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From Probiotics to Psychobiotics: Live Beneficial Bacteria Which Act on the Brain-Gut Axis By: Luis G. Bermúdez-Humarán, et al. Jaylin Wang, Mya Warner Background ● The adult human gut microbiota is composed of 500-1000 bacterial species ● Microbiota is essential for maturation of essential systems...

From Probiotics to Psychobiotics: Live Beneficial Bacteria Which Act on the Brain-Gut Axis By: Luis G. Bermúdez-Humarán, et al. Jaylin Wang, Mya Warner Background ● The adult human gut microbiota is composed of 500-1000 bacterial species ● Microbiota is essential for maturation of essential systems ○ Contribute to showing signs of disorders such as Alzheimer's, anxiety, and autism ● Psychobiotics include prebiotics, stimulating beneficial bacteria that help maintain gut health (bananas, oats, onion, asparagus), and probiotics, digestible microorganisms that provide health benefits (kombucha, kimchi, yogurt) ○ Psychobiotics affect mental health, cognitive function and behavior by regulating neuroimmune axes through interaction with commensal gut bacteria Purpose This review explores recent findings on psychobiotics, emphasizing the interconnection between the microbiota of the intestine, diseases of the nervous system, and potential treatments through neuroimmunomodulation. Highlights the role of probiotic bacteria in influencing the brain-gut axis by producing neuroactive substances. Results Axes of Neuroimmune Control and Regulation ● HPA, SAM, and inflammatory reflex: regulate and control the brain-gut axes ● Neuroimmune axes play a crucial role in diseases affecting the nervous system ○ Affected by psychobiotics (ex: prebiotics fructooligosaccharides (FOS) and galactooligosaccharides (GOS)) ○ Promote healthy gut, improve inflammation and oxidative stress: works on gut and brain Interaction of Microbiota with ENS and Brain-Gut axis ● The ENS plays a crucial role in the gastrointestinal system and is in constant communication with gut microbiota ● Bidirectional communication via the brain-gut axes, meaning both are exchanging feedback from one another constantly ● Microbiota produce NTs such as serotonin, norepinephrine, and endorphins that affect mood, behavior, and gut motility Behavior Cognition and Emotion ● Mice experiment: Administered L. rhamnosus (probiotic); lead to reduced anxiety/depression; downregulation HPA axis ● Presence of a probiotic: lower expression of GABA in hippocampal regions = can modulate inhibitory/excitatory NTs that control stress/anxiety/depression ● prebiotic/probiotic consumption can reduce oxidative stress, pain relief, anxiety/depressive behaviors Author’s Interpretation ● Human microbiota composition and impact of probiotics are important in examining the relationship between microbiota and host health or disease ● Prebiotic intake is important for normal physiological system development, has neuroprotective effects, and enhances brain physiology and learning ● Psychobiotics can alter the gut microbiome to strengthen memory and treat symptoms of mental health disorders and psychiatric conditions Our Interpretation ● The brain-gut axis connects the central nervous system, endocrine and immune systems, and enteric nervous system, so it makes sense that microbiota composition can influence brain function and nervous system development and vice versa, that signals from the CNS can induce microbiota changes in the gut. Modification of microbiota via psychobiotics could be an effective treatment to help conditions and behaviors related to immune, neural, or hormonal mechanisms ● Potential future treatment alternatives for disorders such as depression and anxiety thru supplementation Relation to Lecture ● Discussion of overall communication by signaling pathways for homeostatic control (ex: HPA axis and stress, inflammation, and immune responses, sympathetic/parasympathetic/enteric systems) and their relationship with prebiotic/probiotic intake and gut microbiota composition ● Understanding the gut microbiome, its relationship to physiological development and risk of mood, psychological, neurological, and metabolic diseases, and the potential benefits of probiotic treatments on these conditions could help better understand the importance of diet on microbiota and overall human health. Kaili Valenzuela & Tannen Vagle Circadian Entrainment by Food and Drugs of Abuse Background: - Circadian rhythms are inherent in various organisms, influencing behavioral, anatomical, and molecular levels. - The human sleep-wake cycle is a well-known circadian rhythm, regulated by the day/night cycle and light onset as a zeitgeber. - Biological circadian rhythms (ex. the sleep-wake cycle) exhibit entrained and free-running periods and are regulated by feedback loops with clock genes. - The suprachiasmatic nucleus (SCN) in the hypothalamus is the central pacemaker for light-entrainable circadian rhythms. - The FEO is similar to the SCN as they both entrain food anticipatory activity 1-2 hours before meals (FAAs) → 24 hr periods (anything more found FAAs still at 24hr periods) Purpose: - Searching for the existence and investigating the characteristics of motivation-entrainable oscillators, exploring their relationship with drug abuse, and how they play a role in addiction. Results/Interpretation: - This study focuses on a reward-entrainable oscillator, suggesting that drugs of abuse, through their arousing and locomotor-stimulating properties, might share entraining ability. - Experiments involving female Wistar rats reveal that drugs like methamphetamine and nicotine can entrain anticipatory wheel running, similar to circadian ensuing activity observed after meal delivery. - Distinct types of circadian locomotor activity are observed, with pre-drug and post-drug activity, potentially related to motivation and reward. - Affirmative answers are provided regarding the existence of a drug-entrainable oscillator and its sensitivity to abused drugs. - The study explores the neural basis of entrainment, focusing on the mesocorticolimbic system, dopamine, and glutamate regulation, highlighting their roles in circadian rhythms and more specifically addiction. Conclusions: - Circadian rhythmicity is implicated in drug abuse, with evidence supporting the existence of a reward-entrainable oscillator sensitive to various drugs. - Dopamine and glutamate, crucial neurotransmitters, exhibit circadian regulation and play essential roles in addiction-related neural processes. - The study underscores the potential importance of entrainment in drug craving, habitual drug use, and relapse, opening avenues for further research. Connections to Lecture: - SCN is the central pacemaker of circadian timing→utilizes light in the sleep wake cycle - Primary components of wake-arousal systems→ dopamine & glutamate/clock genes - 3 important components of circadian clocks - Input pathway→drug abuse cycle - Pacemaker→Food/Drug Entrainable Oscillator - Timer→circadian timing of motivation for repeated drug abuse or food seeking behaviors Timing of Light Exposure Affects Mood and Brain Circuits Outline by Daniel Schettini and Hoorig Sarkissian Paper Overview: ● The paper was a literature review that covered how artificial light at night affects emotion and mood regulation. The paper covered how sleep, rhythmic genes, jet lag, seasonal changes, neuroplasticity, and neurotransmission affect the brain based on humans and other animals. Background: ● Light exposure at night has risen from 1 lux to over 300 lux at times with the advent of modern lighting and computer technology. Circadian rhythm disruptions could cause depression and other mood disorders and this needs to be explored. Why Light is Associated with Circadian Rhythms: ● Intrinsically photosensitive retinal ganglion cells (ipRGCs) suppress melatonin and make the circadian system respond to light. ipRGCs project to the suprachiasmatic nucleus (SCN) of the hypothalamus, which is the body’s master clock. The SCN drives the rhythmic cycle via a set of transcriptional-translational feedback loops. Aberrant Light Exposure and the Brain: ● The authors believe that there are both direct (ipRGC projections) and indirect (sleep disruption, gene expression, neuroplasticity, and neurotransmitter and hormone secretion) connections between exposure to artificial light at night and the regulation of our moods. ipRGCS: ● ipRGCs have projections to parts of the brain that control emotions, so the authors believe that light exposure to these cells at unnatural times may affect mood. Sleep: ● Exposure to light during naturally dark times causes melatonin release to be suppressed. Sleep and emotion are believed to be very closely linked, and so the authors believe that sleep disruptions are one possible cause for mood disorders. Rhythmic Expression of Clock Genes: ● Circadian genes have been shown to hold critical roles in mood regulation as mutations in these genes have been linked to behavioral impairments. Rodent studies have shown decreased expression of CLOCK genes when subjects were exposed to nighttime light, causing the authors to believe that disruptions to CLOCK gene expression might affect mood. Jet Lag: ● Jet lag causes phase shifts in biological rhythms leading to a loss of synchronization with environmental rhythms. Multiple studies conducted on humans and rodents have shown that prolonged jet lag leads to impairments in learning and memory as well as other cognitive deficits due to decreased hippocampal cell regeneration and temporal lobe atrophy, respectively. Seasonal Changes in Day Length: ● Changes in day length across seasons have been linked to mood alterations, believed to be driven by shifts in pineal melatonin rhythms due to reduced light exposure throughout the day. Neuroplasticity: ● A feature of major depression is impaired neuroplasticity where the brain has less hippocampal volume, decreased amounts of brain-derived neurotrophic factor (BDNF), and functional plasticity defects. In both nocturnal and diurnal animals, dendritic length decreases, learning deficiencies increase, and depressive behaviors increase when circadian disruptions occur. Neurotransmission: ● Monoamines like serotonin, norepinephrine, and dopamine follow a release pattern that is controlled by circadian rhythms via the SCN. While the regimen of how light is administered matters for how neurotransmission is affected, overall, light has been shown to alter dopamine, DOPA, GABA, and glutamate in rat models. Conclusion: ● The idea is that Circadian Disruptions lead to Clock Gene Disturbances which lead to Neurotransmitter Release Disruptions which can cause depression and other mood disorders. Overall, we agree that light exposure at unnatural times causes effects on sleep, neurotransmitter and hormone release, and neuroplasticity which can all affect people’s moods. Rahul Sobti and Jake Takashima Outline Effects of Diet on Sleep: A Narrative Review Background: 1. Sleep is vital for memory consolidation, restoring energy, and maintaining immune health. Good sleep necessary for overall health and wellbeing is defined as low sleep latency, low number of awakenings during sleep that are greater than 5 minutes, and sleeping a duration of 7-9 hours. 2. 45% of Americans and Australians report not sleeping 7-9 hours a night. 3. An important factor that impacts sleep is dietary intake. a. Previous studies have shown that the consumption of Tryptophan directly influences sleep, as it is converted to a precursor for the sleep inducing hormone melatonin. Hypothesis/Purpose: 1. Since many previous studies examining the relationship between diet and sleep primarily focus on clinical populations, Binks et al. sought to clarify the effects of diet on sleep metrics in generally healthy adults. Materials and Methods: 1. Used data from online databases such as Cochrane, MEDLINE, and Cumulative Index of Nursing and Allied Health Literature (CINAHL) from studies examining the effect of diet on sleep in 1990 to August 2019. 2. Eligible studies used polysomnography (PSG), electroencephalography (EEG), actigraphy, and subjective measures to assess sleep. Results: 1. Tryptophan consumption increases total sleep time, improves sleep efficiency, makes falling asleep easier, and decreases waking at night, total activity, and fragmented sleep. a. Tryptophan depletion prevents the synthesis of serotonin, which subsequently reduces the production of melatonin, which then will reduce sleep quality. 2. Dietary Supplements improve sleep quality or reduce sleep. a. Zinc consumption was shown to significantly decrease the time it takes to fall asleep. b. B vitamin complexes were shown to decrease sleep quality and increase tiredness upon waking up. c. Polyphenols were shown to lower sleep disturbances and increase total sleep duration and quality. d. Crocetins were shown to decrease waking episodes while sleeping. Additionally, participants reported feeling more refreshed and less sleepy upon waking. e. Chlorogenic Acids were shown to decrease the time it takes to fall asleep. f. Gamma-Aminobutyric Acid and Apocynum Venetum were shown to decrease sleep latency. g. Chlorophytum bovivilianum and Velvet Bean improved subjective sleep quality and sleep duration. 3. Food Items a. All studies used actigraphy for sleep metrics. 3 combined subjective measures with actigraphy b. Jerte Valley cherries showed benefits. Effects varied based on cultivar (type of cherry due to suspected variation in melatonin and serotonin concentrations) c. Montmorency tart cherry juice consumption led to less nap time and more sleeping efficiency scores vs baseline + placebo d. Funding was by respective cherry companies 4. Macronutrients a. High glycemic (GI) carbohydrate meal 4hrs before bedtime shortened sleep latency compared to low GI or high GI right before. b. Another study showed 4-day high CHO diet also reduced sleep latency c. Saturated fat intake was associated with less time spent in N3, and sugar was linked with increased arousal d. Consuming more fiber was associated with more time in N3 vs N1 Discussion: ● Authors agreed with study results. We agreed with general importance of nutrition on sleep w/ exception of funding issues and subjectivity of studies Connects to Lecture: ● Tryptophan acts as a precursor for serotonin and melatonin, both modulators of the SCN (responsiveness to light). ● Diabetics and obese patients have less sensitivity to insulin and glucose homeostasis, compromising their ability to efficiently uptake AA/promote Tryptophan:BBB crossing. Angela Tonoyan and Andrew Tran Presentation Outline: I. II. III. IV. V. The Background A. The CNS can regulate cognitive functions through the use of neurotransmitters, however, disturbances caused by lifestyle factors may result in mental illness. The Purpose A. There is an increase in mental disorders, with very little research on preventative measures individuals can take. However, it is unclear if lifestyle factors cause mental illness or affect how they develop as time progresses Major Results/Interpretation A. Physical activity acts as a protective against depression, while sedentary lifestyles increase the risk of depression. However, the review found no effect on schizophrenia or bipolar disorder. B. Smoking was found to have a strong association with depression, especially during adolescence and pregnancy. Furthermore, numerous studies determined that smoking doubles the risk of schizophrenia and psychosis. Lastly, engaging in smoking increases the likelihood of offspring having ADHD. C. Diet can decrease the risk of depression, but generally doesn’t increase it. Healthy foods (Mediterranean diet, low inflammatory foods, vegetables, fish, etc.) were found to decrease the risk of depression. However, unhealthy or neutral foods had no association. The exception that researchers found was that eating sugar increases risk. D. All sleep disturbances (insomnia and poor sleep quality) significantly increase the risk of clinical depression. Additionally, both longer and shorter than average sleep duration were at higher risk of depression Even further, difficulties in falling or staying asleep increase the risk of bipolar disorder. Conclusions A. Many of the mechanisms and interactions behind the results are not fully understood. Researchers expect more lifestyle factors to be discovered in the future. B. Providers should focus more on lifestyle interventions. C. Findings help justify social initiatives and show the potential for wide-reaching preventative care in the near future. Connection to Lecture A. Modern lifestyles have strayed from our evolutionary roots of healthy eating and daily exercise, resulting in higher disease rates. B. A healthy diet and exercise help mitigate the impacts of these lifestyle factors, reducing the risk of diseases like Alzheimer’s and depression, while promoting mental well-being through anxiety reduction, enhanced focus, neurogenesis, and restored energy homeostasis. C. Sleep also plays a crucial role in cognitive function, and sleep deprivation (due to sleep disturbances) can negatively impact mood, concentration, and decision-making. The Neuroscience of Happiness and Pleasure - Yanira Argueta Background: ● Psychologists have been working to map the empirical features of happiness, and neuroscientists are working to investigate the functional neuroanatomy of pleasure which contributes to happiness. ● The goal of this paper is to map the intricate links between pleasure and happiness for the purpose of providing a better understanding of the pleasures of the brain that can offer a general insight into happiness. A Science of Happiness: ● Happiness consists of two aspects: hedonia (pleasure) and eudaimonia (a life well lived; ‘meaning’) ● Scientists have been able to study and measure happiness in the form of self-reports of subjective well-being. ● Scientists use pleasure as an indicator of happiness as it is relevant to our well-being and is involved in happiness; it is also a topic already studied in neuroscience. A Science of Pleasure: ● Happiness has two sides, a positive aims at experiencing strong feelings of pleasure ● and a negative aim for the absence of pain and displeasure ● A crucial component of happiness is pleasure and therefore it has become essential to understand the brain mechanism of pleasure in order to understand the brain mechanisms of happiness. ● All pleasures seem to involve the same hedonic brain systems. Thus, pleasures important to happiness such as socializing with friends and positive hedonic mood traits, likely use the same neurobiological mechanisms that evolved for sensory pleasures. ● Neuroscience research on sensory pleasure has discovered many networks of brain regions and neurotransmitters that are activated by pleasant events, these brain regions that cause pleasure reactions are termed as hedonic hotspots. ● Hedonic hotspots are found in subcortical structures including the nucleus accumbens, ventral pallidum, brainstem and cortical structures including the orbitofrontal cortex, cingulate cortex, medial prefrontal and insular cortices. ● Hedonic hotspots are capable of generating enhancements of “liking” reactions to sensory pleasures such as taste or when stimulated with neurochemical modulators such as opioids and endocannabinoid ● Hedonic hotspots are anatomically distributed but interact to form a functional integrated circuit. These circuits operate largely in a hierarchical fashion and are organized into brain levels where multiple unanimous “votes” from participating hotspots are required to enhance “liking” above normal. Incentive salience causes stimuli to seem attractive by attributing a sense of desirability to them through mesolimbic dopamine neurotransmission. Loss of pleasure: The lack of pleasure is termed anhedonia and it is one of the most important symptoms of many mental illnesses including depression. Hedonic hotspots have close links with the hedonic network and the default network bridging hedonia and eudaimonia.