Monthly Archives: March 2012
Are you an extrovert or an introvert? Personality types are often lumped into one of these categories. Frequent social engagement and novelty-seeking behavior are characteristic of extroverts, whereas introverts prefer to be alone and engage in familiar activities. The differences in brain chemistry that cause these personality traits arise from both ‘nurture’ or individual experiences, and ‘nature’ or genetic predisposition. But which one is more important? This is a classic theme in neuroscience that I will not fully explore here; but new evidence from honey bees scores another point for team nature.
A recent article1 published in Science by Liang et al. investigates the molecular basis for novelty-seeking behavior in the honey bee, Apis mellifera. The authors seek to understand how individual differences in gene expression lead to behavioral variation. They explain that 5-25% of bees within a population continually seek new food sources, even when there is no food shortage. Other individuals stick to the hive and only venture to new sites after the pioneers or “scouts” have told them the way. But how do bees communicate?
Unlike ants or termites, bees can’t leave a trail of pheromones for others to follow because volatile chemicals like pheromones dissipate in the air. Instead honey bees have come up with a creative mapping strategy. They encode the location of newly found food sources within a complicated series of movements called the “waggle dance.” First discovered by Karl von Frisch in 1965, the waggle dance is only performed by scouts2.
So what determines if a bee has what it takes to be a scout? As it turns out, dance moves aren’t the only criteria.
Liang and colleagues collected honey bees that consistently displayed scouting behavior and analyzed gene expression in the brain. Several differences in neurotransmitter signaling were found between scout bees and non-scouts. For example, genes that encode receptors for glutamate, a major excitatory neurotransmitter, had increased expression levels in scouts. A direct relationship between glutamate signaling and novelty-seeking was demonstrated when bees that were given MSG (mono-sodium glutamate) showed increased scouting behavior after administration. Differential expression of DopR1, a gene encoding a subset of dopamine receptors, was also found. Blocking dopamine signaling resulted in an overall 44% decrease in scouting behavior.
The authors point out that both glutamate and dopamine are known to be involved in novelty-seeking behaviors among many vertebrates. Interestingly, DopR1 is known to be involved in drug-seeking behavior in humans3. Although the brain circuits involved in this behavioral dichotomy have not yet been sorted out, it is clear that a similar pattern of gene expression is involved in what I like to call adventurousness. Perhaps a closer analysis of the relationship between genetics and adventurous behavior in other animal models will provide a basis for identifying genetic predisposition to drug addiction or even thrill-seeking in humans.
Written By Alyssa R. Wheeler
1. Liang ZS, Nguyen T, Mattila HR, Rodriguez-Zas SL, Seeley TD, Robinson GE. Molecular determinants of scouting behavior in honey bees. Science. 2012 Mar 9;335(6073):1225-8. PubMed PMID: 22403390.
2. von Frisch K. [The “language” of bees and its utilization in agriculture. 1946]. Experientia. 1994 Apr 15;50(4):406-13. German. PubMed PMID: 8174688.
3. Le Foll B, Gallo A, Le Strat Y, Lu L, Gorwood P. Genetics of dopamine receptors and drug addiction: a comprehensive review. Behav Pharmacol. 2009 Feb;20(1):1-17. Review. PubMed PMID: 19179847.
So imagine my delight in coming across not just one, but two scientific articles about zombies. Both of these papers investigate the real-life phenomenon of zombies in Haiti, where the idea of the zombie originated. The traditional explanation for zombies is sorcery. The Vodun religion (also known as Voodoo) makes a distinction between different elements of a human being. There is the corps cadavre (the physical body), the gwoban anj (the animating principle), and the ti-bon anj (agency, awareness, and memory).
Haitian zombies aren’t really undead. They are the result of a sorcerer taking the ti-bon anj of the victim, leaving a passive and easily-controlled body. These zombies are then believed to be used as free labor on Haitian plantations. Haitian zombies are easily identified by the community. They cannot lift up their heads, have an empty staring expression, and have limited and repetitive speech.
Poisoning was one theory to account for zombification, and in the early 1980s, anthropologist and ethnobotanist Wade Davis traveled to Haiti to investigate. He interviewed Vodun sorcerers and obtained samples of a white powder called coupe poudre that they used to zombify their victims. Analysis of the samples revealed a number of pharmaceutically active ingredients, including cane toad (Bufo marinus) toxins, an irritant produced by a tree frog (Osteopilus dominicensis), and tetrodotoxin, a neurotoxin produced by puffer fish and other marine animals.
Davis hypothesized that the irritant causes small wounds on the skin of the victim, through which the tetrodotoxin enters the bloodstream. The potent toxin can kill by paralysis, but sub-lethal doses result in a significant reduction in heart rate and metabolic activity. Victims, completely paralyzed but fully conscious, are pronounced dead and buried. After a few days, the sorcerer returns and claims the body. The victim is kept enslaved in a permanent state of delirium and disorientation with more drugs, likely containing atropine and scopolamine, toxins with hallucinogenic properties derived from the plants Datura stramonium and Datura metel. In Haiti, both of these plants are known as the “zombie cucumber.”
Recently, scientists publishing in the journal Evidence-Based Complementary and Alternative Medicine revisited Davis’ zombie potions, analyzing the chemical, biological, and pharmacological components of the powders to determine if tetrodotoxin really is the most important ingredient. They came to the same conclusion as Davis and identified four species of puffer fish as the reason behind the poison’s efficacy.
Pufferfish tetrodotoxin blocks sodium channels and prevents neurons from firing. People who ingest the toxin and don’t die within the first 24 hours typically survive, although they often fall into a coma-like state for several days. During this time, they may appear to be dead; reduced metabolic activity decreases the body’s need for oxygen, and the diaphragm muscles may be partially paralyzed, making breathing difficult to detect.
Tetrodotoxin is certainly a potent neurotoxin, but even Davis emphasized that the zombie powder is just one requirement for zombification. Equally important are cultural expectations involving the power of Vodun sorcerers and the effects of the powder, which are learned and ingrained in many parts of Haitian society.
In 1997, the medical journal The Lancet published a medical investigation into three “returned zombies” —individuals whom family members identified as having died and then returned, sometimes decades later, as zombies.
Doctors performed full medical exams on the zombies, including EEG and CT brain scans. The first subject had no neurological damage but was diagnosed with catatonic schizophrenia. The second subject did suffer from brain damage, probably due to lack of oxygen and untreated epilepsy. The last subject was diagnosed with a developmental learning disability, possibly fetal alcohol syndrome.
The most interesting finding came from DNA and fingerprinting tests that revealed that two of the zombies were cases of mistaken identity. They were not the dead relatives that the families identified.
It is unlikely that there is a single explanation for all cases of zombification. Poisoning by tetrodotoxin can cause symptoms typical of Haitian zombies, and it has been shown to be an ingredient in so-called “zombie powder.” But this study suggests a simpler answer: many zombie cases are mistaken identification of wandering mentally ill or neurologically injured people by grieving relatives, primed by their culture to accept the notion of zombies. The authors write that “People with a chronic schizophrenic illness, brain damage, or learning disability are not uncommonly met with wandering in Haiti, and they would be particularly likely to be identified as lacking volition and memory,” instantly recognized zombie characteristics.
Is the mystery of zombification solved? Sort of. It may be that there are as many types of real-life zombies as there are cinematic ones.
Music has incredible power over the human psyche, and in particular over memory. While we’ve now begun to uncover the underlying scientific principles linking music to memory, the phenomenon is something that songwriters and lyricists have known for years. Cole Porter’s classic “Begin the Beguine” explicitly addresses the strength of this connection; throughout the song, the singer recalls that, when the band starts to play music he associates with a former lover,
it brings back the sound
of music so tender
it brings back a night
of tropical splendor
it brings back a memory of green
and that, every time the tune plays, he can’t help but re-live the precious moments spent with the lady he’s lost—even though he tries his best to forget her.
The experience sounds familiar to many of us. When I hear old Clapton ballads, for example, I recall a very particular dance, memories refreshed like a series of old photographs, every detail perfectly catalogued, right down to the curls in my hair and the color of his vest (it was blue). When I go for a run on a warm, blue-skied afternoon and “Sweet Child O’ Mine” pops up on my workout playlist, the song calls to mind every outdoor barbecue, every trip to the beach, every open-windowed drive on hot pavement, every sunny day when that song might have played, and I inevitably find myself grinning, glorying in the beautiful weather and the sound of summer. How can music do this for us? How is it that even a few seconds of a tune, an echo on the radio, can evoke such powerful memories?
The study of music and memory is still relatively young, but what we know thus far is that part of the strength of music as a stimulus or memory trigger seems to be linked to emotion. In the memory field, strong emotions are generally thought to enhance memory formation, as well as memory recall. This concept makes intuitive sense; isn’t it easier to recall exactly how you felt when you had your first kiss, and what you smelled, and saw, and heard, than it is to recall how you felt when you ate that (presumably emotionally neutral) ham sandwich the other day? The effect of emotion on memory formation makes evolutionary sense, too: intense emotional arousal (e.g., fear) would strengthen memories concerning, say, a close encounter with a predator—an important experience for our ancestors to remember (and hopefully avoid in the future)!
This sort of enhancement is mediated in part by a brain structure known as the amygdala. The amygdala makes bi-directional connections to many other parts of the brain, allowing it to communicate with (among other regions) the hippocampus (responsible for memory formation), the pre-frontal cortex (associated with mood and other complex processes) and the hypothalamic-pituitary-adrenal axis (a network that can stimulate the production of hormones that may modulate memory formation and consolidation). About ten years ago, a study found that some of these same brain regions can be activated by music! Specifically, amygdala activation was associated with music that produced the intense feeling of “chills.” Various studies since that time have implicated other components of the limbic (emotion) circuitry in the brain’s response to music, strengthening the apparent connection between what we hear and what we feel. Music has also been shown to enhance our emotional responses to visual stimuli. Imagine Mufasa’s death without the music. Imagine chase scenes in the Bourne movies without the frenzied strings. Considerably less memorable, right?
What’s especially interesting is that music has been linked to the activation of other brain structures, including the nucleus accumbens. Remember the nucleus accumbens? It’s associated with feelings of pleasure, fun, and reward—which, among other reasons, make this brain region integral to addiction behaviors. Still, the activation of reward circuitry by music has a number of interesting implications. Among the most clinically salient, however, are these:
Could we use music to help address mood disorders, or anxiety disorders?
Could we use music to modulate our perception of emotional experiences?
Given the link between music and memory—could we use music to promote memory formation and recall in patients with memory disorders (like Alzheimer’s disease)?
And in fact, these questions are all topics of current and intense research within the field of music perception.
So next time you turn on the radio, think about the songs you hear, and what they might mean to you and to your personal history. Maybe you’ll hear an old love song as you’re driving home from work today; maybe it makes you want to cry. Or laugh. Or feel and remember any of a thousand different things, thrusting you headlong into any of a thousand different moments, each distinct and based upon your own experience—consider it an autobiography of a sort, your life and mine, called to mind, refreshed, re-lived in a series of chords.
Did you ever say to yourself “I will just have a small piece of ________ (cheesecake, ice cream, cake… fill in the blank!)” and end up eating way more than you wanted to? Did you ever notice that when you “fall off the wagon” of eating healthy, it’s harder to get back to eating healthy than it is to give into junk food?
A recent review article in the journal Frontiers in Neuroendocrinology by Johan Alsio, Ph.D. and others illustrates how much our bodies are made for holding onto fat by way of brain changes, variations in hormone levels, and molecular adaptations during overeating.
In our society, we tend to eat not only from hunger, but from food cravings even at the risk of gaining weight, developing diabetes, and increasing our cholesterol levels – if left unchecked making us susceptible to disorders and disease. So, why can’t we stop the bad cycle of indulging too much?
Apparently the link between drug addiction and food addiction is quite closer than we might think because both activate pathways in the brain that affect levels of the neurotransmitter dopamine (aka – the reward system). Get this: the same changes are seen in this pathway in both obese individuals and those that are addicted to cocaine, meth, and heroin! The higher preference there is for sugar correlated to a bigger preference for alcohol, cocaine and speed in rodent models.
Food also acts like a drug in that the more you are exposed to higher fat and higher sugar foods, the more your body will crave them (a ‘feed-forward’ system – ironic, right?). The higher your weight, the bigger the craving for high fat and high sugar foods. So you might wonder what happens if we actively choose to eat super healthy and stay away from junk (easier said than done considering we have pizza, burgers, and ice cream waiting at the back door). Even if you can withstand the higher cravings during ‘dieting’ – this usually leads to higher and longer periods of cravings, making it much easier to give in. Sometimes that salad just doesn’t do it for us, but those steak burritos across the street…..they just sound so yummy In studies done with animals, the longer time period of abstinence from high fat and high sugar foods caused their sugar cravings to increase, they had higher anxiety levels, they were more susceptible and higher tendency to show food-seeking behavior – you can see how this can become a never-ending cycle – like Lindsay Lohan’s frequent visits to rehab. These effects create the yo-yo dieting that is common in our society.
Similar to drug use, there are also withdrawal symptoms after abstaining from high fat/high sugar foods – emotionalism, anxiety, cravings (the neurological symptoms), but also physical symptoms like teeth chattering and tremors (shown in rodents). They mental and physical symptoms are attributed to changes that happen in the brain after exposure to these foods. One that I mentioned before: dopamine levels change and the body’s response to it are altered, but also changes in the receptors for endocannabinoids (think, marijuana), and changes in receptors for opioids. The more we eat junk food, the more we want it – risking health issues and obesity (and get this: the more obese a person is, the less likely they are to become addicted to drugs, because food fills that void). The changes that happen in the brain seem permanent; this is why many people gain the weight back that they lost years ago (so relapsing to bad behaviors doesn’t just happen after short-term healthy eating).
Evolutionarily, seeking out high fat and high sugar foods was crucial in times when food wasn’t readily available… so the problem is that while we have food everywhere now, our bodies haven’t really caught up.
Questions to think about:
1) Can we override the signals in the brain that tell us to seek more food?
2) How well does cognitive behavioral therapy work for overweight and obese patients?
3) To what extent can exercise reverse changes that happen in the brain and body that increase the drive to eat?