By Neuronicus, 16 May 2017.
By Neuronicus, 16 May 2017.
It is April and the Northern Hemisphere is enjoying the sight and smell of blooming magnolias. Fittingly, today is the birthday of the man who described and named the genus. Charles Plumier (20 April 1646 – 20 November 1704) was a French botanist known for describing many plant genera and for preceding Linnaeus in botanical taxonomy. His (Plumier’s) taxonomy was later incorporated by Linnaeus and is still in use today.
Plumier traveled a lot as part of his job as Royal Botanist at the court of Louis XIV. Don’t envy him too much though because the monk order to which he belonged, the Minims, forced him to be a vegan, living mostly on lentil.
Among thousands of other plants described was the magnolia, a genus of gorgeous ornamental flowering trees that put out spectacularly big flowers in the Spring, usually before the leaves come out. Plumier found it in the island of Martinique and named it after Pierre Magnol, a contemporary botanist who invented the concept of family as a distinct taxonomical category.
Interestingly enough, Plumier named other plants either after famous botanists like fuchsia (Leonhard Fuchs) and lobelia (Mathias Obel) or people who helped his career as in begonia (Micheal Begon) and suriana (Josephe Donat Surian), but never after himself. I guess he took seriously the humility tenet of his order. Never fear, the botanists Joseph Pitton de Tournefort and the much more renown Carl Linnaeus named an entire genus after him: Plumeria.
Of interest to me, as a neuroscientist, is that the bark of the magnolia tree contains magnolol which is a natural ligand for the GABAA receptor.
REFERENCE: Plumier, C. (1703). Nova Plantarum Americanum Genera, Paris. http://dx.doi.org/10.5962/bhl.title.59135 FULLTEXT courtesy of the Biodiversity Heritage Library
By Neuronicus, 20 April 2017
The pineal gland held fascination since Descartes’ nefarious claim that it is the seat of the soul. There is no evidence of that; he said it might be where the soul resides because he thought the pineal gland was the only solitaire structure in the brain so it must be special. By ‘solitaire’ I mean that all other brain structures come in doublets: 2 amygdalae, 2 hippocampi, 2 thalami, 2 hemispheres etc. He was wrong about that as well, in that there are some other singletons in the brain besides the pineal, like the anterior or posterior comissure, the cerebellar vermis, some deep brainstem and medullary structures etc.
Descartes’ dualism was the only escape route the mystics at the time had from of the demanding of evidence by the budding natural philosophers later known as scientists. So when some scientists noted that some lizards have a third eye on top of their head, the mystics and, later, the conspiracy theorists went nuts. Here, see, if the soul seat is linked with the third eye, the awakening of this eye in people would surely result in heightened awareness, closeness to the Divinity, oneness with Universe and other similar rubbish that can be otherwise easily and reliably achieved by a good dollop of magic mushrooms. Cheaper, too.
Back to the lizards. Yes, you read right: some lizards and frogs have a third eye. This eye is not exactly like the other two, but it has cells sensitive to light, even if they are not perceiving light in the same way the retinal cells form the lateral eyes are. It is located on the top of the skull, so sometimes is called the parietal organ (because it’s in-between the parietal skull bones, see pic).
It is believed to be a vestigial organ, meaning that primitive vertebrates might have had it as a matter of course but it disappeared in the more evolved animals. Importantly, birds and mammals don’t have it. Not at all, not a bit, not atrophied, not able to be “awakened” no matter what your favorite “lemme see your chakras” guru says. Go on, touch your top of the skull and see if you have some peeking soft tissue there. And no, the soft tissue that babies are born with right there on the top of the skull is not a third eye; it’s a fontanelle that allows for the rapid expansion of the brain during the first year of life.
The parietal organ’s anatomical connection to the pineal gland is not surprising at all for scientists, because the pineal’s role in every single animal that has it is the regulation of some circadian rhythms by the production of melatonin. In humans, the eyes send the information to the pineal that is day or night and the pineal adjusts the melatonin production accordingly, i.e. less melatonin produced during day and more during night. The lizards’ third eye’s main role is to provide information to the pineal about the ambient light for thermoregulatory purposes.
After this long introduction, here is the point: almost twenty years ago Xiong et al. (1998) looked at how this third eye perceives light. In the human eye, light hitting the rods and cones in the retina (reception) launches a biochemical cascade (transduction) that results in seeing (coding of the stimulus in the brain). Briefly, transduction goes thusly: the photon(s) causes a special protein sensitive to light (e.g. rhodopsin) in the photoreceptor cells in the retina to split into its components (photobleaching), one of these components changes its conformation, then activates a G-protein (transducin), which then activates the enzyme phosphodiesterase (PDE), which then destroys a nucleotide called cyclic guanosine monophosphate (cGMP), which results in the closing of the cell’s ion channels, which leads to less neurotransmitter GABA released, which causes the nearby cells (bipolar cells) to release another neurotransmitter (glutamate), which increases the firing rate of another set of cells (ganglion cells) and from there to the brain we go. Phew, visual transduction IS difficult. And this is the brief version.
It turns out that the third eye retina doesn’t have all the types of cells that the normal eyes have. Specifically, it misses the bipolar, horizontal and amacrine cells, having only ganglion and photoreception cells. So how goes the phototransduction in the third eye’s retina, if at all?
Xiong et al. (1998) isolated photoreceptor cells from the third eyes of the lizard Uta stansburiana. And then they did a bunch of electrophysiological recording on those cells under different illumination and chemical conditions.
They found that the phototransduction in the third eye is different from the lateral eyes in that when they expected to see hyperpolarization of the cell, they observed depolarization instead. Also, when they expected the PDE to break down cGMP they found that PDE is inhibited thereby increasing the amount of cGMP The fact that G-protein can inhibit PDE was totally unexpected and showed a novel way of cellular signaling. Moreover, they speculate that their results can make sense only if not one, but two G-proteins with opposite actions work in tandem.
A probably dumb technical question though: the human rhodopsin takes about 30 minutes to restore itself from photobleaching. Xiong et al. (1998) let the cells adapt to dark for 10 minutes before recordings. So I wonder if the results would have been slightly different if they allowed the cell more time to adapt? But I’m not an expert in retina science, you’ve seen how difficult it is, right? Maybe the lizard proteins are different or rhodopsin adaption time has little or nothing to do with their experiments? After all, later research has shown that the third eye has its own unique opsins, like the green-sensitive parietopsin discovered by Su et al. (2006).
REFERENCE: Xiong WH, Solessio EC, & Yau KW (Sep 1998). An unusual cGMP pathway underlying depolarizing light response of the vertebrate parietal-eye photoreceptor. Nature Neuroscience, 1(5): 359-365. PMID: 10196524, DOI: 10.1038/1570. ARTICLE
Tags: whole-cell electrophysiological recordings, perforated-patch electrophysiological recording, phototransduction, rhodopsin, photoreceptor, retina, G-protein, phosphodiesterase (PDE), cyclic guanosine monophosphate (cGMP), adenylyl cyclase, 3-isobutyl-1-methyl-xanthine (IBMX), parietal eye, third eye, lizard, opsin, G-protein, Uta stansburiana
By Neuronicus, 30 March 2017
Whoever didn’t roll out a tongue to catch a few snowflakes? Probably only those who never encountered snow.
The bad news is that snow, particularly urban snow is bad, really bad for you. The good news is that this was not always the case. So there is hope that in the far future it will be pristine again.
Nazarenko et al. (2016) constructed a very clever contraption that reminds me of NASA space exploration instruments. The authors refer to this by the humble name of ‘environmental chamber’, but is in fact a complex construction with different modules designed to measure out how car exhaust and snow interact (see Fig. 1).
After many experiments, researchers concluded that snow absorbs pollutants very effectively. Among the many kinds of organic compounds soaked by snow in just one hour after exposure to fume exhaust, there were the infamous BTEX (benzene, toluene, ethylbenzene, and xylenes). The amounts of these chemicals in the snow were not at all negligible; to give you an example, the BTEX concentration increased from virtually 0 to 50 and up to 380 ug kg-1. The authors provide detailed measurements for all the 40+ compounds they have identified.
Needles to say, many these compounds are known carcinogenics. Snow absorbs them, alters their size distributions, and then it melts… Some of them may be released back in the air as they are volatile, some will go in the ground and rivers as polluted water. After this gloomy reality check, I’ll leave you with the words of the researchers:
“The accumulation and transfer of pollutants from exhaust – to snow – to meltwater need to be considered by regulators and policy makers as an important area of focus for mitigation with the aim to protect public health and the environment” (p. 197).
Reference: Nazarenko Y, Kurien U, Nepotchatykh O, Rangel-Alvarado RB, & Ariya PA. (Feb 2016). Role of snow and cold environment in the fate and effects of nanoparticles and select organic pollutants from gasoline engine exhaust. Environmental Science: Processes & Impacts, 18(2):190-199. doi: 10.1039/c5em00616c. ARTICLE | FREE FULTEXT PDF
By Neuronicus, 26 December 2016
There is no news or surprise that strong hits to the head produce transient or permanent brain damage. But how about mild hits produced by light objects like, say, a volley ball or soccer ball?
During a game of soccer, a player is allowed to touch the ball with any part of his/her body minus the hands. Therefore, hitting the ball with the head, a.k.a. soccer heading, is a legal move and goals marked through such a move are thought to be most spectacular by the refined connoisseur.
A year back, in 2015, the United States Soccer Federation forbade the heading of the ball by children 10 years old and younger after a class-action lawsuit against them. There has been some data that soccer players display loss of brain matter that is associated with cognitive impairment, but such studies were correlational in nature.
Now, Di Virgilio et al. (2016) conducted a study designed to explore the consequences of soccer heading in more detail. They recruited 19 young amateur soccer players, mostly male, who were instructed to perform 20 rotational headings as if responding to corner kicks in a game. The ball was delivered by a machine at a speed of approximately 38 kph. The mean force of impact for the group was 13.1 ± 1.9 g. Immediately after the heading session and at 24 h, 48 h and 2 weeks post-heading, the authors performed a series of tests, among which are a transcranial magnetic stimulation (TMS) recording, a cognitive function assessment (by using the Cambridge Neuropsychological Test Automated Battery), and a postural control test.
Not being a TMS expert myself, I was wondering how do you record with a stimulator? TMS stimulates, it doesn’t measure anything. Or so I thought. The authors delivered brief (1 ms) stimulating impulses to the brain area that controls the leg (primary motor cortex). Then they placed an electrode over the said muscle (rectus femoris or quadriceps femoris) and recorded how the muscle responded. Pretty neat. Moreover, the authors believe that they can make inferences about levels of inhibitory chemicals in the brain from the way the muscle responds. Namely, if the muscle is sluggish in responding to stimulation, then the brain released an inhibitory chemical, like GABA (gamma-amino butyric acid), hence calling this process corticomotor inhibition. Personally, I find this GABA inference a bit of a leap of faith, but, like I said, I am not fully versed in TMS studies so it may be well documented. Whether or not GABA is responsible for the muscle sluggishness, one thing is well documented though: this sluggishness is the most consistent finding in concussions.
The subjects had impaired short term and long term memory functions immediately after the ball heading, but not 24 h or more later. Also transient was the corticomotor inhibition. In other words, soccer ball heading results in measurable changes in brain function. Changes for the worst.
Even if these changes are transient, there is no knowing (as of yet) what prolonged ball heading might do. There is ample evidence that successive concussions have devastating effects on the brain. Granted, soccer heading does not produce concussions, at least in this paper’s setting, but I cannot think that even sub-concussion intensity brain disruption can be good for you.
On a lighter note, although the title of the paper features the word “soccer”, the rest o the paper refers to the game as “football”. I’ll let you guess the authors’ nationality or at least the continent of provenance ;).
Reference: Di Virgilio TG, Hunter A, Wilson L, Stewart W, Goodall S, Howatson G, Donaldson DI, & Ietswaart M. (Nov 2016, Epub 23 Oct 2016). Evidence for Acute Electrophysiological and Cognitive Changes Following Routine Soccer Heading. EBioMedicine, 13:66-71. PMID: 27789273, DOI: 10.1016/j.ebiom.2016.10.029. ARTICLE | FREE FULLTEXT PDF
By Neuronicus, 20 December 2016
If you want to find out how bleach works or what keeps the airplanes in the air or why is the rainbow the same sequence of colors or if it’s dangerous to let your kid play with snails would you ask a scientist or your local priest?
The answer is very straightforward for most of the people. Just that for a portion of the people the straightforwardness is viewed by the other portion as corkscrewedness. Or rather just plain dumb.
Cacciatore et al. (2016) asked about 5 years ago 2806 American adults how much they trust the information provided by religious organizations, university scientists, industry scientists, and science/technology museums. They also asked them about their age, gender, race, socioeconomic status, income as well as about Facebook use, religiosity, ideology, and attention to science-y content.
Almost 40% of the sample described themselves as Evangelical Christians, one of the largest religious group in USA. These people said they trust more their religious organizations then scientists (regardless of who employs these scientists) to tell the truth about the risks and benefits of technologies and their applications.
The data yielded more information, like the fact that younger, richer, liberal, and white people tended to trust scientists more then their counterparts. Finally, Republicans were more likely to report a religious affiliation than Democrats.
I would have thought that everybody would prefer to take advice about science from a scientist. Wow, what am I saying, I just realized what I typed… Of course people are taking health advice from homeopaths all the time, from politicians rather than environment scientists, from alternative medicine quacks than from doctors, from no-college educated than geneticists. From this perspective then, the results of this study are not surprising, just very very sad… I just didn’t think that the gullible people can also be grouped by political affiliations. I though the affliction is attacking both sides of an ideological isle in a democratic manner.
Of course, this is a survey study, therefore a lot more work is needed to properly generalize these results, from expanding the survey sections (beyond the meager 1 or 2 questions per section) to validation and replication. Possibly, even addressing different aspects of science because, for instance, climate change is a much more touchy subject than, say, apoptosis. And replace or get rid of the “Scientists know best what is good for the public” item; seriously, I don’t know any scientist, including me, who would answer yes to that question. Nevertheless, the trend is, like I said, sad.
Reference: Cacciatore MA, Browning N, Scheufele DA, Brossard D, Xenos MA, & Corley EA. (Epub ahead of print 25 Jul 2016). Opposing ends of the spectrum: Exploring trust in scientific and religious authorities. Public Understanding of Science. PMID: 27458117, DOI: 10.1177/0963662516661090. ARTICLE | NPR cover
By Neuronicus, 7 December 2016
Although a complete musical anti-talent myself, that doesn’t prohibit me from fully enjoying the works of the masters in the art. When my family is out of earshot, I even bellow – because it cannot be called music – from the top of my lungs alongside the most famous tenors ever recorded. A couple of days ago I loaded one of my most eclectic playlists. While remembering my younger days as an Iron Maiden concert goer (I never said I listen only to classical music :D) and screaming the “Fear of the Dark” chorus, I wondered what’s new on the front of music processing in the brain.
And I found an interesting recent paper about amusia. Amusia is, as those of you with ancient Greek proclivities might have surmised, a deficit in the perception of music, mainly the pitch but sometimes rhythm and other aspects of music. A small percentage of the population is born with it, but a whooping 35 to 69% of stroke survivors exhibit the disorder.
So Sihvonen et al. (2016) decided to take a closer look at this phenomenon with the help of 77 stroke patients. These patients had an MRI scan within the first 3 weeks following stroke and another one 6 months poststroke. They also completed a behavioral test for amusia within the first 3 weeks following stroke and again 3 months later. For reasons undisclosed, and thus raising my eyebrows, the behavioral assessment was not performed at 6 months poststroke, nor an MRI at the 3 months follow-up. It would be nice to have had behavioral assessment with brain images at the same time because a lot can happen in weeks, let alone months after a stroke.
Nevertheless, the authors used a novel way to look at the brain pictures, called voxel-based lesion-symptom mapping (VLSM). Well, is not really novel, it’s been around for 15 years or so. Basically, to ascertain the function of a brain region, researchers either get people with a specific brain lesion and then look for a behavioral deficit or get a symptom and then they look for a brain lesion. Both approaches have distinct advantages but also disadvantages (see Bates et al., 2003). To overcome the disadvantages of these methods, enter the scene VLSM, which is a mathematical/statistical gimmick that allows you to explore the relationship between brain and function without forming preconceived ideas, i.e. without forcing dichotomous categories. They also looked at voxel-based morphometry (VBM), which a fancy way of saying they looked to see if the grey and white matter differ over time in the brains of their subjects.
After much analyses, Sihvonen et al. (2016) conclude that the damage to the right hemisphere is more likely conducive to amusia, as opposed to aphasia which is due mainly to damage to the left hemisphere. More specifically,
“damage to the right temporal areas, insula, and putamen forms the crucial neural substrate for acquired amusia after stroke. Persistent amusia is associated with further [grey matter] atrophy in the right superior temporal gyrus (STG) and middle temporal gyrus (MTG), locating more anteriorly for rhythm amusia and more posteriorly for pitch amusia.”
The more we know, the better chances we have to improve treatments for people.
unless you’re left-handed, then things are reversed.
1. Sihvonen AJ, Ripollés P, Leo V, Rodríguez-Fornells A, Soinila S, & Särkämö T. (24 Aug 2016). Neural Basis of Acquired Amusia and Its Recovery after Stroke. Journal of Neuroscience, 36(34):8872-8881. PMID: 27559169, DOI: 10.1523/JNEUROSCI.0709-16.2016. ARTICLE | FULLTEXT PDF
2.Bates E, Wilson SM, Saygin AP, Dick F, Sereno MI, Knight RT, & Dronkers NF (May 2003). Voxel-based lesion-symptom mapping. Nature Neuroscience, 6(5):448-50. PMID: 12704393, DOI: 10.1038/nn1050. ARTICLE
By Neuronicus, 9 November 2016
Reference: Russell, B. (10 May 1933). “The Triumph of Stupidity”. In: H. Ruja (Ed.), Mortals and Others: Bertrand Russell’s American Essays, Volume 2, 1931–1935.
The history of the quote and variations of it by others can be found on the Quote Investigator.
By Neuronicus, 6 November 2016