The Neuroscience Behind Visual Experiences & Memory Retrieval

A question regarding memory is whether brain activation in several regions identifies the memory processes of declarative memory regarding to both encoding of memory & retrieval. The use of functional neuroimaging plays an important role in measuring activation in different stages of memory (the process of encoding the current experience into becoming a memory & the storage of memory) to the individual’s experience. Encoded memory that had been processed successfully will be later remembered versus memory that had not been processed successfully (easily forgotten).

Brewer, Zhao, Desmond, & Gary H (1998) article discusses how a specific visual experience is remembered based on neural activity. The introduction to this study briefly discusses a specific region in the brain that is associated with declarative (also known as explicit) memory called the Medial temporal lobe. Declarative memory refers to memories that can be consciously retrieved such as facts. Another region contributing to the memory system is the parahippocampal cortex as well as the right frontal cortex.

For this study 6 participants viewed colored images with indoor & outdoor scenery judging whether the picture was either indoor or outdoor. 30 minutes after they were done they were given an unexpected memory test of the pictures they previously viewed. The memory test consisted of 96 images including additional new images & the participants had to tell whether they have seen the picture or not. 3 different outcomes of memory were reported where the individual have a). Seen the picture (being well remembered) b). The image looked familiar (not well remembered) or c). Pictures weren’t recalled (forgotten).

The results for this study reported that there was a greater activation in the parahippocampal region (associated with long term memory) for remembered pictures then those pictures that were familiar. Activation in the right frontal region proposes memory processes associated with the visuospatial matter of the scenic image so the interaction between those two regions format a long term memory & predicts whether memory will be remembered or forgotten.

Lateralization of brain functioning plays an important role in terms of mental processes that are specialized in memory – we see a significant role in the left laterized region of the brain for both retrieval & working memory. An important note to keep in mind is that the left hemisphere is dominant in language for processing auditory & comprehension of language. Memory involves the temporary storage and manipulation of information & a major component for the manipulation of information is language.


James B. Brewer,* Zuo Zhao, John E. Desmond, Gary H (1998). Making Memories: Brain Activity that Predicts How Well Visual Experience Will Be Remembered

Can you describe a color?

“What does color blue look like?”

This wonderful clip reminded me of the philosophical argument of Mary’s Room.

Mary is a neuroscientist who has dedicated her life in learning about the perception of color and the mechanisms behind light emission.

Here’s the catch: She has never directly experienced color before. Her room is vacant of color.

After she leaves the room with the knowledge she has obtained, she see’s the color red for the very first time thus learning something new: What red looks like.

Was it possible for Mary to have described the color before observing it for the first time?

Review on Mental Health Disorders (Attention Deficit Hyperactivity Disorder- ADHD, Post-Traumatic Stress Disorder, Major Depressive Disorder) & Sugar Consumption


Maintaining glucose metabolism is highly critical for the brains pathological & physiological functioning. Glucose is a form of sugar which is an essential source of energy for nerve cells to provide neurotransmitter synthesis, sensory stimulation and sustaining intracellular pathways. The notion that dietary factors have been known to influence both cognitive & behavioral symptoms of mental health disorders continues to be a debatable subject among researchers today. This article examines the influence of sugar consumption in psychiatric disorders such as Attention deficit hyper activity disorder (ADHD), Post-traumatic stress disorder (PTSD) and Major depressive disorder (MDD).

PART I Attention Deficit Hyperactivity Disorder & Excessive Sugar

Investigating preclinical data, Johnson et al. (2011) hypothesized that excessive sugar intake may be associated with a disruption in dopamine signaling, in such that the D2 receptors are reduced in natural reward-related brain regions such at the prefrontal lobe. This can result in the attempt to correct the dopamine-deficient state by consuming a substantial amount of sugar; leading to symptoms associated with ADHD. The mechanism underlying dopamine release starts with the “sweet” receptors (T1R2 and T1R3) that are located in the tongue and gastrointestinal tract. Johnson mentions previous data in De Araujo 2008 study in regards to the lack of functional taste receptors in mice, however even though they lack these sweet receptors they continue to consume sucrose. This suggests that sugar has a distinct effect on dopamine signaling relating to the metabolic process in such that it alters frontal lobe behavioral mechanisms in response to excessive ingestion of sugar content. Similarly, Volkow et al. (2009) has observed the fontal cortex and the reduced inhibitory signals of postsynaptic dopamine signaling pathway, which could result in the symptoms of ADHD such as impulsive behavior & inattention. For future studies, utilizing neuro feedback to investigate sugar intake & attention deficit would be extremely beneficial. The effects of sugar on the EEG have been studied since the late 30’s. A deficiency of glucose to the brain causes the appearance of slow rhythms in the EEG; demonstrating a significant change in frequency. It could be proposed that an increase in sugar would cause an increase in faster b rhythms in the EEG, or possibly lower theta / alpha waves. This could be demonstrated in higher processing tasks in individuals with ADHD.

PART II  Dietary behavior & Post-Traumatic Stress Disorder

Examining nutritional intake plays a significant role in understanding particular behavioral symptoms of PTSD. The cognitive model, developed by Ehlers and Clark (2000), demonstrates the individual’s inability to appraise the traumatic situation in a way that reduces its effect; which alters the engagement of normal activities. Victims of trauma may often find themselves coping with recurring symptoms of PTSD with stress-induced eating and an unhealthy consumption of food with high sugar content. Hirth et al. (2011) have constructed a cross-sectional study examining unhealthy dietary behaviors in woman in association to their PTSD symptoms. A self-administered questionnaire with questions about health behaviors was given to 3181 women in addition to questions of soda and fast food consumption. A statistical analysis was processed to examine the associations between PTSD symptoms and consumption of sugary soda as well as six unhealthy dieting methods using binary logistic regression on the SAS software. The results for this study revealed that PTSD symptoms are positively associated with the frequency of fast food & excessive sugar consumption. Women who drank more than one soda reported more PTSD symptoms, and a higher proportion of women who reported a higher frequency of fast food eaten on the previous day reported experiencing more PTSD symptoms. In addition, PTSD symptoms that were examined in this study are significantly correlated (p<0.001) with the total number of unhealthy dieting behaviors engaged in over the past 30 days. This study could imply that traumatic experiences may have an “imprinting” effect when consuming high sugar content; triggering a perpetual stress response.

PART III  Correlation between Sugar & Major Depressive Disorder

Abnormalities in neurotransmission have been investigated extensively in major depression for many years. Researcher’s elucidated neural adaptations including changes in dopamine and opioid receptor binding releases; formulating the theory that excessive intake of sugar can have dopaminergic and opioid effects that are similar to psychostimulants. This could exacerbate the symptoms of depression such as withdrawal, anxiety and emotional lability. Rada & Hoebel (2008) have observed behavioral depression in animals using the forced-swim test; which measures swimming escape efforts vs. passive floating. In this experiment, rats were given an initial 5-min forced-swim test in which escape (swimming and climbing) and passive (floating) behaviors. The rats were divided into specific groups, one group that was fed intermittent sucrose & chow, the other group only chow, & libitum with Sucrose. The results for the study has shown that rats who were consuming sucrose /libitum with sucrose demonstrated a decrease in effort to escape that were replaced by passive floating; suggesting the rats were experiencing behavioral depression during withdrawal of their sucrose intake. This withdrawal state involves two neurochemical manifestations. First is a decrease in activity in the accumbens (which functions as the reward circuit of the brain – resulting in the activation of dopamine), and second is the release of acetylcholine (where pain response is activated). These neurochemical adaptations in response to sugar intake mimic the effects of opiates. In summary, the consumption of excessive sugar and the prevalence in depressive symptoms may be correlated. In conclusion, there is a possible impact on specific mental health disorders when consuming an excessive amount of sugar content however further investigation and additional studies need to be done for each disorder.


 Avena, N. M., Rada, P., & Hoebel, B. G. (2008). Evidence for sugar addiction: Behavioral and neurochemical effects of intermittent, excessive sugar intake. Neuroscience and Biobehavioral Reviews, 32(1), 20–39.

De Araujo IE, Oliveira-Maia AJ, Sotnikova TD, Gainetdinov RR, Caron MG, Nicolelis MA, Simon SAFood reward in the absence of taste receptor signaling. 2008 Mar 27; 57(6):930-41.

Ehlers A, Clark DM. A cognitive model of posttraumatic stress disorder. Behav Res Ther. 2000 Apr; 38(4):319-45.

Hirth, J. M., Rahman, M., & Berenson, A. B. (2011). The Association of Posttraumatic Stress Disorder with Fast Food and Soda Consumption and Unhealthy Weight Loss Behaviors Among Young Women. Journal of Women’s Health, 20(8), 1141–1149.

Mergenthaler, P., Lindauer, U., Dienel, G. A., & Meisel, A. (2013). Sugar for the brain: the role of glucose in physiological and pathological brain function. Trends in Neurosciences, 36(10), 587–597.

Millichap, J. G., & Yee, M. M. The diet factor in attention-deficit/hyperactivity disorder (2012).. Pediatrics, 129(2), 330-337. Chicago

Rauch SL, Shin LM, Whalen PJ, Pitman RK. Neuroimaging and the neuroanatomy of PTSD. CNS Spectrums. 1998;3(Suppl. 2):30–41

Richard J. Johnson, Mark S. Gold, David R. Johnson, Takuji Ishimoto, Miguel A. Lanaspa, Nancy R. Zahniser, Nicole M. Avena. Attention-Deficit/Hyperactivity Disorder: Is it Time to Reappraise the Role of Sugar Consumption? Published in final edited form as: Postgrad Med. 2011 Sep; 123(5): 39–49. doi: 10.3810/pgm.2011.09.2458

Volkow ND, Wang GJ, Kollins SH, Wigal TL, Newcorn JH, Telang F, Fowler JS, Zhu W, Logan J, Ma Y, Pradhan K, Wong C, Swanson JM.    Evaluating dopamine reward pathway in ADHD: clinical implications. JAMA 2009 Sep 9; 302(10):1084-91.

Zukerman S, Glendinning JI, Margolskee RF, Sclafani A. T1R3 taste receptor is critical for sucrose but not Polycose taste. Am J Physiol Regul Integr Comp Physiol. 2009;296(4):R866–R876.