Jessica Barson

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Jessica Barson
JessicaBarsonWiki.jpg
NationalityAmerican
Alma materColumbia University, Princeton University
Known forNeurobiological basis of alcohol consumption and fat intake
Scientific career
FieldsNeuroscience
InstitutionsDrexel University College of Medicine

Jessica Barson is an American neuroscientist and associate professor at Drexel University College of Medicine. Barson investigates neuropeptide signalling in the paraventricular nucleus of the thalamus as well as the nucleus accumbens to understand the neurobiological basis of addiction and elucidate targets for therapy.

Contents

Early life and education

From an early age Barson was interested in the brain. She decided to pursue her undergraduate studies in psychology at Columbia College, Columbia University. [1] During her time at Columbia, Barson worked in the lab of Geraldine Downey as a research assistant studying social psychology and developmental psychopathology. During the later part of her time at Columbia, Barson worked in the lab of Jon Horvitz studying the neurobiological basis of learning and memory. Barson obtained her B.A. and graduated summa cum laude from Columbia in 2000 as a member of the Phi Beta Kappa honors society. [1] After her research experiences at Columbia, Barson pursued a Post-Baccalaureate Pre-Medical Program at Columbia, where she continued to work in research as a technician and research assistant at the New York State Psychiatric Institute until 2003. [1]

Continuing on an academic path, Barson pursued her master's degree and graduate research in neuroscience and psychology at Princeton University in 2004. [2] She trained under the mentorship of Bart G. Hoebel studying the regulation of alcohol intake by dietary fat and fat-stimulated neuropeptides. [3] In 2006, Barson obtained her Master of Arts in Psychology and Neuroscience, and then in 2009, Barson obtained her PhD in Psychology and Neuroscience. [2]

Following her graduate training, Barson moved to New York City to complete her postdoctoral research training at The Rockefeller University in Behavioral Neurobiology in 2009. [1] Barson worked under the mentorship of Sarah Fryer Leibowitz continuing to study the role of opioids and orexin in ethanol consumption and feeding. [4] Barson completed her postdoctoral studies in 2014. [3]

Alcohol Consumption and Dietary Fat Intake

During graduate school, Barson explored the relationship between alcohol consumption and fat metabolism to understand how the mechanisms that control reward or food intake may also regulate alcohol consumption. [5] There exists a positive behavioral feedback loop with fat consumption such that fat intake leads to increased consummatory behavior due to orexin and opioid release in the brain. [5] In her work, Barson probed the mechanisms of this positive feedback loop at play during alcohol consumption. [5] She found that ethanol could substitute for fat in this positive feedback loop that decreasing circulating lipid levels leads to decreased ethanol intake. [5] Barson explored this fascinating interconnectivity between fat and ethanol metabolism and their impacts on behavior. [5] Barson found that ethanol increases the same fat-stimulated neuropeptides, orexin and opioids, in the brain and the more ethanol they voluntarily consume, the higher the expression level of these neuropeptides. [5] Further she found that decreases in ethanol consumption, decrease expression of orexin. [5] Probing the effects of opioids on consummatory behavior, Barson injected opioids into brain regions involved in feeding and reward and found increases in alcohol consumption and increases in dopaminergic release in the nucleus accumbens, typically involved in reward behavior. [5]

Barson's work highlighted novel mechanisms driving alcohol intake which create future opportunities for development of targeted strategies to prevent alcohol abuse. [5] In Barson's first author paper published in the journal Alcohol, Barson shows a strategy to intervene the vicious cycle between fat and alcohol, where consumption of the two synergistically act to drive brain processes that drive further consumption. [6] Since both fat and alcohol appear to increase blood triglyceride levels, Barson administered a triglyceride lowering drug called Gemfibrozil which caused a significant reduction in orexigenic peptide and reduced ethanol intake. [7]

Neural Basis of Feeding and Reward

During her postdoctoral studies at Rockefeller, Barson continued to follow up on her graduate work, exploring mechanistically the regulation of neuropeptides in the regulation of addiction and food consumption. Since previous studies showed that, just like the opioid enkephalin, galanin and orexin are also stimulated by dietary fats. [8] Following up on this knowledge, Barson and her team explored which areas of the hypothalamic paraventricular nucleus (PVN) are specifically stimulated by high fat diets as well as exploring whether the ligands or receptors for galanin and orexin are over-expressed in these areas. [8] Interestingly, Barson found strong overlap in galanin expressing cells and enkephalin expressing cells in the medial PVN of rats fed a high fat diet but not rats fed normal chow. [8] Further, they found the same pattern in co-expression of orexin receptor 2 and enkephalin after high fat diet in a region immediately posterior to the medial PVN. [8] These findings show how non-opioid peptides might be interacting with opioid signalling in high fat diets to mediate increased consummatory behavior. [8]

In addition to her work exploring the neurochemical mechanisms of consummatory behavior, Barson also explored how individual variability can account for differences in consummatory behavior. [9] Since alcoholism, and other addictive disorders, show significant variability in both propensity towards addiction and effects of treatments, it is essential to probe the underlying biology of these differences in order to better treat addiction in the fashion of personalized medicine. [9] They first identified subgroups of ethanol naive rats based on two measures known to predispose individuals to high ethanol consumption; high novelty-induced activity and high-fat-induced triglycerides. [9] Barson and her colleagues then trained them to drink ethanol and observed that high activity rats had both increased alcohol intake as well as increased levels of galanin and enkephalin in the PVN as well as increased orexin in the perifornical lateral hypothalamus (PFLH). [9] In the high triglyceride rats, they greater expression in the PVN but reduced orexin in the PFLH showing that while the two predicted high ethanol consumption groups exhibited high alcohol consumption, the endogenous peptide and drug responses markedly differed. [9]

Career and research

Barson worked for one year as a research associate in the lab of Leibowitz, but by 2015 Barson was recruited to Drexel University College of Medicine to become an assistant professor and start her own lab in the Department of Neurobiology and Anatomy. [1] Barson was simultaneously promoted to Adjunct Faculty at The Rockefeller University in 2015, a position she held until 2017 while starting her lab at Drexel. [1] At Drexel, Barson's research program is centered around studying the neural basis of addiction, with a focus on neuropeptidergic actions within the limbic system and their specific role in alcohol disorder and binge eating disorder. [10] In addition to conducting research and teaching, Barson is an editor for Frontiers in Systems Neuroscience, Frontiers in Neuroscience, and previously Frontiers in Psychology. She is also a guest editor for Frontiers in Behavioral Neuroscience and Brain Research. [2]

Paraventricular Nucleus of the Thalamus and Consummatory Behavior

The Paraventricular Nucleus of the Thalamus (PVT) is a markedly understudied brain region found to be implicated in hedonic feeding behavior. [11] Barson became interested in exploring the role of this region in drug and ethanol consumption due to the orexin projections it receives from the hypothalamus and its high level of orexin receptor expression. [11] When rats consumed alcohol, Barson found increases in anterior PVT neuron activity, as indicated by immediate early gene c-Fos immunolabeling. [11] These same cells also showed increased expression of oxytocin receptor 2 and when orexin receptor 2 was inhibited in the anterior PVT they saw decreased ethanol consumption, and this was not seen with inhibition of orexin receptor 1. [11] These results highlighted a highly specific anatomical and molecular substrate for ethanol intake; orexin receptor 2 signalling in the anterior PVT. [11]

Since the PVT appeared to play a role in alcohol consumption behavior, Barson was interested in exploring the role of this area in emotional processing. [11] They found that overall the anterior PVT was implicated in locomotion, but it appeared to have an enhanced role in novelty-induced activity and anxiety-like behavior, implicating its role in the emotional response to stressful stimuli. [11]

Barson and her colleagues then started exploring the relationship between behavioral predictors of high ethanol consumption and neurotensin (NT) levels in the PVT. [12] They found that rats exhibiting high levels of rearing, were high ethanol consumers, and had lower levels of NT in the posterior PVT compared to rats with moderate levels of rearing. [12] Further, they showed that NTS appeared to be low in prone rats, and alcohol consumption did not change NTS levels compared to non-prone rats implicating NTS in mediating high alcohol drinking behavior. [12] To causally probe this hypothesis, they injected NTS into the posterior PVT and found decreases in ethanol drinking as well as decreases in rearing. [12] Their findings directly support the idea that low levels of NTS in the posterior PVT support excessive alcohol consumption. [12]

Recently, the Barson lab implicated pituitary adenylate cyclase-activating polypeptide (PACAP) and its protein isoform, PACAP-27, in regulation of alcohol consumption in the PVT. [13] Alcohol drinking led to an increase in PACAP expression, specifically in the posterior portion of the PVT. [13] Barson's findings have highlighted another way in which the PVT may function in the pathogenesis of alcohol consumptive behaviors. [13]

Science Communication and Advocacy

In addition to her laboratory investigation, Barson is dedicated to science communication and advocacy. Her work has been brought to public attention via LiveScience [14] and the Inquirer, where she describes how her findings lead to an increased understanding of the connection between alcohol consumption and binge eating as well as alcohol consumption and the reliability of memory. [15] Further, Barson participates in local science communication initiatives such as the Taste of Science, where she speaks about her work to the public, educating them on why we might choose unhealthy options to snack on after binge drinking as opposed to healthy options. [16]  Barson is also actively involved in advocating for gender equity in academia. As a member of the Society for Neuroscience and as a mother in science, Barson was invited to speak at the “Fixing the Leaky Pipeline for Women in Science” annual meeting discussing the issues facing new mothers in academia. [1]

Awards and honors

Select publications

Related Research Articles

<span class="mw-page-title-main">Hypothalamus</span> Area of the brain below the thalamus

The hypothalamus is a part of the brain that contains a number of small nuclei with a variety of functions. One of the most important functions is to link the nervous system to the endocrine system via the pituitary gland. The hypothalamus is located below the thalamus and is part of the limbic system. In the terminology of neuroanatomy, it forms the ventral part of the diencephalon. All vertebrate brains contain a hypothalamus. In humans, it is the size of an almond.

<span class="mw-page-title-main">Orexin</span> Neuropeptide that regulates arousal, wakefulness, and appetite.

Orexin, also known as hypocretin, is a neuropeptide that regulates arousal, wakefulness, and appetite. The most common form of narcolepsy, type 1, in which the individual experiences brief losses of muscle tone, is caused by a lack of orexin in the brain due to destruction of the cells that produce it. It exists in the forms of orexin-A and orexin-B.

<span class="mw-page-title-main">Nucleus accumbens</span> Region of the basal forebrain

The nucleus accumbens is a region in the basal forebrain rostral to the preoptic area of the hypothalamus. The nucleus accumbens and the olfactory tubercle collectively form the ventral striatum. The ventral striatum and dorsal striatum collectively form the striatum, which is the main component of the basal ganglia. The dopaminergic neurons of the mesolimbic pathway project onto the GABAergic medium spiny neurons of the nucleus accumbens and olfactory tubercle. Each cerebral hemisphere has its own nucleus accumbens, which can be divided into two structures: the nucleus accumbens core and the nucleus accumbens shell. These substructures have different morphology and functions.

<span class="mw-page-title-main">Dopaminergic pathways</span> Projection neurons in the brain that synthesize and release dopamine

Dopaminergic pathways in the human brain are involved in both physiological and behavioral processes including movement, cognition, executive functions, reward, motivation, and neuroendocrine control. Each pathway is a set of projection neurons, consisting of individual dopaminergic neurons.

Dynorphins (Dyn) are a class of opioid peptides that arise from the precursor protein prodynorphin. When prodynorphin is cleaved during processing by proprotein convertase 2 (PC2), multiple active peptides are released: dynorphin A, dynorphin B, and α/β-neo-endorphin. Depolarization of a neuron containing prodynorphin stimulates PC2 processing, which occurs within synaptic vesicles in the presynaptic terminal. Occasionally, prodynorphin is not fully processed, leading to the release of “big dynorphin.” “Big Dynorphin” is a 32-amino acid molecule consisting of both dynorphin A and dynorphin B.

<span class="mw-page-title-main">Neuropeptide Y</span> Mammalian protein found in Homo sapiens

Neuropeptide Y (NPY) is a 36 amino-acid neuropeptide that is involved in various physiological and homeostatic processes in both the central and peripheral nervous systems. It is secreted alongside other neurotransmitters such as GABA and glutamate. 

Neuropharmacology is the study of how drugs affect function in the nervous system, and the neural mechanisms through which they influence behavior. There are two main branches of neuropharmacology: behavioral and molecular. Behavioral neuropharmacology focuses on the study of how drugs affect human behavior (neuropsychopharmacology), including the study of how drug dependence and addiction affect the human brain. Molecular neuropharmacology involves the study of neurons and their neurochemical interactions, with the overall goal of developing drugs that have beneficial effects on neurological function. Both of these fields are closely connected, since both are concerned with the interactions of neurotransmitters, neuropeptides, neurohormones, neuromodulators, enzymes, second messengers, co-transporters, ion channels, and receptor proteins in the central and peripheral nervous systems. Studying these interactions, researchers are developing drugs to treat many different neurological disorders, including pain, neurodegenerative diseases such as Parkinson's disease and Alzheimer's disease, psychological disorders, addiction, and many others.

<span class="mw-page-title-main">Ventrolateral preoptic nucleus</span> Nucleus of the anterior hypothalamus

The ventrolateral preoptic nucleus (VLPO), also known as the intermediate nucleus of the preoptic area (IPA), is a small cluster of neurons situated in the anterior hypothalamus, sitting just above and to the side of the optic chiasm in the brain of humans and other animals. The brain's sleep-promoting nuclei, together with the ascending arousal system which includes components in the brainstem, hypothalamus and basal forebrain, are the interconnected neural systems which control states of arousal, sleep, and transitions between these two states. The VLPO is active during sleep, particularly during non-rapid eye movement sleep, and releases inhibitory neurotransmitters, mainly GABA and galanin, which inhibit neurons of the ascending arousal system that are involved in wakefulness and arousal. The VLPO is in turn innervated by neurons from several components of the ascending arousal system. The VLPO is activated by the endogenous sleep-promoting substances adenosine and prostaglandin D2. The VLPO is inhibited during wakefulness by the arousal-inducing neurotransmitters norepinephrine and acetylcholine. The role of the VLPO in sleep and wakefulness, and its association with sleep disorders – particularly insomnia and narcolepsy – is a growing area of neuroscience research.

Melanin-concentrating hormone (MCH), also known as pro-melanin stimulating hormone (PMCH), is a cyclic 19-amino acid orexigenic hypothalamic peptide originally isolated from the pituitary gland of teleost fish, where it controls skin pigmentation. In mammals it is involved in the regulation of feeding behavior, mood, sleep-wake cycle and energy balance.

κ-opioid receptor Protein-coding gene in the species Homo sapiens, named for ketazocine

The κ-opioid receptor or kappa opioid receptor, abbreviated KOR or KOP for its ligand ketazocine, is a G protein-coupled receptor that in humans is encoded by the OPRK1 gene. The KOR is coupled to the G protein Gi/G0 and is one of four related receptors that bind opioid-like compounds in the brain and are responsible for mediating the effects of these compounds. These effects include altering nociception, consciousness, motor control, and mood. Dysregulation of this receptor system has been implicated in alcohol and drug addiction.

<span class="mw-page-title-main">Lateral hypothalamus</span>

The lateral hypothalamus (LH), also called the lateral hypothalamic area (LHA), contains the primary orexinergic nucleus within the hypothalamus that widely projects throughout the nervous system; this system of neurons mediates an array of cognitive and physical processes, such as promoting feeding behavior and arousal, reducing pain perception, and regulating body temperature, digestive functions, and blood pressure, among many others. Clinically significant disorders that involve dysfunctions of the orexinergic projection system include narcolepsy, motility disorders or functional gastrointestinal disorders involving visceral hypersensitivity, and eating disorders.

Nesfatin-1 is a neuropeptide produced in the hypothalamus of mammals. It participates in the regulation of hunger and fat storage. Increased nesfatin-1 in the hypothalamus contributes to diminished hunger, a 'sense of fullness', and a potential loss of body fat and weight.

<span class="mw-page-title-main">Median preoptic nucleus</span> Nucleus in the anterior hypothalamus

The median preoptic nucleus is located dorsal to the other three nuclei of the preoptic area of the anterior hypothalamus. The hypothalamus is located just beneath the thalamus, the main sensory relay station of the nervous system, and is considered part of the limbic system, which also includes structures such as the hippocampus and the amygdala. The hypothalamus is highly involved in maintaining homeostasis of the body, and the median preoptic nucleus is no exception, contributing to regulation of blood composition, body temperature, and non-REM sleep.

Psychological dependence is a cognitive disorder that involves emotional–motivational withdrawal symptoms—e.g. anxiety and anhedonia—upon cessation of prolonged drug abuse or certain repetitive behaviors. It develops through frequent exposure to a psychoactive substance or behavior, though behavioral dependence is less talked about. The specific mechanism involves a neuronal counter-adaptation, which could be mediated through changes in neurotransmitter activity or altered receptor expression. Environmental enrichment and physical activity can attenuate withdrawal symptoms. Psychological dependence is not to be confused with physical dependence, which induces physical withdrawal symptoms upon discontinuation of use. However, they are not mutually exclusive.

<span class="mw-page-title-main">SB-334867</span> Chemical compound

SB-334867 is an orexin antagonist. It was the first non-peptide antagonist developed that is selective for the orexin receptor subtype OX1, with around 50x selectivity for OX1 over OX2 receptors. It has been shown to produce sedative and anorectic effects in animals, and has been useful in characterising the orexinergic regulation of brain systems involved with appetite and sleep, as well as other physiological processes. The hydrochloride salt of SB-334867 has been demonstrated to be hydrolytically unstable, both in solution and as the solid. Orexin antagonists have multiple potential clinical applications including the treatment of drug addiction, insomnia, obesity and diabetes.

Hunger is a sensation that motivates the consumption of food. The sensation of hunger typically manifests after only a few hours without eating and is generally considered to be unpleasant. Satiety occurs between 5 and 20 minutes after eating. There are several theories about how the feeling of hunger arises. The desire to eat food, or appetite, is another sensation experienced with regards to eating.

<span class="mw-page-title-main">Central nucleus of the amygdala</span> Nucleus within the amygdala

The central nucleus of the amygdala is a nucleus within the amygdala. It "serves as the major output nucleus of the amygdala and participates in receiving and processing pain information."

While researchers have found that moderate alcohol consumption in older adults is associated with better cognition and well-being than abstinence, excessive alcohol consumption is associated with widespread and significant brain lesions. Other data – including investigated brain-scans of 36,678 UK Biobank participants – suggest that even "light" or "moderate" consumption of alcohol by itself harms the brain, such as by reducing brain grey matter volume. This may imply that alternatives and generally aiming for lowest possible consumption could usually be the advisable approach.

<span class="mw-page-title-main">Alcohol (drug)</span> Active ingredient in alcoholic beverages

Alcohol, sometimes referred to by the chemical name ethanol, is a depressant drug that is the active ingredient in drinks such as beer, wine, and distilled spirits. It is one of the oldest and most commonly consumed recreational drugs, causing the characteristic effects of alcohol intoxication ("drunkenness"). Among other effects, alcohol produces happiness and euphoria, decreased anxiety, increased sociability, sedation, impairment of cognitive, memory, motor, and sensory function, and generalized depression of central nervous system (CNS) function. Ethanol is only one of several types of alcohol, but it is the only type of alcohol that is found in alcoholic beverages or commonly used for recreational purposes; other alcohols such as methanol and isopropyl alcohol are significantly more toxic. A mild, brief exposure to isopropanol, being only moderately more toxic than ethanol, is unlikely to cause any serious harm. Methanol, being profoundly more toxic than ethanol, is lethal in quantities as small as 10–15 milliliters.

Alcoholism is a chronic disease characterized by trouble controlling the consumption of alcohol, dependence, and withdrawal upon rapid cessation of drinking. According to ARDI reports approximately 88,000 people had alcohol-related deaths in the United States between the years of 2006 and 2010. Furthermore, chronic alcohol use is consistently the third leading cause of death in the United States. In consequence, research has sought to determine the factors responsible for the development and persistence of alcoholism. From this research, several molecular and epigenetic mechanisms have been discovered.

References

  1. 1 2 3 4 5 6 7 "Addressing the Leaky Pipeline in Science: Issues Facing New Moms". neuronline.sfn.org. Retrieved 2020-04-28.
  2. 1 2 3 4 "Jessica Barson, PhD: Neurobiology & Anatomy". College of Medicine. 2020-02-21. Retrieved 2020-04-28.
  3. 1 2 "SSIBlings - Jessica R. Barson". academictree.org. Retrieved 2020-04-28.
  4. ↑ "Jessica Barson - Google Scholar Citations". scholar.google.com. Retrieved 2020-04-28.
  5. 1 2 3 4 5 6 7 8 9 Barson, Jessica R (2009). Regulation of alcohol intake by dietary fat and 'fat-stimulated' neuropeptides (Thesis). ProQuest   304980498.
  6. ↑ Barson, Jessica R.; Karatayev, Olga; Chang, Guo-Qing; Johnson, Deanne F.; Bocarsly, Miriam E.; Hoebel, Bartley G.; Leibowitz, Sarah F. (September 2009). "Positive relationship between dietary fat, ethanol intake, triglycerides, and hypothalamic peptides: counteraction by lipid-lowering drugs". Alcohol (Fayetteville, N.Y.). 43 (6): 433–441. doi:10.1016/j.alcohol.2009.07.003. ISSN   1873-6823. PMC   2758659 . PMID   19801273.
  7. ↑ Barson, Jessica R.; Karatayev, Olga; Chang, Guo-Qing; Johnson, Deanne F.; Bocarsly, Miriam E.; Hoebel, Bartley G.; Leibowitz, Sarah F. (September 2009). "Positive relationship between dietary fat, ethanol intake, triglycerides, and hypothalamic peptides: counteraction by lipid-lowering drugs". Alcohol (Fayetteville, N.Y.). 43 (6): 433–441. doi:10.1016/j.alcohol.2009.07.003. ISSN   1873-6823. PMC   2758659 . PMID   19801273.
  8. 1 2 3 4 5 Barson, J. R.; Chang, G. -Q.; Poon, K.; Morganstern, I.; Leibowitz, S. F. (2011-10-13). "Galanin and the orexin 2 receptor as possible regulators of enkephalin in the paraventricular nucleus of the hypothalamus: relation to dietary fat". Neuroscience. 193: 10–20. doi:10.1016/j.neuroscience.2011.07.057. ISSN   0306-4522. PMC   3171948 . PMID   21821102.
  9. 1 2 3 4 5 Barson, Jessica R.; Fagan, Shawn E.; Chang, Guo-Qing; Leibowitz, Sarah F. (January 2013). "Neurochemical heterogeneity of rats predicted by different measures to be high ethanol consumers". Alcoholism: Clinical and Experimental Research. 37 Suppl 1 (1): E141–151. doi:10.1111/j.1530-0277.2012.01858.x. ISSN   1530-0277. PMC   3984010 . PMID   22725682.
  10. 1 2 3 4 5 6 7 8 9 10 11 12 "Jessica Barson Laboratory". Drexel College of Medicine. 2020-02-25. Retrieved 2020-04-28.
  11. 1 2 3 4 5 6 7 Barson, Jessica R.; Ho, Hui Tin; Leibowitz, Sarah F. (2015). "Anterior thalamic paraventricular nucleus is involved in intermittent access ethanol drinking: role of orexin receptor 2". Addiction Biology. 20 (3): 469–481. doi:10.1111/adb.12139. ISSN   1369-1600. PMC   4192116 . PMID   24712379.
  12. 1 2 3 4 5 Pandey, Surya; Badve, Preeti S.; Curtis, Genevieve R.; Leibowitz, Sarah F.; Barson, Jessica R. (2019). "Neurotensin in the posterior thalamic paraventricular nucleus: inhibitor of pharmacologically relevant ethanol drinking". Addiction Biology. 24 (1): 3–16. doi:10.1111/adb.12546. ISSN   1369-1600. PMC   5839915 . PMID   28877396.
  13. 1 2 3 Gupta, Anuranita; Gargiulo, Andrew T.; Curtis, Genevieve R.; Badve, Preeti S.; Pandey, Surya; Barson, Jessica R. (2018). "Pituitary Adenylate Cyclase-Activating Polypeptide-27 (PACAP-27) in the Thalamic Paraventricular Nucleus Is Stimulated by Ethanol Drinking". Alcoholism: Clinical and Experimental Research. 42 (9): 1650–1660. doi:10.1111/acer.13826. ISSN   1530-0277. PMC   6120804 . PMID   29969146.
  14. ↑ January 2017, Agata Blaszczak-Boxe 10 (10 January 2017). "Your Drunken Urge for Pizza and Wings, Explained by Science". livescience.com. Retrieved 2020-04-28.
  15. ↑ Pattani, Aneri (20 September 2018). "Kavanaugh allegations raise questions about alcohol, sexual assault, and the reliability of memory". Inquirer. Retrieved 2020-04-28.
  16. ↑ "The Science of Taste". taste of science. 22 April 2019. Retrieved 2020-04-28.
  17. 1 2 3 "Jessica BARSON | PhD | Drexel University College of Medicine, Philadelphia | Department of Neurobiology & Anatomy". ResearchGate. Retrieved 2020-04-28.
  18. 1 2 "Grantome: Search". Grantome. Retrieved 2020-04-28.
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