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For those curious, the real int/Users/BluJay/Dev/reddit-eli5bot/simpli5/reddit_comment.txteresting findings of this study imo is the actions of GABA in the hippocampus that are distinct from the dlPFC. The dlPFC and vmPFC have anticorrelated activity, I.e. when one is up, the other is down. In depression, for example, persistsnt negative self-rumination is very common and is linked largely to the abnormally low dlPFC activity (necessary for engaging with the external world) and abnormally high vmPFC activity (necessary for introspective processes) often seen in patients with depression. Both are part of the prefrontal cortex (PFC) that projects to both the amygdala (anxiety) and hippocampus (memory and affective interpretation).

The general model has emphasized influences from the dlPFC low activity and hyperactivity of the default network, which is a network of brain regions involved in introspective processing of stimuli. The latter includes the vmPFC and sgACC. The idea is that hyperactivity of this network impairs the persons ability to recruit the dlPFC (or better yet, the fronto-parietal network) when allocating resources enabling engagment with external stimuli. This article shows, however, that the hippocampus plays a larger role in this process that is specific to GABA (the brains most abundant inhibitory neurotransmitter). We already know the hippocampus 'gates' projections from the mPFC and amygdala to brain reward centers, and that this process regulates emotional processing. But this study shows that GABA influences at the hippocampus may be a mechanism contributing to the self-ruminating components typical of disrupted affective processing. 

Do note my research focuses around depression, so my context may be a bit off from the article.

EDIT: 
Lots of questions about treatment and clarity on the network. An easier interpretation of these results is that dysfunction of the hippocampus (I.e. low GABA) might reduce the ability of the frontal lobe (PFC, specifically the dlPFC) to engage in proper executive/cognitive processing. The dlPFC is also assoc. with 'turning down' other brain regions associated with excessive self-rumination. The idea, from my interpretation (sorry I'm on my phone and havent read the whole article), is that lower GABA levels are inhibiting the hippocampus' ability to aid in regulating this introspective processing, I.e. preventing hippocampal regulation over dlPFC processing. Im not familiar with the direct circuit between the hippocampus and dlPFC, though. It is important to note as well that this overall network is very complex, and i can't seem to identify exactly what model the authors are proposing. If you're interested, a good place to start learning is Googling "LCSPT circuits."

Also, for those assuming that taking GABA might help, it is important to remember that all drugs aimed at treating psychopathology act as 'shotguns'. If you take GABA it will influence many different things. A good example are SSRIs aimed at increasing serotonin levels. This also happens in the periphery, thus, often producing sexual dysfunction and weight gain. Please consult a specialist before taking ANYTHING (including supplements), *especiialy* if you are already on medication. 

EDIT 2: 
Also a lot of people making overarching assumptions based on the findings. Two points should be noted. 1) This is a network well-established in the neuroimaging literature, and these findings (I.e. low hippocampus GABA and modulation over dlPFC) are a great addition to it. 2) An important concept to remember in neuroscience is that GABA (being the brains most abundant inhibitory neurotransmitter) does not always equal downstream inhibition. Sometimes you inhibit the inhibitor and create *more* excitation by disinhibting excitatory neurons. This is a exemplified by the mechanisms of ketamine and NMDA receptors. Its also similar with Glutamate (opposite of GABA acting as the brains most excitatory neurotransmitter) which might excitate the inhibitor, providing *more* inhibition. Thus, lower GABA might be a result of a multitude of different mechanisms. Please do not assume that 1) low GABA is causally defined here, and 2) that taking GABA or GABA agonists will help this specific circuit.

LAST EDIT: Thanks for the gold. 

I'd like everyone to understand something very critical to this overall network. The main idea behind some of this research is that patients engage in excessive *negative* self-rumination. This does not mean self-rumination is a bad thing. Please do not think that. Self-rumination /introspection can be *very* beneficial if harnessed correctly. The bad part is when that affective processing hyperfocuses on the "negative" stuff. So, stay positive and think about how your better than that little devil on your shoulder. Dont let your actions or experiences determine how you define your reality. 

LAST LAST EDIT: [Here is a link to the peer-reviewed, open access publication](https://www.nature.com/articles/s41467-017-00956-z). 

Credit goes to /u/sublimal2 for finding the open access pub at the beginning of the thread. The comment got buried very quickly, so Thanks! This is hot off the press and published today. Exciting. Unfortunately I don't have time to read it tonight to double-check my understanding. If you notice a flaw in my understanding please let me know!
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For those curious, the [real int](https://en.wikipedia.org/wiki/Real_interest_rate)/ Users/ [BluJay](https://en.wikipedia.org/wiki/Blujays)/ [Dev](https://en.wikipedia.org/wiki/Dev)/ [reddit](https://en.wikipedia.org/wiki/Reddit)- eli5bot/ simpli5/reddit_comment.txteresting findings of this [study imo](https://en.wikipedia.org/wiki/StudyMode) is the actions of [GABA](https://en.wikipedia.org/wiki/GABA) in the hippocampus that are distinct from the [dlPFC](https://en.wikipedia.org/wiki/DLPFC). The [dlPFC](https://en.wikipedia.org/wiki/DLPFC) and [vmPFC](https://en.wikipedia.org/wiki/VMPFC) have anticorrelated activity, I.e. when one is up, the other is down. In depression, for example, [persistsnt](https://en.wikipedia.org/wiki/Persistent_vegetative_state) negative self- thoughtfulness ([rumination](https://en.wikipedia.org/wiki/Rumination)) is very common and is linked largely to the [abnormally](https://en.wikipedia.org/wiki/Abnormally_Attracted_to_Sin) low dlPFC activity( necessary for engaging with the external world) and [abnormally](https://en.wikipedia.org/wiki/Abnormally_Attracted_to_Sin) high vmPFC activity( necessary for introspective processes) often seen in patients with depression. Both are part of the [prefrontal cortex](https://en.wikipedia.org/wiki/Prefrontal_cortex)( [PFC](https://en.wikipedia.org/wiki/PFC)) that projects to both the [amygdala](https://en.wikipedia.org/wiki/Amygdala)( anxiety) and neural structure ([hippocampus](https://en.wikipedia.org/wiki/Hippocampus))( memory and affective interpretation).

 The general model has emphasized influences from the dlPFC low activity and upset ([hyperactivity](https://en.wikipedia.org/wiki/Hyperactivity)) of the [default network](https://en.wikipedia.org/wiki/Default_network), which is a network of brain regions involved in introspective processing of stimuli. The latter includes the [vmPFC](https://en.wikipedia.org/wiki/VMPFC) and [sgACC](https://en.wikipedia.org/wiki/Sacco_and_Vanzetti). The idea is that upset ([hyperactivity](https://en.wikipedia.org/wiki/Hyperactivity)) of this network impairs the persons ability to recruit the [dlPFC](https://en.wikipedia.org/wiki/DLPFC)( or better yet, the [fronto](https://en.wikipedia.org/wiki/Fronto)- parietal network) when allocating resources enabling engagment with external stimuli. This article shows, however, that the neural structure ([hippocampus](https://en.wikipedia.org/wiki/Hippocampus)) plays a larger role in this process that is specific to [GABA](https://en.wikipedia.org/wiki/GABA)( the brains most abundant inhibitory neurotransmitter). We already know the neural structure ([hippocampus](https://en.wikipedia.org/wiki/Hippocampus))' gates' projections from the [mPFC](https://en.wikipedia.org/wiki/MPFC) and [amygdala](https://en.wikipedia.org/wiki/Amygdala) to brain reward centers, and that this process regulates emotional processing. But this study shows that GABA influences at the neural structure ([hippocampus](https://en.wikipedia.org/wiki/Hippocampus)) may be a mechanism contributing to the self- [ruminating](https://en.wikipedia.org/wiki/Ruminating) components typical of disrupted affective processing.

 Do note my research focuses around depression, so my context may be a bit off from the article.

 EDIT:
 Lots of questions about treatment and clarity on the network. An easier interpretation of these results is that pathology ([dysfunction](https://en.wikipedia.org/wiki/Dysfunction)) of the neural structure ([hippocampus](https://en.wikipedia.org/wiki/Hippocampus))( [I.e.](https://en.wikipedia.org/wiki/I.e.) low GABA) might reduce the ability of the frontal lobe( [PFC](https://en.wikipedia.org/wiki/PFC), specifically the [dlPFC](https://en.wikipedia.org/wiki/DLPFC)) to engage in proper executive/ [cognitive processing](https://en.wikipedia.org/wiki/Cognitive_processing). The [dlPFC](https://en.wikipedia.org/wiki/DLPFC) is also [assoc](https://en.wikipedia.org/wiki/Association_football). with' turning down' other brain regions associated with excessive self- thoughtfulness ([rumination](https://en.wikipedia.org/wiki/Rumination)). The idea, from my interpretation( sorry I'm on my phone and [havent](https://en.wikipedia.org/wiki/Haventec) read the whole article), is that lower GABA levels are inhibiting the hippocampus' ability to aid in regulating this introspective processing, [I.e.](https://en.wikipedia.org/wiki/I.e.) preventing hippocampal regulation over dlPFC processing. I m not familiar with the direct circuit between the neural structure ([hippocampus](https://en.wikipedia.org/wiki/Hippocampus)) and [dlPFC](https://en.wikipedia.org/wiki/DLPFC), though. It is important to note as well that this overall network is very complex, and i can't seem to identify exactly what model the authors are proposing. If you're interested, a good place to start learning is [Googling](https://en.wikipedia.org/wiki/Googling)" LCSPT circuits."

 Also, for those assuming that taking [GABA](https://en.wikipedia.org/wiki/GABA) might help, it is important to remember that all drugs aimed at treating psychopathology act as' shotguns'. If you take [GABA](https://en.wikipedia.org/wiki/GABA) it will influence many different things. A good example are [SSRIs](https://en.wikipedia.org/wiki/SSRIs) aimed at increasing serotonin levels. This also happens in the periphery, thus, often producing [sexual dysfunction](https://en.wikipedia.org/wiki/Sexual_dysfunction) and weight gain. Please consult a specialist before taking thing ([ANYTHING](https://en.wikipedia.org/wiki/Anything_Goes))( including supplements),* especiialy* if you are already on medication.

 EDIT 2:
 Also a lot of people making overarching assumptions based on the findings. Two points should be noted.1) This is a network well- established in the neuroimaging literature, and these findings( [I.e.](https://en.wikipedia.org/wiki/I.e.) low hippocampus GABA and modulation over [dlPFC](https://en.wikipedia.org/wiki/DLPFC)) are a great addition to it.2) An important concept to remember in [neuroscience](https://en.wikipedia.org/wiki/Neuroscience) is that [GABA](https://en.wikipedia.org/wiki/GABA)( being the brains most abundant inhibitory neurotransmitter) does not always equal downstream inhibition. Sometimes you inhibit the substance ([inhibitor](https://en.wikipedia.org/wiki/Inhibitor)) and create* more* excitation by disinhibting [excitatory neurons](https://en.wikipedia.org/wiki/Excitatory_neuron). This is a exemplified by the mechanisms of club drug ([ketamine](https://en.wikipedia.org/wiki/Ketamine)) and [NMDA receptors](https://en.wikipedia.org/wiki/NMDA_receptor). [Its](https://en.wikipedia.org/wiki/Its) also similar with salt ([Glutamate](https://en.wikipedia.org/wiki/Glutamate))( opposite of [GABA](https://en.wikipedia.org/wiki/GABA) acting as the brains most [excitatory neurotransmitter](https://en.wikipedia.org/wiki/Excitatory_neurotransmitter)) which might excitate the substance ([inhibitor](https://en.wikipedia.org/wiki/Inhibitor)), providing* more* inhibition. Thus, [lower GABA](https://en.wikipedia.org/wiki/Lower_Gatara) might be a result of a large number ([multitude](https://en.wikipedia.org/wiki/Multitude)) of different mechanisms. Please do not assume that1) low GABA is causally defined here, and2) that taking [GABA](https://en.wikipedia.org/wiki/GABA) or [GABA agonists](https://en.wikipedia.org/wiki/Gaba_agonists) will help this specific circuit.

 LAST EDIT: Thanks for the gold.

 I'd like everyone to understand something very critical to this overall network. The main idea behind some of this research is that patients engage in excessive* negative* self- thoughtfulness ([rumination](https://en.wikipedia.org/wiki/Rumination)). This does not mean self- thoughtfulness ([rumination](https://en.wikipedia.org/wiki/Rumination)) is a bad thing. Please do not think that. Self- rumination /introspection can be* very* beneficial if harnessed correctly. The bad part is when that affective processing hyperfocuses on the" negative" stuff. So, stay positive and think about how your better than that little devil on your shoulder. Do [nt](https://en.wikipedia.org/wiki/Nt) let your actions or experiences determine how you define your reality.

 LAST LAST EDIT:[ Here is a link to the peer- reviewed, open access publication](https://www.nature.com/ articles/ [s41467](https://en.wikipedia.org/wiki/S-14671)- 017- 00956-z).

 Credit goes to/u/ sublimal2 for finding the [open access pub](https://en.wikipedia.org/wiki/Open_access_publication) at the beginning of the thread. The comment got buried very quickly, so Thanks! This is hot off the press and published today. [Exciting](https://en.wikipedia.org/wiki/Exciting). Unfortunately I don't have time to read it tonight to double- check my understanding. If you notice a failing ([flaw](https://en.wikipedia.org/wiki/Flaw)) in my understanding please let me know!