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Est: June 2013.
Few genes have made the headlines as much as FOXP2. The first gene associated with language disorders, it was later implicated in the evolution of human speech. Girls make more of the FOXP2 protein, which may help explain their precociousness in learning to talk. Now, neuroscientists have figured out how one of its molecular partners helps Foxp2 exert its effects.
The findings may eventually lead to new therapies for inherited speech disorders, says Richard Huganir, the neurobiologist at Johns Hopkins University School of Medicine in Baltimore, Maryland, who led the work. Foxp2 controls the activity of a gene called Srpx2, he notes, which helps some of the brain’s nerve cells beef up their connections to other nerve cells. By establishing what SRPX2 does, researchers can look for defective copies of it in people suffering from problems talking or learning to talk.
Until 2001, scientists were not sure how genes influenced language. Then Simon Fisher, a neurogeneticist now at the Max Planck Institute for Psycholinguistics in Nijmegen, the Netherlands, and his colleagues fingered FOXP2 as the culprit in a family with several members who had trouble with pronunciation, putting words together, and understanding speech. These people cannot move their tongue and lips precisely enough to talk clearly, so even family members often can’t figure out what they are saying. It “opened a molecular window on the neural basis of speech and language,” Fisher says.
A few years later, other researchers showed that the FOXP2 gene in humans differed from the chimp version by only two bases, the “letters” that make up DNA. That small difference may have affected Foxp2 performance such that animal calls could eventually transform into the human gift of gab. In 2009, a team put the human version of the gene in mice and observed that the rodents produced more frequent and complex alarm calls, suggesting these mutations may have been involved in the evolution of more complex speech. But how Foxp2 works has largely remained a mystery.
Huganir didn’t start out trying to solve this mystery. He was testing 400 proteins to see if they helped or hindered the development of specialized junctions between nerve cells, called synapses, which allow nerve cells to communicate with one another. A single neuron can have up to 10,000 synapses, or connections to other neurons, Huganir says. Of the 10 proteins he identified, one that strongly promoted synapse formation was Srpx2, a gene other researchers had linked to epilepsy and language problems.
Huganir and his colleagues examined Srpx2 activity in isolated nerve cells, determining that it stimulated the formation of “excitatory” connections, ones where a “turn on” message was conveyed to the receiving nerve cell. Srpx2 also enhanced the number of excitatory connections in the part of the brain in developing mice that is the equivalent of the human language center, the researchers report online today in Science. Because Foxp2 regulates the activity of several genes, including Srpx2, Huganir and his team took a closer look at how Foxp2affected this gene. When Foxp2 is around, Srpx2 makes fewer excitatory synapses, they report. It may be that the right balance of excitatory synapses and other connections may be necessary for complex vocalizations, Huganir suggests.
As a final test, the researchers looked to see how changing the activity of the Srpx2 gene affected alarm calls of baby mice. Mice pups separated from their moms call for help with squeals too high-pitched for humans to hear. When the researchers artificially inhibited Srpx2’s activity, the mice squealed less. But the pups squealed normally again when gene activity was restored, Huganir and his colleagues report.
The work “shows that Foxp2 affects synapse formation through Srpx2,” says Svante Pääbo, a paleogeneticist at the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, who has studied Foxp2 in primates and in mice. “It is the first target gene of Foxp2 that has a clear function with respect to neuronal function.”
Huganir says his team still doesn’t know whether FOXP2 affects nerve cells that relate to language processing or nerve cells that control muscles involved in talking. Still, he says the link to synapse formation via SRPX2 ”is an important clue how FOXP2 could be regulating language development.”
Image: The language gene FOXP2 may work through a protein partner that stimulates the formation of excitatory connections (green) in nerve cells (magenta). Yoichi Araki, Ph.D.
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Expedit esse deos, et, ut expedit, esse putemus.
Nomenque erit indelebile nostrum.
Nec species sua cuique manet, rerumque novatrix ex aliis alias reparat natura figuras: nec perit in toto quicquam, mihi credite, mundo, sed variat faciemque novat, nascique vocatur incipere esse aliud, quam quod fuit ante, morique desinere illud idem. cum sint huc forsitan illa, haec translata illuc, summa tamen omnia constant.
The default is NBC canon; fleshing out the details will take place, as needed, in each individual thread. Hannibal is fluid, and his concept of truth & history is abstract, to say the least. No truth is immutable. No lie is wholly without backing. I tend to use Harris for more thorough fleshing out, but overlay NBC canon where Harris was just too cracky.
There was a cliff; there was a fall. And where, indeed, did the physical remnants drift to?
One could argue about Hannibal's psychology; he certainly expresses traits common to psychopathy and sociopathy (both loaded terms with their own historical biases) but does not neatly fit into any category. He is articulate, polite, charming, and disarming. A grudge will not be forgotten.
I am not a medical professional. I am not certified to offer medical, psychiatric, or personal advice in any way. This is a roleplay blog—based off of a manipulative, abusive, charming character whom I do not own or in any way represent.
Do not use any of Dr Lecter’s advice. By submitting any ask, you are actively accepting the fact that this is purely entertainment and not any substitution for medical care. By submitting an ask, you are also accepting that I am not responsible for what you choose to do with the completely fictitious content which I produce.
To be very blunt: I don’t know what I’m doing. You should not expect me to. I don’t want to be sued because someone took a fictional character’s fictional advice. (Would you take the advice of a stranger at the bus stop? Your answer should be no, and you should treat this no differently.)
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There is a very large difference between creative grammar/word choice/formatting and purple prose. 'Cerulean orbits' or other such nonsense? That's not creative; it makes no linguistic sense whatsoever. Bend grammar; don't flay the languague, ffs.
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Relationships are not presumed, regardless of canon, without previous discussion.
Hannibal is not a woobie. He is not a sweet, misunderstood gentleman who just ‘happens’ to have a penchant for eating people whom he finds crass. Hannibal is a self-aware sociopath*; a calculating, cold-blooded monster hiding in a very fine suit. Please do not be surprised when he acts accordingly.
Your character has high odds of being maimed, murdered, and/or consumed.
On various spectra, I would categorise Hannibal as grey-panromantic (generally presenting as aromantic) and grey-pansexual (presenting as asexual). The vast majority of his physical sexuality is a power play; getting under his skin to something less constructed is extremely unlikely.
It should go without saying that this entire show is a giant trigger & ergo this blog will contain consistently mature/disturbing fictional content. Gore, NSFW images, and NSFW threads are not usually behind readmores. I will not make a habit of tagging gore, murder, cannibalism, etc, since doing so would be redundant.
However, if you would like a specific trigger tagged or put behind a readmore, please let me know. I’m more than happy to oblige.
And finally:
disclaimer: Hannibal Lecter is not my creative property, and I own nothing here except my own prose. This is all in good fun; I thank you in advance for not suing me.
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