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April 16, 2021

[Brain Image]    

PSY 340 Brain and Behavior

Class 26: Attack & Escape Behaviors

   
[Attack...Escape]

A. Attack Behaviors!

Behavior = Violence, fighting, or aggression, but

Emotions = anger, rage, fury, resentment, hostility, etc.

What are the Environmental and Heredity Factors which have been shown to lead toward violence?

   Environmental Factors
Lead vs. Murder
   Genetic factors
No single gene has been found strongly connected to aggressive behavior
> Genetic x Environmental Effects

MAOA and Early Trauma 

    Effects of Hormones: Testosterone
   Serotonin Synapses & Aggressive Behavior
As the nervous system uses serotonin, it continually reabsorbs or takes back up the serotonin molecules in the synaptic cleft or the serotonin molecules are cut apart by MAO-A. Thus, we can't measure directly how much serotonin an animal's nervous system is using. But, as serotonin is used, it creates a metabolite, 5-HIAA (5-hydroxyindoleacetic acid), which does remain in the synaptic cleft. Hence, measuring how much 5-HIAA exists give us an index of how much "turnover" of serotonin has taken place.
        Low serotonin turnover = a relative decrease in the amount of serotonin released and taken back into the pre-synaptic neuron.

Summary: There appears to be some relationship between increased violence and various biological functions (hormones, low serotonin, genetic x environmental interactions). But

B. Escape! Behaviors: Fear and Anxiety

Fear, Anxiety, and the Amygdala

Is there an inborn or unlearned form of fear? Loud noise = startle reflex (present in babies, too) which occurs 2/10th of a second after the sound. Muscles of neck tense up.

Basal GangliaThe basic research on the neuroscience of fear has been conducted at the lab of Joseph LeDoux at New York University. He has focused upon the role of the amygdala in the formation of emotional responses. While our text mentions LeDoux earlier in the module, his work is generally ignored in the rest of the module. I intend to focus much more on LeDoux than our text author does.

[Temporal Lobe]

Amygdala

[Amygdala Connections]

1. Studies in Rats

  • Conditioned stimulus (CS, e.g. bell) paired with an unconditioned stimulus (UCS, e.g., electrical shock) leads eventually to the development of a conditioned response (CR), i.e., fearfulness.
  • Learning takes place via changes of cell connections in the lateral amygdala
  • Damage to the amygdala interferes with learning fearfulness
  • Implications: Changes in the amygdala are implicated in human anxiety problems such as PTSD, phobias, & panic disorder. It may become overly sensitive to threats in the environment.

2. Studies in Monkeys

Klüver-Bucy Syndrome (Nahm & Pribram, 1998): Damage to the amygdala. This syndrome is found (rarely) in humans. When it is patients with this syndrome have usually experienced either bilateral trauma to the amygdala or been infected with Herpes simplex encephalitis which damaged the amygdala.

  • Taming: Placid, loss of aggression
  • Psychic Blindness: Inability to recognize objects by sight: No longer fear stimuli such as snakes
  • Responsiveness to many small visual cues ("hypermetamorphosis" [Danek, 2007])
  • Hyperorality: Examine objects by licking, biting, & chewing
  • Hypersexuality
3. Studies in Humans
PET & fMRI: Increased activity in amygdala to pictures of faces showing strong emotions, e.g., fearful, angry, happy

Amygdala will signal the ANS even if shown emotional images too quickly to be consciously comprehended
  • [Thalamic-Cortical Tracts & Amygdala]Originally LeDoux spoke of two "roads" by which we respond to emotional (NOT just FEARFUL) information
    • "high road" through the sensory cortex which provides conscious (explicit) recognition after 30-40 ms
    • "low road" directly from the thalamus to the amygdala at an unconscious (implicit) level of processing within 12 ms

However, in this model, it looked like the amygdala itself produced the conscious emotion of fear. LeDoux did not mean to suggest this.

Emotion as a Conscious Cognitive State. Since 2016 LeDoux has argued that, in human beings, after receiving information from the sensory systems of the body, the amygdala does not function itself as a "fear" circuit in the brain. It does not produce the emotions of fear or anxiety. Rather, he argues that the amygdala is one of several "defensive survival circuits [that] are evolutionarily wired to detect and respond to innate threats and to respond to novel threats that have been learned about in the past....Defensive survival circuits indirectly contribute to the feeling of fear, but their activity does not constitute fear" (LeDoux & Brown, 2017, p. 2, emphasis added) In LeDoux's argument, both fear (an emotion that responds to a threat NOW) and anxiety (an emotion that responds to a threat in the FUTURE) only become real when we become conscious of the threat and of our unconscious responses. 

Newer LeDoux
                model

An alternative and updated diagram of his model is shown below (and based on his August 2017 talk at the APA meeting in DC).

  • In this model, the experience of fear (or any other emotion) arises in our conscious working memory from multiple elements that are processed in our working memory at an unconscious level. 
LeDoux Diagram

Urbach-Wiethe Disease [aka Lipoid proteinosis] (Siebert, Markowitch, & Bartel, 2003)
Patients experience degeneration of the amygdala. Siebert et al. report that, compared to normal subjects, these patients had major difficulty in judging all emotions in facial expression, remembering negative and positive pictures, and dealing with an odor-figure association test.


SM Amygdala  Facial
                Expression

Patient S.M.
  • Shows no fear of objects and animals (e.g., snakes & spiders) which she claims she fears.
  • She has also put herself in dangerous situations, e.g., she has been robbed at gunpoint and physically assaulted a number of times.
  • S.M. and other patients with Urbach-Wiether Disease only experienced anxiety and, indeed, a panic attack when exposed to high levels of carbon dioxide (CO2) instead of oxygen. However, even after this experience which was described as terrible, these patients were willing to go through the same experience a week later and did not think about it. 
  • Damage to amygdala leads to difficulty in recognizing fearful facial expressions and in making social judgments about others' trustworthiness. It appears that such patients focus on the nose and mouth of others rather than either the eyes and, thus, are unable to actually read the actual emotion on the face.
(Note this disease has other primary physical symptoms including eyelid beading; thickened woody tongue; hoarseness of voice; skin lesions; seizures)
Conclusion: Amygdala seems to be deeply involved in the processing and interpretation of sensory stimuli for its emotional importance or meaning. This means that the amygdala is involved in more than just fear!

C. Anxiety Disorders
Anxiety disorders include generalized anxiety disorder, panic disorder, phobias, and post-traumatic stress disorder (PTSD).

Panic Disorder

OK City BombingPost-Traumatic Stress Disorder (PTSD)

Events include soldiering in war, rape, severe automobile accidents, torture, exposure to natural or human-caused disasters (e.g., Oklahoma City Bombing, 9/11, or the Boston Marathon bombing).

While many people have strong stress reactions immediately after a trauma, most do not develop PTSD (that is, <50% exposed to serious trauma actually develop PTSD).  Why do some people develop the disorder and others not? [Valium]Relief from Anxiety

1. Pharmacological Relief (Medications). The medical treatment of anxiety disorders in the short-term often employs a class of drugs called the benzodiazepines.
[GABAa
            Receptor Complex Diagram]Central to the action of the benzodiazepines is the GABA-A receptor complex on the membrane of neurons in the amygdala and hypothalamus (see illustration on right). More specifically, the receptor has five protein subunits.* These subunits each have multiple possible binding sites and the inhibitory neurotransmitter molecule, GABA (gamma-Aminobutyric acid), binds to at least one of these sites. When the GABA molecule attaches to the receptor, a channel opens to let negative chloride ions (Cl-) into the neuron. This serves to hyperpolarize the postsynaptic neuron, i.e., make it less likely to fire, an inhibitory effect.
  
Benzodiazepines which bind to GABA-nergic sites in the amygdala appear to decrease overall levels of anxiety and fearfulness. How? This may be due to the drug's ability to block the amygdala's processing of fear-inducing information or stimuli.

* Kalat and the literature in general tends to be wrong. During the 1980s and early 1990s, the GABA-A receptor was thought to consist of four subunits. But, more recent research points to five subunits. See <http://www.bioscience.org/1998/v3/d/homanics/3.htm>


[Budweiser Beer
              Can]2. Alcohol as an Anxiety Reducer. Another chemical which binds to the GABA-A complex is ethyl alcohol (ethanol). It appears to change the shape of the receptor complex in such a way that GABA molecules themselves bind much more easily. This results in the antianxiety and intoxicating effects of alcohol. Note that these conclusions are tentative and active research into the specific binding sites for ethanol is still ongoing (Harris et al. 2008).

Hoffmann-LaRoche developed a drug, Ro15-4513, which blocks many of the effects of alcohol (it functions as an inverse agonist to GABA). Hence, Ro15-4513 blocks not only the anti-anxiety and other depressant effects of alcohol, but also the motor coordination impairment caused by drinking.

Why is Ro15-4513 not available on the market as a "sobering up" medication? Hoffman-LaRoche realized it was too risky legally:

3. Relearning to Erase Anxiety



References

Beckley, A. L., Caspi, A., Broadbent, J., Honalee, H., Houts, R. M., Poulton, R., ... Moffitt, T. E. (2018). Association of childhood blood lead levels with criminal offending. JAMA Pediatrics, 172, 166– 173.

Byrd, A. L., Manuck, S. B. et al (2019) The interaction between monoamine oxidase A (MAOA) and childhood maltreatment as a predictor of personality pathology in females: Emotional reactivity as a potential mediating mechanism. Development and Psychopathology, 31(1), 361-377. doi: 10.1017/S0954579417001900

Carver, C. S., Johnson, S. L., & Joormann, J. (2008). Serotonergic function, two-mode models of self-regulation, and vulnerability to depression: What depression has in common with impulsive aggression. Psychological Bulletin, 134(6), 912-943. Retrieved 03/31/09 from http://0-search.ebscohost.com.library.lemoyne.edu/login.aspx?direct=true&db=psyh&AN=2008-14745-005&site=ehost-live

Danek, A. (2007). ["Hypermetamorphosis". Heinrich Neumann's (1814-1984) legacy]. Nervenzart, 78(3), 342-346. [Abstract. Article in German]

Frazzetto, G., Di Lorenzo, G., Carola, V., Proietti, L, Sokolowska, E., Siracusano, A, Gross, C., & Troisi, A. (2007). EarlY trauma and increased risk for physical aggression during adulthood: The moderating role of MAOA genotype. PLoS ONE, 2(5), e486. doi: 10.1371/journal.pone.0000486

Harris, R. A., Trudell, J. R., & Mihic, S. J. (2008, July 15). Ethanol's molecular targets [Abstract]. Science Signaling, 1(28), p. re7. doi: 10.1126/scisignal.128re7 Abstract retrieved 03/31/09 from http://stke.sciencemag.org/cgi/content/abstract/1/28/re7

Hayman, L. A., Rexer, J. L., Pavol, M. A., Strite, D., & Meyers, C. A. (1998). Klüver-Bucy syndrome after bilateral selective damage of amygdala and its cortical connections. Journal of Neuropsychiatry and Clinical Neuroscience, 10, 354-358. Retrieved 04/07/08 from http://neuro.psychiatryonline.org/cgi/content/full/10/3/354

Kamarck, T. W., Haskett, R. F., Muldoon, M., Flory, J. D., Anderson, B., Bies, R., Pollock, B., & Manuck, S. B. (2009). Citalopram intervention for hostility: Results of a randomized clinical trial. Journal of Consulting and Clinical Psychology, 77(1), 174-188. Retrieved 03/31/09 from http://0-search.ebscohost.com.library.lemoyne.edu/login.aspx?direct=true&db=psyh&AN=2009-00563-009&site=ehost-live

Kindt, M. (2018). The surprising subtleties of changing fear memory: A challenge for translational science. Philosophical Transactions of the Royal Society-B, 373. doi: 10.1098/rstb.2017.0033

LeDoux, J. (2007, Oct 23). Amygdala. Current Biology, 17(20), R868-R874. Retrieved 04/07/08 from http://www.current-biology.com/content/article/fulltext?uid=PIIS0960982207017794

LeDoux, J. (nd) Amygdala. Scholarpedia [online] Retrieved 4/8/08 from http://www.scholarpedia.org/article/Amygdala

LeDoux, J., & Brown, R. (2017). A higher-order theory of emotional consciousness. Proceedings of the National Academy of Sciences. doi:10.1073/pnas.1619316114

Nahm, F. K. D., & Pribram, K. H. (1998). Heinrich Klüver. May 25, 1897-February 8, 1979. Biographical Memoirs. Vol. 73. Washington, DC: National Academy Press (NAP). Retrieved 04/09/05 from  http://books.nap.edu/html/bio73h/kluver.html

Raine, A. (2019). A neurodevelopmental perspective on male violence. Infant Mental Health Journal, 40, 84-97.

Seo, D., Patrick, C. J., & Kennealy, P. J. (2008). Role of serotonin and dopamine system interactions in the neurobiology of impulsive aggression and its comorbidity with other clinical disorders. Aggression and Violent Behavior, 13(5), 383-395. Retrieved 03/31/09 from http://0-search.ebscohost.com.library.lemoyne.edu/login.aspx?direct=true&db=psyh&AN=2008-12517-005&site=ehost-live

Siebert, M., Markowitsch, H. J., & Bartel, P. (2003). Amygdala, affect and cognition: Evidence from 10 patients with Urbach-Wiethe disease. Brain, 126(12), 2627-2637. <Abstract>

 
This page was first posted April 10, 2005