory is called the life-course-persistent. These are the offenders, mostly males, who start behaving antisocially early and continue through to adulthood, often escalating in the seriousness of their acts.

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3
Q

What is heredity?

A

Heredity is the transmission of genetic information from one generation to the next.

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4
Q

Is there evidence of intergenerational criminality?

A

There is a high correlation between the fathers criminality and the sons criminality. This applies equally to boys and girls.

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5
Q

What is also of influence in the transmission of crime from parent to child?

A

Other factors such as parental monitoring and disciplining practices, having a father with a poor work record, and living in poor housing are also important. Official police and court processing may also be of influence.

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6
Q

How can ‘assertive mating’ explain the transmission of crime from parent to child?

A

83% of boys grew up and married women who also had criminal records.

Family criminality was the best predictor of anti-social behavior for any family member.

When the mother was arrested,the chance of the father having been arrested was five times more likely.

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7
Q

What does a higher concordance rate in monozygotic (MZ) twins compared to dizygotic (DZ) twins suggest?

A

It suggests that heredity has a stronger influence on the trait being studied.

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8
Q

What were the concordance rates for criminality found by Lange (1929) for MZ and DZ twins?

A

MZ twins: 77% concordance
DZ twins: 12% concordance

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9
Q

What concordance rates for criminality were found by Christiansen (1970) and Dalgaard?

A
  • Christiansen (1970): 35% for MZ twins, 12% for DZ twins.
  • Dalgaard: 26% for MZ twins.
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10
Q

What is the equal environments assumption in twin studies?

A

The assumption that identical twins (MZ) and fraternal twins (DZ) experience similar environments, so differences in concordance rates are primarily due to genetics.

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11
Q

What did Grove et al. (1990) find about MZ twins raised apart and antisocial personality disorder?

A

They found a 29% concordance rate for antisocial personality disorder, consistent with other twin studies on crime.

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12
Q

What is the discordant MZ-twin method, and what does it aim to uncover?

A

It assumes MZ twins raised together do not share exactly the same environments. This method helps identify potential specific environmental causes, holding genetics constant.

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13
Q

In Caspi et al. (2004), what did researchers conclude about the role of maternal treatment in child aggression?

A

Negative maternal emotions strongly predicted child aggression, suggesting that maternal treatment, not genetics, explained child aggressiveness.

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14
Q

What factors are analyzed in adoption studies on criminal behavior?

A

Adoption studies analyze:
(a) The criminal history of biological parents.
(b) The criminal history of adoptive parents.
(c) Combinations of criminality in biological and adoptive parents.

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15
Q

What did a study of over 14,000 adoptees in Denmark (1924-1947) reveal about genetic influences on criminality?

A
  • Adoptees with criminal biological parents raised by noncriminal adoptive parents had a conviction rate of 20%, compared to 13.5% for those with noncriminal biological and adoptive parents.
  • This suggests a modest genetic influence on criminal behavior (effect size: 0.03).
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16
Q

What genetic correlations did Barnes et al. (2014a) estimate for criminological traits?

A

Barnes et al. (2014a) estimated genetic correlations between criminological traits to range from 0.30 to 0.60.

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17
Q

How does heritability of behavioral issues vary with severity?

A
  • Severe behavioral problems (e.g., major depression, antisocial behavior) have a stronger genetic component.
  • Life-course-persistent offenders show heritability of up to 70%, compared to 35% for adolescence-limited offenders.
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18
Q

What differences in heritability were observed between genders in severe antisocial behavior?

A

Females with life-course-persistent offending showed stronger genetic influences compared to males.

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19
Q

What did Harden et al. (2008) and Armour and Haynie (2007) find about early sexual activity and delinquency?

A

Contrary to prior research, Harden et al. found that early sexual activity was associated with lower delinquency, highlighting the complexity of the relationship.

Armour and Haynie (2007) noted that early sexual debut increased the risk of delinquency by 20%, though causation remains unclear.

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20
Q

What are the 2 levels in which the nature-nurture interaction can proceed?

A
  • There is the molecular genetic level
  • There is a higher level of the behavioral markers representing the biological systems that underlie criminal conduct.
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21
Q

What does the MAOA gene do?

A

School attachment and repeating a grade, both risk factors for delinquency, interact with the MAOA gene.The MAOA gene is widely regarded to influence aggression via serotonin and dopamine neurotransmission.

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22
Q

Give 5 biological markers indicative of biological system processes that may interact with environmental factors:

A
  • Sensation seeking
  • High energy
  • Low self-control
  • Emotionality
  • Callousness
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23
Q

What did Lombroso conclude about criminals after observing a convict’s brain?

A
  1. Criminals biologically resemble lower-order animals.
    1. They behave like animals with few inhibitions, as “biological throwbacks” to an earlier evolutionary stage.
    2. Some criminals are “born bad.”
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24
Q

What is the limbic system, and why is it called the “old brain”?

A

The limbic system is a brain circuit controlling basic emotions and motivations. It is called the “old brain” because it developed early in evolution and is similar to structures in lower-level animals.

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25
Q

What did Charles Goring’s (1913) and Hooten (1939) study reveal about the physical differences between convicts and non-convicts?

A

Goring found no significant physical differences between 3,000 English convicts and groups of university students, hospital patients, and soldiers.

Hooten found differences in 19 of 33 physical characteristics, with criminals having low foreheads, protruding ears, and being generally physically inferior.

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26
Q

What is plasticity, and how does it affect the brain?

A

Plasticity is the brain’s ability to adapt, with neurons assuming the functions of damaged areas. The brain is more plastic during youth than adulthood.

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27
Q

What are William Sheldon’s three body types, and how do they relate to delinquency?

A
  1. Ectomorph: Thin and fragile.
    1. Endomorph: Overweight and round.
    2. Mesomorph: Muscular and athletic.
      The Gluecks (1950) found that delinquents were more likely to be mesomorphs.
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28
Q

How do the limbic system and the prefrontal cortex interact in violent behavior?

A

Violent behavior depends on processes in both the limbic system (emotions and motivations) and the prefrontal cortex (impulse control and executive functioning).

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29
Q

What racial differences did Rushton and Jensen propose regarding intelligence and behavior?

A

They argued that:
1. Asians are the most advanced in intelligence, temperament, and social organization.
2. Caucasians are intermediate.
3. Blacks are the least advanced.

Note: This theory is highly controversial and criticized for its lack of scientific validity and its racial bias

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30
Q

What is the role of the frontal lobes in behavior?

A

The frontal lobes are responsible for attention, planning, impulse control, and executive functioning. Development continues until around age 25, influencing the “age-crime curve.”

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31
Q

What is the “cad” strategy in evolutionary criminology?

A

The “cad” strategy refers to men using deceitful or aggressive tactics to reproduce while avoiding paternal responsibilities, in contrast to “dads” who commit to monogamy and child-rearing.

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32
Q

How are frontal lobes different in white-collar criminals compared to other criminals?

A

White-collar criminals tend to have greater gray matter thickness in their frontal lobes compared to average criminals.

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33
Q

What are the two main types of life-course-persistent offenders?

A
  1. Moffitt’s neuropsychological type: Individuals with neuropsychological problems, difficult temperaments, and poor socialization experiences.
    1. Psychopaths: Individuals pursuing a strategic “life history” to maximize mating success without significant neuropsychological deficits.
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34
Q

What are the traits of a difficult temperament in a child?

A
  1. Intense reactions to stimuli.
    1. Generally negative mood.
    2. Slowness to adapt to change.
    3. Irregularity in sleep, hunger, and other bodily functions.
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35
Q

What is passive avoidance learning, and how does it teach self-control?

A

Passive avoidance learning teaches self-control through fear reduction:
1. Antisocial behavior is punished, producing fear.
2. Fear discourages the behavior, and its reduction reinforces inhibition.

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36
Q

What is the “age-crime curve”, and how is it linked to brain development?

A

The age-crime curve shows that antisocial behaviors peak in late adolescence and decline in early adulthood. This pattern is linked to delayed development of the frontal lobes.

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37
Q

How do criminals differ from noncriminals in reproductive behavior?

A

Criminals tend to:
* Begin sexual activity earlier.
* Have children earlier.
* Have more sexual partners.

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38
Q

What did the Dunedin Study reveal about neuropsychological tests and delinquency?

A

Poor neuropsychological test performance, especially in verbal abilities, predicted delinquency at age 18.

This was most strongly associated with life-course-persistent male delinquents but not with adolescent-limited delinquents.

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39
Q

What is the outcome of criminals mating with partners with similar temperaments and social backgrounds?

A

They experience higher levels of failed intimate partnerships, poorer health, and higher mortality rates.

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40
Q

What does Moffitt’s biosocial model suggest about chronic criminality?

A

Chronic criminality arises from a combination of:
* Biological factors: Neuropsychological deficits (poor verbal skills, impulsiveness).
* Psychosocial factors: Negative environments that amplify these biological risks.

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41
Q

Do biological factors directly cause crime?

A

No, biological factors do not directly cause crime but can increase the likelihood of antisocial behavior, especially in adverse environmental conditions.

42
Q

How do neuropsychological deficits contribute to life-course-persistent offending?

A

Deficits like poor verbal skills, impulsiveness, and attention issues increase the likelihood of persistent offending, especially when combined with adverse social environments.

43
Q

What are the four main areas where neurobiology plays a role in criminology?

A
  1. Understanding criminal behavior.
    1. Early detection, prediction, and intervention in deviant behavior.
    2. Criminal proceedings: assessing responsibility and informing sentencing.
    3. Forensic rehabilitation and treatment.
44
Q

Why is the maturity gap important in understanding adolescent behavior?

A

The maturity gap occurs because adolescents desire adult status but lack full neurophysiological maturity, contributing to impulsive and antisocial behaviors.

45
Q

What percentage of variance in criminal behavior is attributed to genetic influences?

A

About 40–60% of the variance in criminal behavior is attributed to genetic influences.

46
Q

How does neurological impairment in the frontal lobe and limbic system affect life-course-persistent offenders?

A

Impairments contribute to persistent antisocial behavior, distinguishing life-course-persistent offenders from those whose behavior is developmentally limited.

47
Q

How do biological predispositions and environmental factors interact?

A

Biological predispositions influence how individuals react to the environment, while environmental factors can affect gene expression, hormone and neurotransmitter levels, and brain structure and functioning.

48
Q

What combination of factors increases the likelihood of persistent criminal behavior?

A

Persistent criminal behavior results from biological factors (e.g., genetics, neurophysiological deficits) combined with negative social environments.

49
Q

What does neurobiological research aim to achieve in criminology?

A
  1. Understand the neurobiological characteristics of antisocial behavior.
    1. Predict antisocial behavior using neurobiological risk factors.
    2. Study interactions between neurobiological, psychological, and environmental factors.
50
Q

What is temperament, and how is it related to personality?

A

Temperament refers to inherent and stable tendencies to respond to the environment. It is the biological precursor to personality and explains the heritability of personality.

51
Q

What ethical concerns arise with neurobiological approaches to predicting and intervening in deviant behavior?

A
  1. Stigmatization of individuals labeled as “at-risk.”
    1. Risk of false positives leading to unnecessary interventions.
    2. Negative impacts on self-esteem and treatment outcomes.
    3. Questions about decision-making autonomy for children labeled as at-risk.
52
Q

What are the main challenges of using neurobiological tools in detecting and intervening in antisocial behavior?

A
  1. Balancing public safety and the risk of inducing stigma.
    1. Ensuring cost-effectiveness of population-wide screening.
    2. Deciding who makes treatment decisions for identified children.
53
Q

What are the two interrelated temperamental traits linked to delinquency and life-course-persistent offenders?

A
  1. High stimulation-seeking combined with low self-control.
    1. Negative emotionality, which includes facets like aggression, alienation, and stress reactions.
54
Q

What is “neuro-determinism,” and why is it a concern?

A

“Neuro-determinism” is the belief that biological factors alone drive behavior. It risks fostering false assumptions, stigmatization, and reliance on “quick fixes” while overlooking psychological and socio-economic factors.

55
Q

What is a “poorness of fit,” and how does it contribute to behavioral problems?

A

A poorness of fit occurs when a child’s difficult temperament mismatches with caregivers’ or teachers’ approaches, leading to exacerbated behavioral problems.

56
Q

How can neurobiological evidence support the criminal justice system?

A

Neurobiological evidence can:
1. Help assess responsibility and cognitive impairments.
2. Inform sentencing decisions.
3. Refine forensic psychiatric reports.
4. Improve mental health rehabilitation and treatment.

57
Q

How does neurophysiological underarousal contribute to sensation-seeking and criminal behavior?

A

Individuals with low baseline arousal may seek stimulation to “wake up” their systems, predisposing them to risky and criminal behaviors, especially when combined with low self-control.

58
Q

What are the risks of over-reliance on neurobiological evidence in court?

A
  1. Fostering “neuro-determinism.”
    1. Overestimating its accuracy in proving reduced responsibility or dangerousness.
    2. Misinterpretation leading to biased sentencing outcomes.
59
Q

How can forensic mental health interventions benefit from neurobiological insights?

A
  1. Accurate diagnostics can guide treatment to reduce recidivism.
    1. Non-invasive neuro-interventions (e.g., neurofeedback, transcranial magnetic stimulation) show promise.
    2. Combining biological and psychological approaches ensures balanced rehabilitation.
60
Q

Why do individuals with antisocial personalities struggle with learning self-control?

A

They often exhibit reduced fear responses and slower dissipation of physiological fear markers, impairing their ability to learn from punishment.

61
Q

What risks are associated with emphasizing biological determinism in offender treatment?

A
  1. Increased stigma and harmful stereotypes.
    1. Lower patient motivation for recovery.
    2. Viewing disorders as untreatable or permanent, which can hinder outcomes.
62
Q

How do sensation-seeking tendencies differ between offenders and non-offenders?

A

Offenders tend to score higher on sensation-seeking measures and often report feeling a “rush” from engaging in criminal acts.

63
Q

How does neurobiological evidence influence sentencing?

A

It can mitigate accountability by highlighting cognitive impairments or brain deficits, but misuse or over-reliance may lead to biased decisions or neglect of other important factors.

64
Q

What is the neurophysiological arousal hypothesis in relation to crime?

A

It suggests that some offenders engage in criminal acts for the sensation-seeking thrill, due to their underactive neurophysiological systems.

65
Q

What is antisocial behavior (AB), and why is it significant?

A

Antisocial behavior includes aggression, violence, and rule-breaking, with significant financial, social, and emotional costs to society, perpetrators, victims, and their families.

66
Q

What is callous-unemotional (CU)?

A

Callous-unemotional traits (CU) are distinguished by a persistent pattern of behavior that reflects a disregard for others, and also a lack of empathy and generally deficient affect.

67
Q

How does heterogeneity manifest in youth with antisocial behavior?

A

Youth with AB differ in onset, duration, and severity of behavior. Subtypes include:
1. Early-onset AB (greater genetic risk).
2. Adolescent-onset AB (less severe trajectory).
3. AB with callous-unemotional (CU) traits, linked to higher levels of AB.

68
Q

How does the heritability of aggression differ from rule-breaking?

A
  • Aggression: More heritable (65%) with less environmental influence (5%).
    • Rule-breaking: Less heritable (48%) with greater environmental influence (18%).
69
Q

What are the genetic heritability differences for AB with and without CU traits?

A
  • AB with CU traits: 81% heritable.
    • AB without CU traits: 30% heritable.
70
Q

What findings have adoption studies revealed about AB?

A
  1. Severe AB in biological parents predicts greater CU traits in children.
    1. Positive parenting by adoptive parents reduces CU traits.
71
Q

What neurotransmitter systems are often studied in relation to AB?

A
  1. Dopaminergic system: Altered dopamine levels may contribute to heightened reward sensitivity.
    1. Serotonergic system: Greater serotonin is linked to poor impulse control and irritability.
72
Q

Which genes are associated with AB in molecular genetic studies?

A
  1. Dopaminergic genes: Linked to reward sensitivity and AB.
    1. Serotonin transporter polymorphism: Short allele linked to AB.
    2. Monoamine oxidase-A (MAOA) gene: Involved in serotonin breakdown, linked to AB.
73
Q

What is a gene-environment (GxE) interaction, and how does it relate to AB?

A

In a GxE interaction, genetic variation predicts AB only in specific environmental contexts. For example, genetic predispositions may only lead to AB under adverse environmental conditions.

74
Q

What is the goal of genome-wide association studies (GWAS) in the context of AB?

A

GWAS examines whether individual differences in AB are associated with allelic differences across the genome. However, detecting genetic effects requires large sample sizes due to the small effect size of individual genetic variants.

75
Q

What brain regions are implicated in AB, and how do they function?

A
  1. Amygdala: Linked to heightened fear responses.
    1. Prefrontal cortex: Associated with disinhibition and impulse control.
    2. Striatum: Tied to reward sensitivity.
      AB is often marked by heightened amygdala activity, lower prefrontal activation, and reduced amygdala-prefrontal connectivity.
76
Q

What disorders are associated with aggression?

A
  • Intermittent Explosive Disorder (IED) - characterized by frequent and problematic impulsive aggressive outbursts.
  • Borderline Personality Disorder (BPD) - characterized by instability in self-image, in interpersonal relationships as well as impulsivity and affect .
  • Antisocial Personality Disorder (AsDP) - characterized by a pattern of disregard for, and violation of, the rights of others.
77
Q

What is serotonin (5-HT), and what functions does it regulate?

A

Serotonin is a monoamine neurotransmitter derived from L-tryptophan, regulating mood, appetite, sleep, gastrointestinal muscle contractility, and self-injurious behavior.

78
Q

What factors influence serotonin’s action in the brain?

A
  1. The specific receptor subtype it binds to.
    1. The amount of 5-HT available in the synapse.
    2. The level of enzymatic activity.
    3. Availability of agonists or antagonists for competitive binding.
79
Q

How is serotonin linked to impulsive aggression?

A

Low serotonin levels in emotion-regulating brain regions (e.g., prefrontal cortex, anterior cingulate cortex) predispose individuals to impulsive aggression.

Reduced serotonin metabolites (e.g., 5-HIAA in CSF) are associated with violent and suicidal behaviors.

80
Q

What did early studies (1976–1979) reveal about serotonin and aggression?

A
  1. Sheard et al.: Lithium carbonate (serotonin-enhancing agent) reduced impulsive aggression in prison inmates.
    1. Asberg et al.: Lower 5-HIAA levels in CSF correlated with violent and suicidal behaviors.
    2. Brown et al.: Found a strong inverse relationship between 5-HIAA levels and aggression, with MHPG levels positively linked to aggression.
81
Q

What role do serotonin receptors play in aggression regulation?

A
  1. 5-HT1a receptor agonists: Typically reduce aggression, though effects vary by brain region.
    1. 5-HT1b receptor agonists: Can increase aggression under specific conditions.
    2. 5-HT2a and 5-HT2c receptor activation: Generally reduces aggression, especially in the mesocorticolimbic pathway.
    3. 5-HT transporters: Activation reduces pathological aggression.
82
Q

How does serotonin interact with dopamine in aggression?

A
  • Low serotonin levels are linked to dopaminergic hyperactivity, particularly in the prefrontal cortex.
    • This imbalance may drive impulsive aggression.
    • Studies show elevated dopamine in the nucleus accumbens and reduced serotonin in the frontal cortex during aggression.
83
Q

Does serotonin increase or decrease aggression?

A
  • Serotonin generally decreases aggression by modulating emotion-regulating brain regions.
    • Low serotonin availability or function leads to impulsive and violent behaviors.
84
Q

What is the significance of serotonin metabolites like 5-HIAA in aggression?

A

Lower 5-HIAA levels in cerebrospinal fluid (CSF) are strongly correlated with violent, suicidal, and aggressive behaviors.

85
Q

What is dopamine (DA), and what are its primary functions?

A

Dopamine is a catecholamine neurotransmitter involved in cognition, movement, sleep, mood, attention, learning and memory, and reward pathways related to behaviors like drug use, eating, and sexual activity.

86
Q

How does dopamine influence aggressive behavior?

A
  • Increased DA activity, particularly in the nucleus accumbens (NAc) and anterior hypothalamus (AH), is associated with greater aggression.
    • Dopamine receptor antagonists targeting these areas reduce aggression, indicating DA’s role in modulating aggressive behaviors.
87
Q

What role does the COMT gene play in aggression?

A

The low-activity Met/Met genotype of the COMT gene is linked to aggression and impulsivity, as seen in conditions like borderline personality disorder, bipolar disorder, and major depressive disorder.

88
Q

How does dopamine receptor activity in the anterior hypothalamus (AH) influence aggression?

A
  • D2-like receptor antagonists in the AH suppress aggression without affecting mobility or sociability.
    • D5 receptors in the lateral AH may modulate aggression through non-GABAergic pathways.
89
Q

What is the significance of dopamine receptor antagonists in aggression studies?

A

Dopamine receptor antagonists targeting D1-like and D2-like receptors reduce aggression, providing evidence that heightened dopaminergic activity contributes to aggressive behaviors.

90
Q

What is norepinephrine (NE), and what are its primary functions?

A

NE is a catecholamine neurotransmitter and stress hormone involved in the “fight-or-flight” response, modulating physiological reactions like heart rate and glucose release, as well as aggression and stress responses.

91
Q

How does norepinephrine (NE) affect aggression?

A

Low NE levels are linked to increased aggression.
* High NE levels are associated with reduced aggression, especially in certain treatment contexts.

92
Q

How does norepinephrine (NE) modulate aggression in humans?

A
  • Patients with schizophrenia treated with clozapine (which increases NE levels) exhibited reduced aggression compared to those treated with other antipsychotic drugs.
    • This suggests NE helps modulate aggression in clinical context
93
Q

How does norepinephrine (NE) interact with other neurotransmitter systems?

A

NE interacts with systems like serotonin, influencing aggression in complex ways:
* Decreased NE activity can lead to depression and self-directed aggression.
* Increased NE activity can cause irritability and violent aggression in some cases.

94
Q

What is Gamma-aminobutyric acid (GABA), and what is its primary function?

A

GABA is the primary inhibitory neurotransmitter in the central nervous system (CNS). It regulates neurological function by reducing neuronal activity, often producing calming effects.

95
Q

How does GABA influence aggression in animal studies?

A
  1. Increased GABA levels (e.g., in GAT1−/− mice) are linked to reduced aggression.
    1. GABA(B) receptor activation in the dorsal raphe nucleus increases aggression by modulating serotonin.
    2. GABA(A) receptor activation, particularly in alcohol-treated mice, has been linked to heightened aggression, especially in alcohol-induced scenarios.
96
Q

What do human studies suggest about GABA’s role in aggression?

A
  1. Higher cerebrospinal fluid (CSF) GABA levels are linked to impulsivity but not directly to aggression.
    1. Reduced GABA(B) receptor activity correlates with increased impulsivity, a trait often linked to aggression.
97
Q

Does GABA increase or decrease aggression?

A
  • GABA generally decreases aggression due to its inhibitory role in the CNS.
    • However, the effect varies by receptor subtype (e.g., GABA(A), GABA(B)) and brain region, with some GABA receptor activation increasing aggression (e.g., in the dorsal raphe nucleus).
98
Q

How does GABAergic dysfunction affect aggression in the anterior hypothalamus (AH)?

A

Reduced GABAergic inhibition in the anterior hypothalamus, often influenced by dopamine D2 receptor activity, is associated with increased aggression.

99
Q

Why is GABA’s role in aggression considered context-dependent?

A

GABA’s effects on aggression depend on:
1. Receptor subtype (e.g., GABA(A), GABA(B)).
2. Brain region (e.g., dorsal raphe nucleus, anterior hypothalamus).
3. Interaction with other neurotransmitter systems, like dopamine and serotonin

100
Q

What role does vasopressin play in aggression?

A

Higher cerebrospinal fluid (CSF) vasopressin levels are positively associated with increased aggression, particularly in males with personality disorders. This relationship persists even after accounting for serotonin function.

101
Q

How is oxytocin linked to aggression?

A

Lower CSF oxytocin levels are associated with a greater history of aggressive behavior, suggesting an inverse relationship between oxytocin levels and aggression.

102
Q

What effect do opioids have on aggression?

A
  • Elevated opioid activity is linked to increased aggression.
    • Mu opioid receptor density is higher in violent suicide victims, and opioid administration in healthy subjects increases aggression.
    • Opioid antagonists like naltrexone reduce self-injurious behaviors, supporting opioids’ role in aggression modulation.