The Atlantic cod is driven to extinction by overfishing and global warming

Say bye-bye to this tasty beauty. Atlantic cod (Gadus morhua) picture by Hans Hillewaert (CC BY-SA 4.0)
Say bye-bye to this tasty beauty: the Atlantic cod (Gadus morhua). Picture by Hans Hillewaert released under CC BY-SA 4.0 license.

Pershing et al. (2015) analyzed a lot data from 1982-2013 about the Gulf of Maine temperatures, cod population metrics, and global warming indices. Global warming has hit the Gulf of Maine harder than anywhere else on the planet, with temperatures rising much faster than the rest of the global ocean during the last decade (about 0.23 Cº per YEAR). As a direct consequence, the cod population has declined very rapidly in the last two decades: “The most recent assessment found that the spawning biomass in this stock is now less than 3,000 mt, only 4% of the spawning stock biomass that gives the maximum sustainable yield” (p. 2)., which means, to my non-marine biologist understanding, that 96% of the little fishes required to make a sustainable pool for fishing are dead.

The authors go further and analyze predator behavior, zooplankton availability (which has declined due to… you are correct, that pesky global warming again) coupled with the recent heat waves and they say that, despite the horribly rapid decline in the population, the cod would have bounced back if it wasn’t for overfishing. That’s right, folks! Is not enough that global warming (which is also man-made, the nay-sayers are deluded, period) has jeopardized this species, but we made sure is on the brink of extinction by overfishing it. The quotas set for the fishing industry failed to take into the account the global warming effect of the population, setting fishing quotas for a steady-state system, which obviously the Gulf of Maine is not.

You may say, “All righty, then. Let’s fish some less cod until it bounces back. Some major fisheries will go bankrupt, but, hey, we’re saving the fishes so we can eat them later. Easy-peasy”. Not so fast. The gravity of the situation is further accentuated by the very doom and gloom predictions of a basic population dynamics model that the authors publish in the form of Fig. 3 of the paper. The cod population may bounce back, if we stop the fishing now COMPLETELY. Not a little bit, not a few here and there, not the slow and the weak, but ALL fishing needs to stop now if we want to rebuild the cod stock population. And you don’t get to say “damn the cod, I don’t eat it anyway’, because you don’t know what else might be driven to extinction by the disappearance of the cod.

I am not exaggerating here with metaphors. Read the paper and take a look at the scientists’ simulations and predictions yourselves.

Reference: Pershing AJ, Alexander MA, Hernandez CM, Kerr LA, Le Bris A, Mills KE, Nye JA, Record NR, Scannell HA, Scott JD, Sherwood GD, & Thomas AC (Epub 29 October 2015). Slow adaptation in the face of rapid warming leads to collapse of the Gulf of Maine cod fishery. Science, DOI: 10.1126/science.aac9819. Article | FREE FULLTEXT PDF

By Neuronicus, 30 October 2015

Grooming only half side of the body

Grooming only half side of the body. Credit: http://www.bajiroo.com/2013/04/23-guys-with-half-shaved-beard/
Grooming only half side of the body. Credit: http://www.bajiroo.com/2013/04/23-guys-with-half-shaved-beard/

Contrary to popular belief, rats and mice are very fastidious animals; they keep themselves scrupulously clean by engaging in a very meticulous routine of self-grooming. The routine is so rigorous that allows the researchers to divide the grooming sequence into four different phases, starting with the nose and whiskers and ending with the genitalia and tail. It is also a symmetrical behavior (no whisker left ungroomed, no paw unlicked).

Grooming is sensitive to dopaminergic manipulations, so Pelosi, Girault, & Hervé (2015) sought to see what happens if they destroy the dopamine fibers in the mouse brain. So they lesioned the medial forebrain bundle, which is a bunch axon fibers that contains over 80% of the midbrain dopaminergic axons. But they were tricky, they lesioned only one side.

And the results were that the lesioned mice not only exhibited less self-grooming on the opposite side to the lesion, but the behavior was rescued by L-DOPA, which is medication for Parkinson’s. That is, they gave the mice some L-DOPA and they began to merrily self-groom again on both sides of the body. The authors discuss in depths other findings, like the changes (or absence thereof) in grooming bouts, grooming time, grooming bouts, completeness of grooming etc.

The findings have significance in the Parkinson’s research, where the mild to moderate phases of the disease often present with asymmetrical motor behavior.

Reference: Pelosi A, Girault J-A, & Hervé D (23 Sept 2015). Unilateral Lesion of Dopamine Neurons Induces Grooming Asymmetry in the Mouse. PLoS One. 2015; 10(9): e0137185. doi: 10.1371/journal.pone.0137185. PMCID: PMC4580614. Article | FREE FULLTEXT PDF

By Neuronicus, 29 October 2015

Fat & afraid or slim & brave (Leptin and anxiety in ventral tegmental area)

A comparison of a mouse unable to produce leptin thus resulting in obesity (left) and a normal mouse (right). Courtesy of Wikipedia. License: PD
A comparison of a mouse unable to produce leptin thus resulting in obesity (left) and a normal mouse (right). Courtesy of Wikipedia. License: PD

Leptin is a small molecule produced mostly by the adipose tissue, whose absence is the cause of morbid obesity in the genetically engineered ob/ob mice. Here is a paper that gives us another reason to love this hormone.

Liu, Guo, & Lu (2015) build upon their previous work of investigating the leptin action(s) in the ventral tegmental area of the brain (VTA), a region that houses dopamine neurons and widely implicated in pleasure and drug addiction (among other things). They did a series of very straightforward experiments in which the either infused leptin directly into the mouse VTA or deleted the leptin receptors in this region (by using a virus in genetically engineered mice). Then they tested the mice on three different anxiety tests.

The results: leptin decreases anxiety; absence of leptin receptors increases anxiety. Simple and to the point. And also makes sense, given that leptin receptors are mostly located on the VTA neurons that project to the central amygdala, a region involved in fear and anxiety (curiously, the authors cite the amygdala papers, but do not comment on the leptin-VTA-dopamine-amygdala connection). For the specialists, I would say that they are a little liberal with their VTA hit assessment (they are mostly targeting the posterior VTA) and their GFP (green fluorescent protein) is sparsely expressed.

Reference: Liu J, Guo M, & Lu XY (Epub ahead of print 5 Oct 2015). Leptin/LepRb in the Ventral Tegmental Area Mediates Anxiety-Related Behaviors. International Journal of Neuropsychopharmacology, 1–11. doi:10.1093/ijnp/pyv115. Article | FREE PDF

By Neuronicus, 28 October 2015

How grateful would you feel after watching a Holocaust documentary? (Before you comment, READ the post first)

form Fox et al. (2015)
form Fox et al. (2015)

How would you feel if one of your favourite scientists published a paper that is, to put it in mild terms, not to their very best? Disappointed? Or perhaps secretly gleeful that even “the big ones” are not always producing pearl after pearl?

This is what happened to me after reading the latest paper of the Damasio group. Fox et al. (2015) decided to look for the neural correlates of gratitude. That is, stick people in fMRI, make them feel grateful, and see what lights up. All well and good, except they decided to go with a second-hand approach, meaning that instead of making people feel grateful (I don’t know how, maybe giving them something?), they made the participants watch stories in which gratitude may have been felt by other people (still not too too bad, maybe watching somebody helping the elderly). But, the researchers made an in-house documentary about the Holocaust and then had several actual Holocaust survivors tell their story (taken from the SC Shoah Foundation Institutes Visual History Archive), focusing on the part where their lives were saved or they were helped by others by giving them survival necessities. Then, the subjects were asked to immerse themselves in the story and tell how grateful they felt if they were the gift recipients.

I don’t know about you, but I don’t think that after watching a documentary about the Holocaust (done with powerfully evocative images and professional actor voice-overs, mind you!) and seeing people tell the horrors they’ve been through and then receiving some food or shelter from a Good Samaritan, gratitude would not have been my first feeling. Anger perhaps? That such an abominable thing as the Holocaust was perpetrated by my fellow humans? Sorrow? Sadness? Sick to my stomach? Compassion for the survivors? Maybe I am blatantly off-Gauss here, but I don’t think Damasio et co. measured what they thought they were measuring.

Anyway, for what is worth, the task produced significant activity in the medial prefrontal cortex (which is involved in so many behaviors that is not even worth listing them), along with the usual suspects in a task as ambiguous as this, like various portions of the anterior cingulate and orbitofrontal cortices.

Reference: Fox GR, Kaplan J, Damasio H, & Damasio A (30 September 2015). Neural correlates of gratitude. Frontiers in Psycholology, 6:1491. doi: 10.3389/fpsyg.2015.01491. Article | FREE FULLTEXT PDF

By Neuronicus, 27 October 2015

Save

The F in memory

"Figure 2. Ephs and ephrins mediate molecular events that may be involved in memory formation. Evidence shows that memory formation involves alterations of presynaptic neurotransmitter release, activation of glutamate receptors, and neuronal morphogenesis. Eph receptors regulate synaptic transmission by regulating synaptic release, glutamate reuptake from the synapse (via astrocytes), and glutamate receptor conductance and trafficking. Ephs and ephrins also regulate neuronal morphogenesis of axons and dendritic spines through controlling the actin cytoskeleton structure and dynamics" (Dines & Lamprecht, 2015, p. 3).
“Figure 2. Ephs and ephrins mediate molecular events that may be involved in memory formation. Evidence shows that memory formation involves alterations of presynaptic neurotransmitter release, activation of glutamate receptors, and neuronal morphogenesis. Eph receptors regulate synaptic transmission by regulating synaptic release, glutamate reuptake from the synapse (via astrocytes), and glutamate receptor conductance and trafficking. Ephs and ephrins also regulate neuronal morphogenesis of axons and dendritic spines through controlling the actin cytoskeleton structure and dynamics” (Dines & Lamprecht, 2015, p. 3).

When thinking about long-term memory formation, most people immediately picture glutamate synapses. Dines & Lamprecht (2015) review the role of a family of little known players, but with big roles in learning and long-term memory consolidation: the ephs and the ephrines.

Ephs (the name comes from erythropoietin-producing human hepatocellular, the cancer line from which the first member was isolated) are transmembranal tyrosine kinase receptors. Ephrines (Eph receptor interacting protein) bind to them. Ephrines are also membrane-bound proteins, which means that in order for the aforementioned binding to happen, cells must touch each other, or at least be in a very very cozy vicinity. They are expressed in many regions of the brain like hippocampus, amygdala, or cortex.

The authors show that “interruption of Ephs/ephrins mediated functions is sufficient for disruption of memory formation” (p. 7) by reviewing a great deal of genetic, pharmacologic, and electrophysiological studies employing a variety of behavioral tasks, from spatial memory to fear conditioning. The final sections of the review focus on the involvement of ephs/ephrins in Alzheimer’s and anxiety disorders, suggesting that drugs that reverse the impairment on eph/ephrin signaling in these brain diseases may lead to an eventual cure.

Reference: Dines M & Lamprecht R (8 Oct 2015, Epub 13 Sept 2015). The Role of Ephs and Ephrins in Memory Formation. International Journal of Neuropsychopharmacology, 1-14. doi:10.1093/ijnp/pyv106. Article | FREE FULLTEXT PDF

By Neuronicus, 26 October 2015

The FIRSTS: the discovery of the telomerase (1985)

WIKI-Working_principle_of_telomerase, licensed under the Creative Commons Attribution-Share Alike 3.0 Unported license.
Telomerase at work. Credit: Fatma Uzbas. License: CC BY-S.A. 3.0

A telomere is a genetic sequence (TTAGGG for vertebrates) that is repeated at the end of the chromosomes many thousands of times and serves as a protective cap that keep the chromosome stable and protected from degradation. Every time a cell divides, the telomere length shortens. This shortening had been linked to aging or, in other words, the shorter the telomere, the shorter the lifespan. But in some cells, like the germ cells, stem cells, or malignant cells, there is an enzyme that adds the telomere sequence back on the chromosome after the cell has divided.

The telomerase has been discovered in 1984 by Carol W. Greider and Elizabeth Blackburn in a protozoan (i.e. a unicellular eukaryotic organism) commonly found in puddles and ponds called Tetrahymena. I wanted to give a synopsis of their experiments, but who better to explain the work then the authors themselves? Here is a video of Dr. Blackburn herself explaining step by step in 20 minutes the rationale and the findings of the experiments for which she and Carol W. Greider received the Nobel Prize in Physiology or Medicine in 2009. If 20 minutes of genetics just whet your appetite, perhaps you will want to watch the extended 3 hours lecture (Part 1, Part 2, Part 3).

Reference: Greider, C.W. & Blackburn, E.H. (December 1985). Identification of a specific telomere terminal transferase activity in Tetrahymena extracts. Cell. Vol. 43, Issue 2, Part 1, pg. 405-413. DOI: 10.1016/0092-8674(85)90170-9. Article | FREE FULLTEXT PDF

By Neuronicus, 25 October 2015

The FIRSTS: Axon description (1865)

Human medulla oblongata sectioned at the level of the olivary nuclei. Drawing by Deiters (1965). Original caption: Fig. 15. Durchschnitt der medulla oblongata des Menschen in der Höhe der Olive (OL). R.R Raphe, Hyi). Nervus hypoglossus. Vag. Nervus vagus, deren Kerne in V und H liegen, aber in der Zeichnung nicht feiner ausgeführt sind. Den Haupttlißil der Figur nimmt die Formatio reticularis ein mit ihren zerstreuten Ganglienzellen, und die Olive mit den zu ihr hinzutretenden Fasern des Stratum zonale; C.c crura cerebelli ad medullam oblongatam; P Pyramidenstrang.
Human medulla oblongata sectioned at the level of the olivary nuclei. Drawing by Deiters (1865). Original caption: “Fig. 15. Durchschnitt der medulla oblongata des Menschen in der Höhe der Olive (OL). R.R Raphe, Hyi). Nervus hypoglossus. Vag. Nervus vagus, deren Kerne in V und H liegen, aber in der Zeichnung nicht feiner ausgeführt sind. Den Haupttlißil der Figur nimmt die Formatio reticularis ein mit ihren zerstreuten Ganglienzellen, und die Olive mit den zu ihr hinzutretenden Fasern des Stratum zonale; C.c crura cerebelli ad medullam oblongatam; P Pyramidenstrang”.

In 1863, using the microscope, a german neuroanatomist from the University of Bonn by the name of Otto Friedrich Karl Deiters describes in exquisite detail the branch-like processes of the neuron (i. e. dendrites) and the long, single “axis cylinder” (i.e. axon). Deiters’ nucleus is named after him (the place where a good portion of the cranial nerve VIII ends).

The book with the findings is published in German, posthumously (in 1865), with preface and under the editorial guidance of Max Schultze, another famous German anatomist. I got the information from Debanne et al. (2011), which is nice review on axon physiology (my German is kindda rusty due to lack of use). But I got my hands on the original German book (see link below) and, like a kid that doesn’t know how to read yet, all I could do was marvel at the absolutely stunning drawings by OFK Deiters. Which are truly and unequivocally beautiful. See for yourself.

Neurons with axons and dendrites. Drawings buy Deiters (1865.)
Neurons with axons and dendrites. Drawings by Deiters (1865.)

Reference: Debanne D, Campanac E, Bialowas A, Carlier E, & Alcaraz G (April 2011). Axon physiology. Physiological Reviews, 91(2):555-602. doi: 10.1152/physrev.00048.2009. Article | FREE FULLTEXT PDF

Original citation: Deiters OFK (1865). Untersuchungen über Gehirn und Rückenmark des Menschen und der Säugethiere. Ed. Max Schultze, Braunschweig: Vieweg, 1865. doi: 10.5962/bhl.title.15270. Book | PDF

By Neuronicus, 24 October 2015

You were not my first choice either!

lego
Sexually receptive female mice prefer a Lego brick over a male if their prefrontal oxytocin neurons are silenced.

Over the past five years or so, dopamine stepped down from the role of the “love molecule” in favor of oxytocin, a hormone previously known mostly for its crucial role in pregnancy, labor, delivery, lactation, and breastfeeding. Since some interesting discoveries in monogamous vs. polygamous voles (a type of rodent) pointing to oxytocin as essential for bonding, many studies implicated the chemical in all sorts of behaviors, from autistic to trusting, from generosity to wound healing.

Nakajima, Görlich, & Heintz (2015) add to that body of knowledge by finding that only a small group of cells in the medial prefrontal cortex express oxytocin receptors: a subpopulation of somatostatin cortical interneurons. Moreover, these neurons are gender dimorphic, meaning they differ from male to female: the female ones have twice as many action potentials upon application of oxytocin as compared to male’s.

And here is the more interesting part:
– Females in the sexually receptive phase of their estrus whose oxytocin neurons were silenced preferred to interact with a Lego brick over a male mouse (which, as you might have guessed, in not what they typically choose).
– Females that were not in their sexually receptive phase when their oxytocin neurons were silenced still preferred to interact with a mouse (male or female) over the Lego brick.
– Silencing of other neurons had no effect on their choice.
– Silencing had no effect on the males.

Hm… there are such things out there as oxytocin inter-nasal sprays… How soon do you think until the homeopaths, naturopaths, and other charlatans market oxytocin as a potent aphrodisiac? And it will take some deaths until the slow machine of beaurocracy turns its wheels and tightens the regulations on the accessibility to the hormone. Until then… as the cartoons say, don’t try this at home! Go buy some flowers or something for your intended one… it would work better, trust me on this.

Reference: Nakajima M, Görlich A, & Heintz N (9 October 2014). Oxytocin modulates female sociosexual behavior through a specific class of prefrontal cortical interneurons. Cell. 159(2): 295–305. doi:10.1016/j.cell.2014.09.020. Article | FREE FULLTEXT PDF

By Neuronicus, 23 October 2015

Are you in love with an animal?

Sugar Candy Hearts by Petr Kratochvil. License: PD
Sugar Candy Hearts by Petr Kratochvil taken from publicdomainpictures. License: PD

Ren et al. (2015) gave sweet drink (Fanta), sweet food (Oreos), salty–vinegar food (Lays chips) or water to 422 people and then asked them about their romantic relationship; or, if they didn’t have one, about a hypothetical relationship. For hitched people, the foods or drinks had no effect on the evaluation of their relationship. In contrast, the singles who received sweets were more eager to initiate a relationship with a potential partner and evaluated more favorably a hypothetical relationship (how do you do that? I mean, if it’s hypothetical… why wouldn’t you evaluate it favorably from your singleton perspective?) Anyway, the singles who got sweets tend see things a little more on the rosy side, as opposed to the taken ones.

The rationale for doing this experiment is that metaphors alter our perceptions (fair enough). Given that many terms of endearment include reference to the taste of sweet, like “Honey”, “Sugar” or “Sweetie”, maybe this is not accidental or just a metaphor and, if we manipulate the taste, we manipulate the perception. Wait, what? Now re-read the finding above.

The authors take their results as supporting the view that “metaphorical thinking is one fundamental way of perceiving the world; metaphors facilitate social cognition by applying concrete concepts (e.g., sweet taste) to understand abstract concepts (e.g., love)” (p. 916).

So… I am left with many questions, the first being: if the sweet appelatives in a romantic relationship stem from an extrapolation of the concrete taste of sweet to an abstract concept like love, then, I wonder, what kind of concrete concept is being underlined in the prevalence of “baby” as a term of endearment? Do I dare speculate what the metaphor stands for? Should people who are referred to as “baby” by their partners alert the authorities for a possible pedophile ideation? And what do we do about the non-English cultures (apparently non-Germanic or non-Mandarin too) in which the lovey-dovey terms tend to cluster around various small objects (e.g. tassels), vegetables (e.g. pumpkin), cute onomatopoeics (I am at a loss for transcription here), or baby animals (e.g. chick, kitten, puppy). Believe me, such cultures do exist and are numerous. “Excuse me, officer, I suspect my partner is in love with an animal. Oh, wait, that didn’t come out right…”

Ok, maybe I missed something with this paper, as half-way through I failed to maintain proper focus due to an intruding – and disturbing! – image of a man, a chicken, and a tassel. So take the authors’ words when they say that their study “not only contributes to the literature on metaphorical thinking but also sheds light on an understudied factor that influences relationship initiation, that of taste” (p. 918). Oh, metaphors, how sweetly misleading you are…

Please use the “Comments” section below to share the strangest metaphor used as term of endearment you have ever heard in a romantic relationship.

Reference: Ren D, Tan K, Arriaga XB, & Chan KQ (Nov 2015). Sweet love: The effects of sweet taste experience on romantic perceptions. Journal of Social and Personal Relationships, 32(7): 905 – 921. DOI: 10.1177/0265407514554512. Article | FREE FULLTEXT PDF

By Neuronicus, 21 October 2015

Giving up? Your parvalbumin neurons may have something to do with it

Cartoon from http://i393.photobucket.com/albums/pp20/saisi24/dontgivedup.jpg, licensing unknown
Cartoon from Photobucket, licensing unknown.

One of the most ecologically-valid rodent models of depression is the learned helplessness paradigm. You get a rat or a mouse and you confine it in a cage with an electrified grid. Then you apply mild foot shocks at random intervals and of random duration for an hour (which is one session). The mouse initially tries to escape, but there is no escape; the whole floor is electrified. After a couple of sessions, the mouse doesn’t try to escape anymore; it gives up. Even when you put the mouse in a cage with an open door, so it can flee to no-pain freedom, it doesn’t attempt to do so. The interpretation is that the mouse has learned that it cannot control the environment, no matter what he does, he’s helpless, so why bother? Hence the name of the behavioral paradigm: learned helplessness.

All antidepressants on the market have been tested at one point or another against this paradigm; if the drug got the mouse to try to escape more, then the drug passed the test.

Just like in the higher vertebrate realm, there are a few animals who keep trying to escape longer than the others, before they too finally give up; we call these resilient.

Perova, Delevich, & Li (2015) looked at a type of neuron that may have something to do with the capacity of some of the mice to be resilient; the parvalbumin interneurons (PAI) from the medial prefrontal cortex (mPFC). These neurons produce GABA, the major inhibitory neurotransmitter in the brain, and modulates the activity of the nearby neurons. Thanks to the ability to genetically engineer mice to have a certain kind of cell fluoresce, the researchers were able to identify and subsequently record from and manipulate the function of the PAIs. These PAIs’ response to stimulation was weaker in helpless animals compared to resilient or controls. Also, inactivation of the PAI via a designer virus promotes helplessness.

Reference: Perova Z, Delevich K, & Li B (18 Feb 2015). Depression of Excitatory Synapses onto Parvalbumin Interneurons in the Medial Prefrontal Cortex in Susceptibility to Stress. The Journal of Neuroscience, 35(7):3201–3206. doi: 10.1523/JNEUROSCI.2670-14.2015. Article | FREE FULLTEXT PDF

By Neuronicus, 21 October 2015