Adolescent Brain: Plasticity to Counter the Perfect Storm

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08/02/20 Psychology Reference this

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This paper will focus on the presentation of Dr. Chiye Aoki titled “Adolescent Brain: Plasticity to Counter the Perfect Storm”, hosted by Dr. Katya Likhtik. Dr. Aoki received her doctorate from Rockefeller University where she demonstrated that neuronal plasticity changes cytoskeletal activity inside neurons (Presentation, Oct.22). After this, Dr. Aoki went on to Cornell, where she worked on researching the distribution on NMDA receptors in axons and synapses, as a function of activity or inactivity (Presentation, 2018). Today, inspired by the changes she saw when her children reached adolescence, she is studying anxiety, resilience, and feeding behaviors, within the context of anorexia nervosa at NYU (Presentation, 2018). Furthermore, Dr. Aoki is involved in a leading position in BP-Endure Hunter/NYU program (Presentation, 2018).

Before delving into the literature and presentation given by Dr. Aoki, a brief exploration of the background of anorexia nervosa is warranted. Anorexia nervosa is a mental illness that is characterized by an irrational fear of gaining weight, although the inflicted individual is of normal weight or even underweight (APA, 2013). Anorexia nervosa is also defined by high levels of anxiety because of this fear of gaining weight, which is handled though self-imposed starvation (Kaye, 2004) and excessive exercise (Beumont, 1994). Anorexia has the highest mortality rate of all mental disorders (Arcelus, 2011). This illness also has a twenty-five percent relapse (Hudson, 2007). Furthermore, this illness is about nine times more prevalent in females than in males, according to Dr. Aoki’s presentation, and there are no accepted pharmacological treatments for this illness (Presentation, Oct.22). Finally, according to twin studies, there appears to be a strong genetic component to this illness, with as much as fifty to seventy percent of the condition being genetically heritable. (Bulik, 2007).

To gauge the background of the information provided in her presentation, a close look was given to two papers that Dr. Aoki authored, “Enlargement of Axo-Somatic Contacts Formed by GAD-Immunoreactive Axon Terminals onto Layer V Pyramidal Neurons in the Medial Prefrontal Cortex of Adolescent Female Mice Is Associated with Suppression of Food Restriction-Evoked Hyperactivity and Resilience to Activity-Based Anorexia.” and “Synaptic changes in the hippocampus of adolescent female rodents associated with resilience to anxiety and suppression of food restriction-evoked hyperactivity in an animal model for anorexia nervosa.” In the first paper, Dr. Aoki and her team were able to discover that negative correlations exist between glutamic acid decarboxylase terminal contact lengths onto L5P and Activity Based Anorexia (ABA) in the context of wheel running behavior (Chen, 2015). More specifically, this study indicated that ABA induction among adolescent female mice had an impact on the prefrontal cortex circuitry and could potentially contribute to the prevention of weight loss caused by food restriction-evoked hyperactivity (Chen, 2015).

In the second paper, Dr. Aoki and her research team focused on the role of a GABAergic mechanism in the hippocampus, and its role in regulating an individual’s anxiety, which is highly correlated to an individual’s propensity for ABA. More specifically, the research of this paper found that ionotropic GABAA receptors with the subunits alpha4 and delta, play a role in suppressing pyramidal neurons, via shutting inhibition (Aoki, 2017). This is important in the context of anorexia, given that hippocampal pyramidal neurons are known to become more excitable during ABA (Aoki, 2017). The hippocampus itself is not part of the brain’s feeding center, however, it is a valuable in the context of anorexia since this illness is also an anxiety disorder, and the hippocampus along with the amygdala and the prefrontal cortex play a role in the experience of anxiety. (Adhikari, 2010)

 In the presentation, Dr. Aoki started by focusing on the way the brain develops over a lifetime. While a lot of changes take place in infancy the brain reaches its adult volumetric size by the age of five. At this age, humans have most of the cellular mass that constitutes the human brain, however, many synaptic changes take place as well. In adolescence, there is a window in which synaptogenesis takes place at an immense rate, followed by a pruning that leads to a finalized adult brain. Nevertheless, the human brain continues to develop for over a decade, with the prefrontal cortex experiencing changes in myelination up to the age of twenty-six (Presentation, 2018). Dr. Aoki went on to say that it is suspected that the cause of the discrepancy in the prevalence of anorexia between the two genders would seem to indicate a hormonal component. She also informed us of a derivative of estradiol, THP (allopregnanolone), a female associated hormone, has the ability to modulate brain circuitry to great extents while estrogens generally inhibit food intake (Young, 1991).

 Then, prior to engaging in the molecular and biological aspects that she’s been exploring, Dr. Aoki made sure to let us know that anorexia is not a lack of appetite, but a suppression of hunger. She also said that exercise is a form of showing stress and that animal subjects would be appropriate to to carry such experiments because they seem to experience the foraging instinct associated with hunger, just as humans do. In other words, if mice are accustomed to a running wheel and then food deprived, their activity will overall increase. The individual differences come in when some of the subjects continue to exercise even when food is presented, while others don’t exhibit this behavior (Presentation, 2018). 

 For the actual experiments elaborated in the presentation, Dr. Aoki took Wild-Type mice, let them acclimate to the wheel for four days, and then subjected them to food restriction. As expected, some mice increased their level of activity, while others stayed consistent with their activity prior to food restriction. It is also important to note that the wheel is an enrichment element and is seen to be enjoyed even if placed in a non-captive environment. Mice that become hyperactive in induced starvation conditions, exhibit the odd behavior of continuing to exercise even during times when food is available. The behavior can be so chronic that they can die of exhaustion (Presentation, 2018).

 Food restriction hyperactivity also causes abnormal activity patterns. Under normal conditions, mice sleep during the day and are active during the night. As per Dr. Aoki’s presentation, food restricted mice exhibit activity as much during the day as during the night. These mice also peak just before feeding time, food-anticipatory activity, as well as after the feeding session, referred to as post-prandial. These experiments yielded a correlation positive between anxiety level and wheel running (Presentation, 2018).

 Dr. Aioki proceeded to tell the audience why she focused her research on the brain structures that she did. Brain structures that are thought to play a role in anorexia include prefrontal cortex, amygdala, and the hippocampus. The prefrontal cortex plays a role in decision-making, based on integration of sensory input and internal state. The amygdala encodes information about danger, safety, and adverse stimuli. Finally, the hippocampus has also been associated with playing a role in anxiety. The more excited the hippocampus, the more anxiety-like behavior (Presentation, 2018).

Dr. Aioki discovered that the more GABA is present in the hippocampus, the more dampening of anxiety takes place. She also found that NR2A, an NMDAR subunit, appears to have a correlation with the amount of weight loss experienced by food restricted subjects. Specifically, the more synapses expressed NR2B, the more severe the weight loss. If NR2A was located in the membrane, the animal was more inflicted by severe weight loss, while if it was located in the cytoplasm, it seems to be protective against this event. The movement of NR2A from the cytoplasm happens with the aid of Drebrin, which stands for “Developmentally Regulated Brain Protein”. The more Drebrin animals express, the more NR2A is localized in their cell membranes (Presentation, 2018).

  As for the role of GABA in the hippocampus, α4βδ-GABAA receptors work with the inhibitory neurotransmitter and are present at excitatory synapses so they can repress over excitation. This makes the excitatory synaptic inputs less effective and reduces anxiety, but also impairs cognition. In behavior, this manifested as the ability to better suppress running impulse. The question here was whether the GABA receptor was different, or if the amount of GABA changed as well. After further analysis, it was discovered that there is a disparity between the frequency of GABA release between individuals, not the receptors themselves, contributing to the differences in behavior (Presentation, 2018).

 Finally, Dr. Aoki talked about using DREADD, designer receptors exclusively activated by designer drugs, to activate or suppress neurons at a given time. This allowed her to activate receptors in the prefrontal cortex just before feeding started, which resulted in suppression of physical activity during the meal time (Presentation, 2018).

 Current scientific literature suggests that similar conclusions as Dr. Aoki’s body of work. Puberty in mice is found increased expression of α4βδ-GABA receptors in the hippocampus. The expression of these receptors also negatively impacts spatial learning in a hippocampal-dependent task. These impairments were not seen in knock-out mice for α4βδ-GABA. Current literature also reaffirms that α4βδ GABARs are a sensitive target for steroids such as THP which ultimately results in increased anxiety, disproportionately in women (Smith, 2013).

In summary, Dr. Aoki’s presentation demonstrated that animal models are helpful in identifying cell and molecular differences in adolescents. Furthermore, NR2B, Drebrin and GABA inhibition in the hippocampus affected anxiety levels. Finally, excitation of the prefrontal cortex helps with the exercising behavior.

Works Cited

  1. Presentation, 2018. Aoki C., 2018 “Adolescent Brain: Plasticity to Counter the Perfect Storm”
  2. APA, 2013. Diagnostic and Statistical Manual of Mental Disorders DSM-5, Washington, DC.
  3. Kaye, W.H., et al., 2004. Comorbidity of anxiety disorders with anorexia and bulimia nervosa. Am. J. Psychiatry 161, 2215–2221.
  4. Beumont, P.J., et al., 1994. Excessive physical activity in dieting disorder patients: proposals for a supervised exercise pro- gram. Int. J. Eat. Disord. 15, 21–36.
  5. Arcelus, J., et al., 2011. Mortality rates in patients with anorexia nervosa and other eating disorders. A meta-analysis of 36 studies. Arch. Gen. Psychiatry 68, 724–731.
  6. Hudson, J.I., et al., 2007. The prevalence and correlates of eating disorders in the National Comorbidity Survey Replication. Biol. Psychiatry 61, 348–358.
  7. Bulik, C.M., et al., 2007. The genetics of anorexia nervosa. Annu. Rev. Nutr. 27, 263–275.
  8. Chen, Y. W., Wable, G. S., Chowdhury, T. G., & Aoki, C. (2015). Enlargement of axo-somatic contacts formed by GAD-immunoreactive axon terminals onto layer V pyramidal neurons in the medial prefrontal cortex of adolescent female mice is associated with suppression of food restriction-evoked hyperactivity and resilience to activity-based anorexia. Cerebral Cortex26(6), 2574-2589.
  9. Aoki, C., Chowdhury, T. G., Wable, G. S., & Chen, Y. W. (2017). Synaptic changes in the hippocampus of adolescent female rodents associated with resilience to anxiety and suppression of food restriction-evoked hyperactivity in an animal model for anorexia nervosa. Brain research1654, 102-115.
  10. Adhikari, A., Topiwala, M.A., Gordon, J.A., 2010. Synchronized activity between the ventral hippocampus and the medial prefrontal cortex during anxiety. Neuron 65, 257–269.
  11. Young, J.K., 1991. Estrogen and the etiology of anorexia nervosa. Neurosci. Biobehav. Rev. 15, 327–331.
  12. Smith, S. S. (2013). α4βδ GABAA receptors and tonic inhibitory current during adolescence: effects on mood and synaptic plasticity. Frontiers in neural circuits7, 135.
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