Attention: How a Possible Function of SSRIs Could Be Staring Us in the Face

Image by Mara Potter

When TV commercials sing the famous jingle, “Nausea, heartburn, indigestion, upset stomach, diarrhea,” Pepto Bismol fans rejoice. There’s an appreciation out there when multiple problems have a single solution.  However, when we look at the suite of disorders for which selective seretonin reuptake inhibitors (SSRIs) are prescribed — depression, panic disorder, obsessive compulsive disorder, social anxiety disorder, and anorexia to name a few [1] [2] — there isn’t the same “Huzzah!” as for Pepto.  Run “SSRI” through a YouTube search query and the results are peppered with scared and angry people declaring SSRIs to be dangerous, even going so far as to claim that they are a direct cause of homicidal behavior.

Wild speculation is, to some extent, understandable when we aren’t sure exactly how a psychoactive drug works, yet prescribe it for a number of common ailments.  Relevant experts in pharmaceuticals and neuroscience are still not sure how exactly serotonin reuptake inhibition has a therapeutic effect for the disorders for which it’s prescribed. [1] [2] [5]  Research is still trying to pin down the mechanism behind SSRIs that produce their varied long term effects. But an increasing number of studies are making headway by focusing on subtle, unconscious changes in attention that occur after short term SSRI use and precede noticeable changes in mood or voluntary behavior.  Some of the most immediate observed effects of SSRIs are altered tendencies of visual fixation — like how one goes about reading a person’s face.
background checkLooking in the Eye

This year, Simplicio et. al have published their research studying the short-term effects of SSRI drugs on facial exploration using eye tracking data.  Eye tracking during the viewing of images has become a valuable technique for assessing behaviors associated with affective disorders and their treatments, allowing unique insight into attention and instantaneous reactions to stimuli.  By holding the head still and recording gaze over an image, abnormal attentional biases have been identified in several affective disorders. [4]  Various forms of neuroticism have been associated with avoidant viewing patterns of faces, leading Simplicio et. al to wonder how this avoidant behavior would be affected by SSRI use. [3]

Participants were screened for traits of high neuroticism, characterized by “a predisposition to negative affect and increased vulnerability to emotional disorders.” [3]  These highly neurotic individuals were asked to look at series of pictures of faces during eye tracking to measure the areas and duration of attention paid to each face.  Compared to participants rated as having low neuroticism, highly neurotic participants (High N’s) spent less time focused on the eyes and more focused on the mouth, and spent less time overall looking at the face.  Within the High N population, those who maintained a longer gaze over the eyes rated fewer faces as having hostile characteristics, suggesting that increased focus on the eyes can lead to less anxious interpretations of facial expression. [3]raphe nulcei projections

Half of the High N participants were given repeated regular dosage of Citalopram, an SSRI noted as being the most selective for serotonergic synapses, over seven days.  The other half received a placebo.  The Citalopram group increased both overall face scanning time and maintenance of gaze on the eyes for all facial expressions significantly more than the placebo.  They also demonstrated a lower requirement of expression-intensity in order to correctly identify positive vs. negative emotions.  Also notable, the Citalopram population did not lose their bias for the mouth region over the eye region, suggesting that the SSRI produces a nonspecific effect on facial gaze maintenance.  These effects were seen without subjective reporting of mood change in either group.  Simplicio et. al acknowledge that because participants were explicitly cued to respond to the faces, ability to compare their results to natural behavior is limited as the behavior may have been altered by task-driven strategy in a way that wouldn’t be seen in a natural setting. [3]

Simplicio et. al do speculate about how these results may be involved in the long term therapeutic effects of SSRIs.  Though it’s too big of a jump to make with confidence, it’s possible that SSRIs make an intervention in the facial avoidance patterns associated with high neuroticism, and that these patterns could be partially causal to the persistent interpersonal difficulties characteristic of this group.  If this small behavioral change allows for fewer misattributions of facial stimuli, the early effects of SSRI use could be crucial in disrupting a cycle of anxious symptoms. [3]

Participants in this study were selected for high neuroticism, thus limiting the ability for its implications to be applied in the grand scheme of SSRI administration.  However, it does push research to explore the way that facial exploration is affected in more diverse populations.  Working with a broader range of disorders, as well as more specific dimensions of neuroticism (for instance, including Low N’s), will get us closer to understanding SSRIs function in a way that will allow us to improve its use and to pacify a skeptical public.  As progress is made in better understanding drug efficacy, a more trusting relationship can be developed between patients and providers.

Although, if it makes you feel any better, no one’s exactly sure why Pepto works either.


References:

1. Edwards JG. Selective serotonin reuptake inhibitors. BMJ. 1992;304:1644–1646. doi: 10.1136/bmj.304.6843.1644. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3651296/
2. David J. Nutt, Sam Forshall, Caroline Bell, Ann Rich, John Sandford, Jon Nash, Spilios Argyropoulos, Mechanisms of action of selective serotonin reuptake inhibitors in the treatment of psychiatric disorders, European Neuropsychopharmacology, Volume 9, Supplement 3, July 1999, Pages S81-S86, ISSN 0924-977X, http://dx.doi.org/10.1016/S0924-977X(99)00030-9. http://www.sciencedirect.com/science/article/pii/S0924977X99000309
3. Martina Di Simplicio, Sonia Doallo, Giulia Costoloni, Gustavo Rohenkohl, Anna C Nobre and Catherine J Harmer, ‘Can you look me in the face?’ Short-term SSRI Administration Reverts Avoidant Ocular Face Exploration in Subjects at Risk for Psychopathology, Neuropsychopharmacology advance online publication 13 August 2014; doi: 10.1038/npp.2014.159. http://www.nature.com/npp/journal/vaop/ncurrent/full/npp2014159a.html#bib14
4. Armstrong T., Olatunji B. O. (2012). Eye tracking of attention in the affective disorders: a meta-analytic review and synthesis. Clin. Psychol. Rev. 32, 704–72310.1016/j.cpr.2012.09.004. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4172016/
5. Meera Vaswani, Farzana Kadar Linda, Subramanyam Ramesh, Role of selective serotonin reuptake inhibitors in psychiatric disorders: a comprehensive review, Progress in Neuro-Psychopharmacology and Biological Psychiatry, Volume 27, Issue 1, February 2003, Pages 85-102, ISSN 0278-5846, http://dx.doi.org/10.1016/S0278-5846(02)00338-X. http://www.sciencedirect.com/science/article/pii/S027858460200338X

Categories: Blog, Front Page Tags: , , , ,

REFERENCES

    1.  Edwards JG. Selective serotonin reuptake inhibitors. BMJ. 1992;304:1644–1646. doi: 10.1136/bmj.304.6843.1644.  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3651296/
    2.  David J. Nutt, Sam Forshall, Caroline Bell, Ann Rich, John Sandford, Jon Nash, Spilios Argyropoulos, Mechanisms of action of selective serotonin reuptake inhibitors in the treatment of psychiatric disorders, European Neuropsychopharmacology, Volume 9, Supplement 3, July 1999, Pages S81-S86, ISSN 0924-977X, http://dx.doi.org/10.1016/S0924-977X(99)00030-9.  http://www.sciencedirect.com/science/article/pii/S0924977X99000309
    3.  Martina Di Simplicio, Sonia Doallo, Giulia Costoloni, Gustavo Rohenkohl, Anna C Nobre and Catherine J Harmer, ‘Can you look me in the face?’ Short-term SSRI Administration Reverts Avoidant Ocular Face Exploration in Subjects at Risk for Psychopathology, Neuropsychopharmacology advance online publication 13 August 2014; doi: 10.1038/npp.2014.159. http://www.nature.com/npp/journal/vaop/ncurrent/full/npp2014159a.html#bib14
    4.  Armstrong T., Olatunji B. O. (2012). Eye tracking of attention in the affective disorders: a meta-analytic review and synthesis. Clin. Psychol. Rev. 32, 704–72310.1016/j.cpr.2012.09.004. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4172016/
    5.  Meera Vaswani, Farzana Kadar Linda, Subramanyam Ramesh, Role of selective serotonin reuptake inhibitors in psychiatric disorders: a comprehensive review, Progress in Neuro-Psychopharmacology and Biological Psychiatry, Volume 27, Issue 1, February 2003, Pages 85-102, ISSN 0278-5846, http://dx.doi.org/10.1016/S0278-5846(02)00338-X.  http://www.sciencedirect.com/science/article/pii/S027858460200338X

Food for Thought: How Your Brain Controls What You Eat

Image by Torsten Mangner, licensed under public domain via Wikimedia Commons.

One of the most frequent decisions we make is what to eat, but just because it’s a common task doesn’t mean it’s a simple one—at least when it comes to what happens in our brains. When making food choices, our brains integrate multiple sensory inputs to come to the conclusion of what we should eat, as well as how much of it to eat.

The food decision-making process begins before a single bite of food reaches our lips. After all, the first way we sense our food is through sight. Functional MRI (fMRI) scans have shown that looking at pictures of food activates multiple brain regions, most notably the orbitofrontal complex (OFC).[1] This region, involved in decision-making, is also activated by the scent of food.[2] In the OFC, these visual and olfactory stimuli are integrated to provide a measure of the pleasantness and desirability of the food—the greater the perceived pleasantness of the food, the greater the OFC activation.[2]

The most important factor influencing the appeal of a food is, of course, how it tastes. fMRI scans of the human brain show that taste information is primarily processed in the anterior insula and frontal operculum, with secondary processing occurring in the OFC.[2] Activations in the anterior insula and frontal operculum indicate both the identity and intensity of a taste.[2] In the OFC and anterior cingulate cortex, this information is integrated with visual, olfactory, and even textural information to produce a measure of the pleasantness of the food’s flavor.[2]

A food’s nutritive value also helps to determine its appeal, and the brain has ways of detecting nutrition independently of taste. Studies in mice and fruit flies have shown that both prefer sucrose (a nutritive sugar that contains calories[3]) over sucralose (a nonnutritive, no-calorie sugar) even when their taste receptors were knocked out.[4] How could they tell the difference between the two? Their brains contain nutritive-sugar-activated neurons that release dopamine upon ingestion of sucrose.[4] While these results have yet to be replicated in humans, experiments have shown that the ingestion of different types of sugars does cause differences in human eating behavior.[5] So even if you’re not consciously thinking about the nutritional content of the food you’re eating, your brain is likely considering it.

Food desirability can further be modified by how it’s marketed. For example, human study subjects showed increased OFC activation when drinking an “expensive” wine than when drinking a “cheap” wine, or so they were told—the same wine was used for both treatments.[6] In a different study, increased activation of the OFC (and a related region, the pregenual cingulate cortex) was also detected when subjects were exposed to a flavor stimulus labeled “rich and delicious flavor,” versus when the same stimulus was labeled “boiled vegetable water.”[7] These examples show that how desirable a food is may depend on more than just the food’s appeal to the senses; cognitive factors also play a role.

Once you’ve decided what to eat, how do you know when you’ve had enough of it? One way the brain controls appetite is by decreasing OFC activation in response to a particular food after it’s eaten, reducing its desirability.[2] Overall satiation level is controlled through hormone signals secreted by gastrointestinal organs in the presence of foods, which travel to the brain to promote feelings of satiation.[8] Gut distension, or the expansion of the stomach, also triggers the release of these signals.[9] The control of appetite is truly a well-orchestrated collaboration between the gastrointestinal, endocrine, and nervous systems.

The next time you’re hankering for a snack and debating between, say, Swedish fish, roasted peanuts, or licorice, you probably won’t want to spend too much time mulling over the relative merits of each choice. Thankfully, your brain has you covered, so you can spend more time doing what’s really important—enjoying your food.


References:

1. Van der laan LN, De Ridder DT, Viergever MA, Smeets PA. The first taste is always with the eyes: a meta-analysis on the neural correlates of processing visual food cues. Neuroimage. 2011;55(1):296-303.
2. Rolls ET. Taste, olfactory and food texture reward processing in the brain and the control of appetite. Proc Nutr Soc. 2012;71(4):488-501.
3. Nutritive and Nonnutritive Sweetener Resources. (n.d.). Retrieved November 4, 2014, from http://fnic.nal.usda.gov/food-composition/nutritive-and-nonnutritive-sweetener-resources
4. Yapici N, Zimmer M, Domingos AI. Cellular and molecular basis of decision-making. EMBO Rep. 2014;15(10):1023-1035.
5. Ochoa M, Lallès JP, Malbert CH, Val-laillet D. Dietary sugars: their detection by the gut-brain axis and their peripheral and central effects in health and diseases. Eur J Nutr. 2014;
6. Plassmann H, O’Doherty J, Shiv B, Rangel A. Marketing actions can modulate neural representations of experienced pleasantness. Proc Natl Acad Sci USA. 2008;105(3):1050-4.
7. Grabenhorst F, Rolls ET, Bilderbeck A. How cognition modulates affective responses to taste and flavor: top-down influences on the orbitofrontal and pregenual cingulate cortices. Cereb Cortex. 2008;18(7):1549-59.
8. Suzuki K, Simpson KA, Minnion JS, Shillito JC, Bloom SR. The role of gut hormones and the hypothalamus in appetite regulation. Endocr J. 2010;57(5):359-72.
9. Wang GJ, Tomasi D, Backus W, et al. Gastric distention activates satiety circuitry in the human brain. Neuroimage. 2008;39(4):1824-31.
10. Image by Torsten Mangner, licensed under public domain via Wikimedia Commons.

Categories: Blog, Front Page

REFERENCES

    1. Van der laan LN, De Ridder DT, Viergever MA, Smeets PA. The first taste is always with the eyes: a meta-analysis on the neural correlates of processing visual food cues. Neuroimage. 2011;55(1):296-303.
    2. Rolls ET. Taste, olfactory and food texture reward processing in the brain and the control of appetite. Proc Nutr Soc. 2012;71(4):488-501.
    3. Nutritive and Nonnutritive Sweetener Resources. (n.d.). Retrieved November 4, 2014, from http://fnic.nal.usda.gov/food-composition/nutritive-and-nonnutritive-sweetener-resources
    4. Yapici N, Zimmer M, Domingos AI. Cellular and molecular basis of decision-making. EMBO Rep. 2014;15(10):1023-1035.
    5. Ochoa M, Lallès JP, Malbert CH, Val-laillet D. Dietary sugars: their detection by the gut-brain axis and their peripheral and central effects in health and diseases. Eur J Nutr. 2014;
    6. Plassmann H, O'Doherty J, Shiv B, Rangel A. Marketing actions can modulate neural representations of experienced pleasantness. Proc Natl Acad Sci USA. 2008;105(3):1050-4.
    7. Grabenhorst F, Rolls ET, Bilderbeck A. How cognition modulates affective responses to taste and flavor: top-down influences on the orbitofrontal and pregenual cingulate cortices. Cereb Cortex. 2008;18(7):1549-59.
    8. Suzuki K, Simpson KA, Minnion JS, Shillito JC, Bloom SR. The role of gut hormones and the hypothalamus in appetite regulation. Endocr J. 2010;57(5):359-72.
    9. Wang GJ, Tomasi D, Backus W, et al. Gastric distention activates satiety circuitry in the human brain. Neuroimage. 2008;39(4):1824-31.
    10. Image by Torsten Mangner, licensed under public domain via Wikimedia Commons.

A Bee’s Perspective: Cocaine and Reward Processing

Image by USGS Bee Inventory and Monitoring Lab. Licensed under public domain via Wikimedia Commons.

Cocaine affects reward processing in the brain resulting in feelings of well-being and euphoria. Because of such effects, the drug is helping researchers interested in how reward centers are related to motivation and learning.

In a controlled experiment, scientists administered cocaine to bees and monitored them as they traveled to different food sources. Upon returning to the hive those bees under the influence of cocaine danced a higher percentage of times (communicating the position of discovered food caches) than the bees without cocaine. They also found that these bees had a higher sensitivity to poorer food sources (with a very low percentage of sucrose).

These results suggest that cocaine skews the bees’ perception of the reward. The bees responded more strongly to poor resources by dancing more often to indicate to their hive that the food source is worth a second trip. Of course, this is detrimental to the hive as they are wasting time and energy to gather food that is not very nutritious.

Because medium to high doses of cocaine can affect insects’ motor control, the experimenters used low doses to try and lessen this effect. On this dose the bees’ did not show signs of motor control changes as drugged bees were not hyperactive and they only danced at socially appropriate times. These observations suggest that the dancing was not caused by motor control over-stimulation, but that it was an effect of reward processing instead.

Interestingly, the researchers also found that learning was not impaired while the bees’ were on cocaine but it was statistically lower while bees’ were going through withdrawal [1]. In a similar study, rats given cocaine and tested on reversal learning after a 30-day withdrawal period had “severe … learning impairments” [2]. Unlike other experiments of the time, researchers tested withdrawal after self-administration of the drug, known as contingent drug exposure. This condition allows the organism to learn the causal relationship between drug and effect and more closely resembles human addiction [2]. The researchers argue that the withdrawal learning deficit may contribute to the characteristic poor decision making of drug addicts.

Many factors contribute to human reward and motivation which can make it difficult to discern the causal relationships between the behavior and stimulus. However, these two studies show that learning and reward evaluation is affected (in animal models) by the presence of cocaine and may contribute to addiction behaviors.


References:

1. Barron AB, Maleszka R, Helliwell PG, Robinson GE (2009) Effects of cocaine on honey bee dance behaviour. The Journal of experimental biology 212: 163–168
2. Calu DJ, Stalnaker TA, Franz TM, Singh T, Shaham Y, Schoenbaum G. Withdrawal from cocaine self-administration produces long-lasting deficits in orbitofrontal-dependent reversal learning in rats. Learn Mem. 2007;14(5):325-8.

Categories: Blog, Front Page

REFERENCES

    1. Barron AB, Maleszka R, Helliwell PG, Robinson GE (2009) Effects of cocaine on honey bee dance behaviour. The Journal of experimental biology 212: 163–168
    2. Calu DJ, Stalnaker TA, Franz TM, Singh T, Shaham Y, Schoenbaum G. Withdrawal from cocaine self-administration produces long-lasting deficits in orbitofrontal-dependent reversal learning in rats. Learn Mem. 2007;14(5):325-8.

Tapeworms on the Brain

Image from the CDC

For most people, the mere thought of a parasite setting up residence in their tissues is enough to induce a serious case of the creeps. There is something particularly horrifying about sharing something so personal (yeah, your insides) with an unwelcome intruder.

Taenia solium, better known as the pork tapeworm, is one such parasite. As an adult, the parasite attaches to the intestinal wall of its host (including humans) and grows anywhere from 2 to 7 m long producing an average of 50 million eggs1.

The life cycle of T. solum. Source: the CDC.

Figure 1. The life cycle of T. solum. Image source: the CDC.

However, more serious than the intestinal infection caused by the adult T. solum, is the infection caused by the larvae. The tapeworm is typically introduced into the human intestinal tract after consuming undercooked pork, where it then matures (Figure 1). But, if the eggs are consumed by another human (via inadvertent ingestion of contaminated fecal mater, for example) and develop into a larval stage within their host, the result is rather unsavory: larvae will burrow into the muscle and subcutaneous tissue of their host. This is an infection known as Cysticercosis1,2.

As unsettling as it may be to imagine these parasitic larvae burrowing into your muscles, it gets worse – both in clinical severity and general yuck-factor. A subset of cysticerosis infections is described by appending the prefix neuro.

Neurocysticerosis is the class of T. solium cyst infections of the central nervous system (CNS), which include the eyes, spinal cord, and brain2. Brain tissue is extremely sensitive to insult. As the tapeworm larvae burrow into brain structures, their occupancy disrupts brain function, which results in a series of clinically relevant neurological symptoms such as: migraine, psychiatric problems, arachnoiditis, vasculitis, and hydrocephalus2,3.

Among the most common symptoms is seizure4,5. Indeed, neurocysticercosis is the leading cause of epilepsy in underdeveloped communities and is becoming increasingly common in the United States5.

Figure 2. In this brain many neurocysticercosis induced cysts have formed. Source: Discover magazine.

Figure 2. In this brain many neurocysticercosis induced cysts have formed. Image source: Brane Space.

Efforts are being made to eradicate the prevalence of T. solium infections in endemic areas such as Latin America, Asia, and Africa. The World Health Organization is planning a pilot program in 2015, which, if successful, will be scaled “up in selected endemic countries by 2020.6

The pathology of all parasitic infections is interesting and neurocysticercosis is no exception. But, because it can infect the human brain, I find T. solium a bit more disgusting than the rest.

Interested in more parasites? Check out Carl Zimmer’s book on the subject.


References:

1. Centers for Disease Control and Prevention. http://www.cdc.gov/dpdx/taeniasis/index.html
2. Serpa, J. A., Machicado, J. (2013). Taenia solium and cysticercosis. ClinicalKey. Retrieved from: https://www-clinicalkey-com.offcampus.lib.washington.edu/#!/content/medical_topic/21-s2.0-2001693
3. Palacios, E., Lujambio, P.S., Jasso, R.R. 1997. Computed tomography and magnetic resonance imaging of neurocysticercosis. Seminars in Roentgenology, 32(4): 325-334.
4. Centers for Disease Control and Prevention. http://www.cdc.gov/parasites/cysticercosis/disease.html
DeGiorgio, C.M., Medina, M.T., Durón, R., Zee, C. Escueta, S.P. 2004. Neurocysticercosis. Epilepsy Currents. 4(3): 107-111.
5. The World Health Organization. http://www.who.int/mediacentre/factsheets/fs376/en/

 

Grey Matters Welcome Meeting

fall2014welcomeflyer

Grey Matters Journal is having a welcome party meeting. Come learn more about the journal, our work, and how you can get involved. We will meet Thursday, October 2 at 6:30 p.m. in Allen Library.

Food and prizes to accompany brain geekery.

 

Know Your Claustrum!

A general schematic of the claustrum, as shown in the Crick and Koch paper "What is the function of the claustrum?"

Figure 1 A general schematic of the claustrum, as shown in the Crick and Koch paper “What is the function of the claustrum?”

It seems like consciousness is always on everyone’s mind. Scientists constantly probe every millimeter of brain they can, from the frontal cortex to the brainstem, with hopes of mapping out the physiological underpinnings of consciousness. Until now, a tucked away brain region called the claustrum has slid by under the radar. But a recent case-study published in Epilepsy & Behavior provided interesting insight into how this sneaky slice of brain may relate to the black box of consciousness.

A modest, subcortical region, the claustrum is known to have widespread connectivity with many regions of the cerebral cortex – most of which loop back to the claustrum in some way. It also sends projections to more internal brain regions like the thalamus, hippocampus, and amygdala [1, 2].

While performing electrical brain stimulation to examine the nature of a patient’s epilepsy, researchers and clinicians led by Mohamad Z. Koubeissi, director of George Washington University’s Epilepsy Center, uncovered the ability to selectively arrest consciousness in an awake, behaving patient. The location of the crucial stimulation, shown as a red dot (Figure 2), was suspiciously close to the claustrum. This, coupled with the attention it has received by influential neuroscientists in the past, makes the claustrum a piece of the brain that might be worth knowing [3].

Location of stimulation by Koubeissi et. al. shown in three dimensions. Red circles (NOT to scale) indicate location of stimulation in relation to claustrum (yellow region). Adapted from “Electrical stimulation of a small brain area reversibly disrupts consciousness”.

Figure 2 Claustrum stimulation in three dimensions. Red circles (NOT to scale) indicate location of stimulation in relation to claustrum (yellow region). Adapted from Koubeissi et. al.

In relation to epilepsy, it makes sense that a region with very broad connections would be a good place to probe while examining a patient, but can the same be said for consciousness?

Neuroscientists Cristof Koch and Francis Crick put forth an interesting argument for the claustrum as a potential structure involved in our conscious experience for precisely this reason. Its interconnectivity with various brain regions endows it with the potential to act as a “conductor coordinating a group of players in the orchestra”, effectively synchronizing our senses in a timely manner [1].

But before waving our hands any more than we already have about the claustrum’s role in consciousness, certain points should be considered. First, it should be noted that the claustrum is in close association with other brain regions, particularly the insula, as noted by Koubeissi et. al., so it could be that stimulation affected both regions [3]. However, the researchers who took part in the study note that the region stimulated to knock out consciousness was the closest to the claustrum, and report that stimulation of nearby regions (within 5 mm) did not produce the same result.  What may be more cause for skepticism, however, is that these results have only been seen in one patient, on one side of the brain. Until more trials have been run, the claims should be held under strict scrutiny.

Considering the implications of such a finding it will be exciting to see what research follows. Are we closer to placing a piece in the puzzle of consciousness? Or are we stumbling down a convincing dead end? At this point, it appears the best way to find out is to know your claustrum.


References:

1. F.C. Crick, C. Koch. What is the function of the claustrum? Philos Trans R Soc Lond B Biol Sci, 360 (1458) (2005), pp. 1271–1279. PMCID: PMC1569501.
2. Mohamad Z. Koubeissi, Fabrice Bartolomei, Abdelrahman Beltagy, Fabienne Picard, Electrical stimulation of a small brain area reversibly disrupts consciousness, Epilepsy & Behavior, Volume 37, August 2014, Pages 32-35. PMID: 24967698.
3. Rastislav Druga. The Structure and Connections of the Claustrum. From: The Claustrum: Structural, Functional, and Clinical Neuroscience, Chapter 2.

Categories: Blog, Front Page Tags: , , ,

REFERENCES

    1. F.C. Crick, C. Koch. What is the function of the claustrum? Philos Trans R Soc Lond B Biol Sci, 360 (1458) (2005), pp. 1271–1279. PMCID: PMC1569501.
    2. Mohamad Z. Koubeissi, Fabrice Bartolomei, Abdelrahman Beltagy, Fabienne Picard, Electrical stimulation of a small brain area reversibly disrupts consciousness, Epilepsy & Behavior, Volume 37, August 2014, Pages 32-35. PMID: 24967698.
    3. Rastislav Druga. The Structure and Connections of the Claustrum. From: The Claustrum: Structural, Functional, and Clinical Neuroscience, Chapter 2.

Spring Quarter Welcome Meeting

spring-welcome-meeting

Hello Neuroscience Enthusiasts,

Spring is here! Let’s celebrate the sunshine and cherry blossoms by geeking out about the brain. Grey Matters is an undergraduate neuroscience journal whose mission is to enhance public understanding, grow the neuroscience community, and develop accomplished science communicators.

You can learn more about the journal – and how to get involved – by joining us this Thursday at 6:30 p.m. in Thompson 134.

Love Actually (it’s neuroscience)

 

Love is an insane neurochemical flood.

For those of us lucky enough to have experienced it, this comes as no surprise.

A wide variety of neurochemicals have been implicated in this mess, including: oxytocin, sex hormones testosterone and estrogen, dopamine, vasopressin, serotonin, and norepinephrine[1]. Each of these chemicals has a diverse array of targets within the brain, so their combined impact is multifaceted and far-reaching. In fact, you can see a really neat graphic depicting a variety of these effects here. However, there is one class of compounds in particular that deserves some extra attention.

Nerve growth factors (NGFs), or neurotrophins (NTs), are proteins which mediate the survival and upkeep of neurons throughout the CNS, and they have been found at elevated levels in the brains of newly in-love couples.  This study, conducted by Enzo Emanuele and his colleagues at the University of Pavia, Italy, compared plasma levels of four separate NTs from couples who had fallen in love within six months of the trial to those from couples in long-term relationships and also individuals not involved in a romantic relationship.

The lovebirds had significantly higher NT levels than both long-term couples and singles.  On top of this, the degree to which NT levels were elevated was positively correlated with the “intensity” of romantic love experienced, as indicated through subjects’ responses on the Passionate Love Scale (yes, there is actually a test which is thought to reliably indicate the intensity of romantic love of an individual).

In short, while in love, our brains are bathed with heightened concentrations of proteins which help keep our neurons alive.

Evidently, the neurochemical effects of head-over-heels love wear off eventually. And heartbreak is accompanied by its own list of stressors, which can in some cases lead to severe depression.  It is currently unknown whether the impacts of love-induced NT elevation have any long-terms effects on an individual’s health.

Perhaps future research will reveal whether it is, in fact, better to have loved and lost, than to never have loved at all.


References:

1. Zeki, S. (2007). The neurobiology of love. FEBS Letters,581(14), 2575-2579. Retrieved from http://www.sciencedirect.com/science/article/pii/S0014579307004875

Categories: Blog, Front Page

REFERENCES

    1. Zeki, S. (2007). The neurobiology of love. FEBS Letters,581(14), 2575-2579. Retrieved from http://www.sciencedirect.com/science/article/pii/S0014579307004875

Killer Whales Are Non-Human Persons

What makes humans so special? Is it their ability to use language and empathize with others? Their ingenuity? Their tool making? It has been known for some time that other non-human primates are avid tool users, too. Yet it does not stop there – a plethora of other species including birds, invertebrates, rodents etc. have also been found to use tools specialized to their environments and needs. It’s also been made clear that, though our language has a highly developed level of syntax and grammar, other species do have lingual forms of their own. These are only a few of the many attributes once thought to be merely human that have been recognized, in their own forms, in species around the world.

Figure 1. This MRI coronal section image was taken midway through a developed, post-mortem killer whale's brain. Of particular note are the enlarged limbic lobes on the medial surface of both hemispheres above the corpus callosum on the dorsal aspect of the brain.

Figure 1. This MRI coronal section image was taken midway through a developed, postmortem killer whale’s brain. Of particular note are the enlarged limbic lobes on the medial surface of both hemispheres above the corpus callosum on the dorsal aspect of the brain. (Citation 1)

The species of topic today is one who has demonstrated many human-like qualities including intelligence, language, and an exquisite sense of emotional capability: Orcinus orca, the killer whale. These massive toothed whales are home in the cold waters of the North Atlantic, North Pacific, and Antarctic but dwell in vast expanses around these areas, sometimes swimming hundreds of miles a day. The largest killer whale ever found stretched up to about 10 meters and weighed about 10 tons. However, not only are their bodies massive; so too are their brains. Postmortem MRI studies of the killer whale brain have shown that it is on the scale of 3.5-6.5 times as massive as a common bottlenose dolphin, another cetacean species that has demonstrated non-human-person-like qualities1. Their brain also demonstrates an exquisite level of cortical folding similar to humans and other higher mammals (chimpanzees, but not macaques, for example), which indicates high amounts of cortical processing, as seen in Figure 1.

This image depicts the relative size difference of post-mortem Killer Whale and human brains.

This image depicts the relative size difference of post-mortem Killer Whale and human brains. (Citation 6)

Three areas of particular interest stand out when observing intact killer whale brains that are enlarged with respect to human brains: the insular cortex, its surrounding operculum, and the limbic lobe. First, the frontal operculum is correlated with speech in humans, while the insular cortex is involved with audition, or the ability to hear and process sound. These areas reside on the upper surface of the temporal cortex. It has also been hypothesized that a part of the operculum in killer whales innervates the nasal respiratory tract, the origin of killer whale vocalization2. As such, it has been speculated that this area serves similar functions as the speech-related operculum in humans. Indeed, the vocal patterns found within orca pods demonstrate levels of communication beyond mere sounds. Similarly, the structural differences of sound patterns between different orca pods is suggestive of dialectical variation as well as the fact that sound may be a learned behavioral trait used for communication3.

The third structure of particular importance is the enlarged limbic lobe, located on the medial surface between the two hemispheres, directly above the corpus callosum. In humans, the limbic system is associated with emotional life and behavior as well as the formation of memories. Humans only have one cingulate gyrus, located medial above the corpus callosum, associated with the limbic system. Orcas’ cingulate gyrus, or limbic lobe, on the other hand is vastly enlarged and made up of three separate lobes separated by two clefts: the limbic and paralimbic clefts, as seen in Figure 1. Beyond the enlargement of these areas, the cellular architecture also gives clues to the extent of their aptitude for emotional expression. Spindle cells, associated with the limbic system processing of social organization and empathy, were once thought to be unique to the great apes but have since been found in whale species including orcas. In fact the relative number of spindle cells in killer whales is larger than that of even the human brain4!

Killer whales’ demonstration of extremely coordinated group behavior and social interaction including both vocal and non-vocal cues arguably correlates with this vast expanse of the cortical areas mentioned above5. It certainly is true that upon observing killer whales, both in the wild and in captivity, that they exhibit a range of emotions from joy, fear, frustration, and anger, as well as self-awareness. As such, this generates a new set of ethical questions regarding the ways humans continue to interact with killer whales and other whale species by keeping them in captivity and killing them unnecessarily for food. As research continues, it might be time to reconsider the cognitive status of certain other life forms as non-human persons capable of intelligent inter- and intraspecies interactions.

If you want to learn more about the sad story of killer whales in captivity and the efforts being undertaken to free them check out the movie Blackfish (2013).


References:

1. Marino, L., Sherwood, C. C., Delman, B. N., Tang, C. Y., Naidich, T. P., & Hof, P. R. (January 01, 2004). Neuroanatomy of the killer whale (Orcinus orca) from magnetic resonance images. The Anatomical Record. Part A, Discoveries in Molecular, Cellular, and Evolutionary Biology, 281, 2, 1256-63. http://onlinelibrary.wiley.com/doi/10.1002/ar.a.20075/full
2. Morgane PJ, Jacobs MS, MacFarland WL. 1980. The anatomy of the brain of the bottlenose dolphin (Tursiops truncatus): surface configurations of the telencephalon of the bottlenose dolphin with comparative anatomical observations in four other cetacean species. Brain Res Bull 5 (Suppl 3): 1–107. http://www.sciencedirect.com/science/article/pii/0361923080902725
3. Deecke, V. B., Ford, J. K. B., & Spong, P. (November 01, 2000). Dialect change in resident killer whales: implications for vocal learning and cultural transmission. Animal Behaviour, 60, 5, 629-638. http://www.sciencedirect.com/science/article/pii/S0003347200914544
4. Bekoff, M. (2007). The emotional lives of animals: A leading scientist explores animal joy, sorrow, and empathy–and why they matter. Novato, Calif: New World Library. http://books.google.com/books
5. Marino, L., Connor, R. C., Fordyce, R. E., Herman, L. M., Hof, P. R., Lefebvre, L., Lusseau, D., … Whitehead, H. (May 01, 2007). Cetaceans Have Complex Brains for Complex Cognition. Plos Biology, 5, 5.) http://www.plosbiology.org/article/info%3Adoi%2F10.1371%2Fjournal.pbio.0050139
6. Whiting, Candace C. “Orca Brains Are Large And Complex.” Seattlepi.com. SeattlePi, 13 July 2009. Web. 07 Dec. 2013. http://blog.seattlepi.com/candacewhiting/2009/07/13/orca-brains-are-large-and-complex/