Basal forebrain vs. basal ganglia?

I'm trying to understand the differences between these two, both functionally and anatomically. I read that basal forebrain includes the ventral basal ganglia, but confused as to why + how we differentiate these structures.

Thanks in advance!

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📅︎ May 27 2021
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Basal forebrain cholinergic neurons selectively drive coordinated motor learning in mice biorxiv.org/content/10.11…
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👤︎ u/sburgess86
📅︎ Apr 25 2021
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Brain waves: basal forebrain neurons fine-tune consciousness by synchronizing rhythms in the cortex sciencedaily.com/releases…
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📅︎ Dec 03 2019
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Motivation to bully is regulated by brain reward circuits. Individual differences in the motivation to engage in or to avoid aggressive social interaction (bullying) are mediated by the basal forebrain, lateral habenula circuit in the brain medicalxpress.com/news/20…
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👤︎ u/Wagamaga
📅︎ Jul 10 2016
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Scientists identify that dopamine receptor type-2 expressing cells in the basal forebrain, control risky decision making nature.com/nature/journal…
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Study finds amyloid-beta begins to accumulate in basal forebrain neurons as early as age 20; aggregates continue to form throughout life and are more numerous in individuals who have Alzheimer's disease. This is the first study to show amyloid-beta aggregates occurring in such young brains. brain.oxfordjournals.org/…
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👤︎ u/marc5387
📅︎ Mar 02 2015
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BMP9 induces the transcriptome of basal forebrain cholinergic neurons ncbi.nlm.nih.gov/pmc/arti…
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Study finds amyloid-beta begins to accumulate in basal forebrain neurons as early as age 20; aggregates continue to form throughout life and are more numerous in individuals who have Alzheimer's disease. This is the first study to show amyloid-beta aggregates occurring in such young brains. brain.oxfordjournals.org/…
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👤︎ u/marc5387
📅︎ Mar 02 2015
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Study finds amyloid-beta begins to accumulate in basal forebrain neurons as early as age 20; aggregates continue to form throughout life and are more numerous in individuals who have Alzheimer's disease. This is the first study to show amyloid-beta aggregates occurring in such young brains. /r/neur. reddit.com/r/neuroscience…
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👤︎ u/eleitl
📅︎ Mar 03 2015
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Differential expression of galanin in the cholinergic basal forebrain of patients with Lewy body disorders [Acta Neuropathol Commun., Dec 2015 — free full-text] doi.org/10.1186/s40478-01…
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👤︎ u/isosafrole
📅︎ May 30 2016
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Study finds amyloid-beta begins to accumulate in basal forebrain neurons as early as age 20; aggregates continue to form throughout life and are more numerous in individuals who have Alzheimer's disease. This is the first study to show amyloid-beta aggregates occurring in such young brains. brain.oxfordjournals.org/…
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👤︎ u/marc5387
📅︎ Mar 02 2015
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Electrical stimulation of cholinergic neurons in the brainstem hyperpolarizes GABAergic interneurons of the thalamic reticular nucleus, which in turn disinhibits thalamic relay cells from firing properly

I think this is critical and honestly, it would be worth reading the entirety of the research article as it's all very illuminating, but I'm going to try to provide and highlight the most relevant sections as it contains what I see as several "smoking guns" both for my specific case and anyone similarly afflicted.

It says point blank what activation or stimulation of the cholinergic neurons of the brainstem does. They project directly to the thalamic reticular nucleus, the thalamus' pacemaker core, and hyperpolarize GABAergic interneurons there. This reduces the amount of firing from GABAergic interneurons.

Someone may ask "But isn't that bad? Don't we want GABAergic interneurons of the thalamic reticular nucleus to fire more?" No. It's counterintuitive, but that is not the case. GABAergic interneurons of the thalamic reticular nucleus are (as you can ascertain from being GABAergic and being interneurons) are inhibitory. But they are, when not constrained by brainstem cholinergic projections driven by acetylcholine, inhibiting the thalamocortical relay cells from firing properly. Visual noise over signal is increased and faithful relay of finely tuned visual information to the V1 (visual cortex of the cerebral cortex) is then disturbed.

Cholinergic neurons of the brainstem have to modulate, constrain or inhibit GABAergic interneurons of the TRN so the end result will be disinhibition of thalamocortical relay cells, including ones of the dorsal lateral geniculate nucleus (visual portion of the thalamus).

(From the American College of Neuropsychopharmacology)

> Structure and Function of Cholinergic Pathways in the Cerebral Cortex, Limbic System, Basal Ganglia, and Thalamus of the Human Brain

> **The cerebral cortex, thalamus, and basal ganglia of the human brain provide neural templates for the transformation of simple movements and sensations into exceedingly complex psychological acts and experiences. These transformations occur through the orderly transfer of information along parallel and serial pathways that lead to the formation of large-scale distributed networks. The thousands of neural pathways that contribute to the formation of these networks can be divided into two major groups. One group contains point-to-point (discrete) projections such as those that interconnect individual thalamic nuclei with their cortical targets. The second group contains equally important regulatory (diffuse) neural projections which (a) innervate

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📅︎ Dec 23 2021
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Neuronal Activity in Brainstem Cholinergic Nuclei Related to Tonic Activation Processes in Thalamocortical Systems

Unfortunately I've only located the full version of this available in a PDF. I will again note and just include a few crucial sections here.

Note: Remember that "oscillations" in this context are brainwaves.

Note especially the section at the end.

> The Journal of Neuroscience, August 1990

> M. Steriade, S. Datta, D. Pare, G. Oakson, and R. Curro Dossi

> Laboratoire de Neurophysiologie, Faculté de Médecine, Université Laval, Québec, Canada G1K 7P4

> This study was performed to examine the hypothesis that thalamic-projecting neurons of mesopontine cholinergic nuclei display activity patterns that are compatible with their role in inducing and maintaining activation processes in thalamocortical systems during the states of waking (W) and rapid-eye-movement (REM) sleep associated with desynchronization of the electroencephalogram (EEG). A sample of 780 neurons located in the peribrachial (PB) area of the pedunculopontine tegmental nucleus and in the laterodorsal tegmental (LDT) nucleus were recorded extracellularly in unanesthetized, chronically implanted cats. Of those neurons, 82 were antidromically invaded from medial, intralaminar, and lateral thalamic nuclei; 570 were orthodromically driven at short latencies from various thalamic sites; and 45 of the latter elements are also part of the 82 cell group, as they were activated both antidromically and synaptically from the thalamus.

> The desynchronization of EEG activity, also termed EEG activation because of the simultaneous increase in thalamic and cortical responsiveness (see Steriade et al., 1990a) consists of at least 2 major components: the disruption of spindle oscillations that takes place in the thalamus and the blockade of high amplitude slow (0.5 - 4 Hz) or delta waves. As yet, the precise origin of the latter waves is not elucidated. The cortical origin is most often suggested. In the cerebral cortex, delta waves probably originate from synaptic inhibitory processes, but especially from the exceedingly long-lasting calcium-dependent potassium currents (see Steriade and Buzsaki, 1990). Their disruption can be realized by a series of transmitters used by neuronal systems with direct access to the cerebral cortex: basal forebrain cholinergic neurons, ventrolateral posterior hypothalamic histaminergic neurons, and locus coeruleus noradrenegic neurons. The suppressing action of these transmitters upon calcium-dependent potassium currents are now established (Reiner and

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📅︎ Dec 24 2021
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Synaptic mechanisms underlying cholinergic control of thalamic reticular nucleus neurons

The thalamic reticular nucleus, seen as a form of pacemaker of the thalamus and in turn, a stabilizing force for thalamocortical rhythms and perhaps optimum functioning of neural oscillations (brainwaves) and their patterns.

This will be the true beginning of a series on research I've pored over for months and which I believe is intimately relevant to my own case and possibly contains implications for others here. This will be a longer post, but I think it's important information.

Dr. Diana Driscoll, an optometrist and author, as well as creator of the Parasym Plus supplement, is the one who spoke some time ago about vision disturbances reflective of the same symptoms described by people now being recognized as VSS cases long being considered in the community of optometrists and ophthalmologists as having a cholinergic mechanism (being related to cholinergic damage/dysfunction). Unfortunately, I tried that specific supplement much earlier in the year along with many others and it had zero positive effect for me. I believe I've come to understand why.

I do not think acetylcholinesterase inhibitors (inhibitors which disrupt the activities of the enzyme which breaks down endogenous acetylcholine), acetylcholine precursors like choline (found in foods like eggs and poultry as well as specific choline supplements) required for production of endogenous acetylcholine, or even partial or nonselective agonists/activators are enough to stimulate and activate the receptors involved with an equal or greater degree of force to the extent to which they were antagonized to reverse the process said antagonism caused.

Acetylcholine is one of the principal neurotransmitters of the entire central nervous system (brain and spinal cord), like GABA, glutamate, serotonin, dopamine, norepinephrine, and so on. Yet unlike GABA which is mostly inhibitory or glutamate which is mostly excitatory, acetylcholine can be inhibitory or excitatory. It can excite inhibitory neurons into proper action and functioning, or even inhibit inhibitory neurons (such as GABAergic interneurons of the thalamic reticular nucleus) from maladaptively inhibiting in turn the necessary function of thalamic relay cells. Thus, it epitomizes the role of a true neuromodulator.

It does this through changing a cell's resting membrane potential via depolarization or hyperpolarization. Remember that depolarization shifts a cell's resting membrane potential to a more positive value, making it more likely to

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📅︎ Dec 22 2021
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Theories of Consciousness - List

Hey guys, I made a list of all the theories of consciousness I could find. Made a short description of each one. Would appreciate feedback if I missed anything or if my description is inaccurate. Also, let's pointlessly argue about which one is the most correct one. Looking forward to your inputs.

Ps. In each section, the first theory or two is most established one in the field (take into account that all the theories are untestable, thus what makes a theory more popular is its applicability to AI, and not how accurate it represents consciousness in the brain). Also, I didn't include theories that were refuted, such as the OrchOr theory.

Models:

  1. **Synchrony theory** (Singer, Engel): Neurons that fire in the same phase (rhythm) at the gamma range (above 30 action potentials per sec) send together stimulus information to consciousness. The purpose of consciousness is binding features into objects (eg binding the shape of a box with its color, sound, location. etc). The theory is now considered incomplete, and is the basis of most theories below.

System-Integration models: Consciousness emerges when information from different sources is processed in a closed network.

  1. **Integrated information theory** (Tononi): Subjective experience is a side effect of a large scale simultaneous processing of incoming information in a closed network/ensemble of neurons. The information forms conscious shapes (quale) in the conscious space (qualia space) by integrating together all the possible dimensions of informations (q-arrows). The posterior parietal cortex (attention center) is a hot-zone for eliciting consciousness due to receiving more incoming information than other regions (but to a lesser degree consciousness occurs also in other brain parts). The model was formed by analyzing the properties of subjective experience (and not by examining the brain).

  2. **Supramodular Interaction theory of Consciousness** (Morsella): Conflict resolution of movement is the only behavior that cannot occur subconsciously (ie it is encapsulated). In order to determine which body movement to execute, our brain enables cross talk between many different regions. The purpose of consciousness is to delay gratification (exert volitional control over the muscle system).

  3. **Postdiction model of Consciousness** (Eagleman, Michel & Doerig): Sensory stimuli arrives to consciousness at different times, but we experience it simultaneously. T

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📅︎ Oct 31 2021
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Acetylcholine and hallucinations: disease-related compared to drug-induced alterations in human consciousness

I recommend visiting the parent thread I posted on this topic, but I wanted to separate this and another into formally distinct topic threads lest the length and subject matter become unwieldy as I think this info shouldn't get lost in the shuffle.

Again, direct implications for anyone who has taken an anticholinergic medication in any form prior to onset of VSS symptoms.

(Original thread)

https://www.reddit.com/r/visualsnow/comments/rltpz6/synaptic_mechanisms_underlying_cholinergic/

> Acetylcholine and hallucinations: disease-related compared to drug-induced alterations in human consciousness

> Newly proposed criteria for Lewy body dementia include alterations in consciousness. Lewy body dementia is also associated with a disturbance in cholinergic transmission; neocortical cholinergic deficits in this disorder are more extensive than in Alzheimer's disease and are correlated with symptoms commonly associated with delirium, such as visual hallucinations. The traditional view that derangements of the basal forebrain cholinergic system in Alzheimer's disease relate specifically to memory impairment is assessed in terms of a more general role for cortical acetylcholine in consciousness. This extends the concept that cortical acetylcholine enhances neuronal signal to noise ratio. It is suggested that muscarinic receptor activation in the cortex is involved in confining the contents of the discrete self-reported conscious "stream." In the absence of cortical acetylcholine, currently irrelevant intrinsic and sensory information, which is constantly processed in parallel at the subconscious level, enters conscious awareness. This is consistent with the ability of anti-muscarinic drugs administered medically, recreationally, or ritualistically to induce visual hallucinations and other perceptual disturbances. The hypothesis is explored through comparisons between muscarinic and nicotinic receptor psychopharmacology and between the pathology of the basal forebrain as opposed to pedunculopontine cholinergic systems in different diseases of the human brain affecting consciousness and cognition. The paradoxical effects of muscarinic receptor blockade to induce hallucinations and of REM sleep-associated cholinergic activation of the thalamus to induce dreaming may be related to the differential distribution and activity of muscarinic receptor subtypes or to the differing responses of intrinsic GABA neurons in cortex and thalamus.

> https://pubm

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📅︎ Dec 22 2021
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Hard physiological evidence for Jung’s concept of the Self, which subsequently validates the scientific legitimacy of the concepts of the archetypes and the collective unconscious.

https://www.frontiersin.org/articles/10.3389/fpsyg.2017.01424/full

Jung said, “I have long thought that, if there is any analogy between psychic and physiological processes, the organizing system of the brain must lie subcortically on the brain stem. This conjecture arose out of considering the psychology of an archetype [the Self] of central importance and universal distribution represented in mandala symbols. … The reason that lead me to conjecture a localization of a physiological basis for this archetype in the brain stem was the psychological fact that besides being specifically characterized by the ordering and orienting role, its uniting properties are predominantly affective. I would conjecture that such a subcortical system might somehow reflect characteristic of the archetypal form of the unconscious.”

And the paper I’m sharing concluded, “Although dominant neurocognitive paradigms typically co-locate subjective life to the highest levels of the brain organization, primarily as the consequence of accumulating individual memories that are stored within neuroplastic forebrain circuits, a large amount of neuro-ethological evidence shows that non-human animals (mammals, birds, and perhaps also other vertebrates) also have forms of subjectivity that emerge from the activity of old evolutionary subcortical brainstem, diencephalic, and basal forebrain areas. These findings clearly indicate that subjectivity is an inherited disposition routed on the instinctual archaic action-foundations of our brain, and they confirm Jung’s view that before reflexive self-consciousness [the ego] is developmentally acquired by infants, a primordial-instinctual affective form of Self already exists, expressing itself in the form of a affective-psychic intentionality that can interact effectively, in an evaluative way, with the material, deterministic world.”

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👤︎ u/KingThommo
📅︎ Aug 20 2021
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MF MOASS LEVEL UP!!!!!

Ok hi, so I'm a psychology ape with experience in clinical work (Dyadic Developmental Psychotherapy/attachment theory) and research focused on genetics and addiction. I love stonks but I'm no DD god so this is my contribution to the community.

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Post breakdown:

  1. Three 10/10 phrases applicable to the post and this entire situation.
  2. Meet n' greet with your brain.
  3. Why feelings matter for MOASS.
  4. MF MOASS LEVEL UP!!!

Knowledge is power.

It is not the strongest or smartest who survive, it's is those who can adapt.

Manage how you feel THEN manage how you exit.

Time to meet your brain! Why? because knowledge is power, thats why.

The three major brain divisions.

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The brain is broken into three parts:

  1. Primal brain (Basal Ganglia) - hindbrain
  2. Emotional brain (Limbic System) - midbrain
  3. Rational brain (Neocortex) - forebrain

Guess what? Your limbic system and neocortex are constantly communicating but they can only communicate in one direction at a time. Please allow me to introduce you to top-down and bottom-up processing.

Top-down and bottom-up structural processes.

Right, so do you want to think like a predator ready to take down a HF or a paper-handing prey? Oh you say predator? Well then listen the f up.

Your limbic system is responsible for all your feelies while your neocortex is responsible for managing those feelies.

When we are excited or scared, our brain goes into a 'fight or flight' response which operates on bottom-up processing. In simple words, if you become excited or scared during the MOASS (a likely response) then you may be irrational and could act on impulse.

No one wants to be, and no one wants you to be, an irrational ape during the MOASS. So it looks like your feelings really do matter (and fuck anyone who tells you they don't. no seriously, fuck them).

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👤︎ u/Limecandi
📅︎ Apr 14 2021
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SERIOUS: This subreddit needs to understand what a "dad joke" really means.

I don't want to step on anybody's toes here, but the amount of non-dad jokes here in this subreddit really annoys me. First of all, dad jokes CAN be NSFW, it clearly says so in the sub rules. Secondly, it doesn't automatically make it a dad joke if it's from a conversation between you and your child. Most importantly, the jokes that your CHILDREN tell YOU are not dad jokes. The point of a dad joke is that it's so cheesy only a dad who's trying to be funny would make such a joke. That's it. They are stupid plays on words, lame puns and so on. There has to be a clever pun or wordplay for it to be considered a dad joke.

Again, to all the fellow dads, I apologise if I'm sounding too harsh. But I just needed to get it off my chest.

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📅︎ Jan 15 2022
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Altruism and group cohesion. Why this subreddit is a phenomena and one of your greatest resources for the MOASS.

Break down of post:

  • Some basic psychology to provide a foundation for building understanding.
  • What is altruism, where does it come from and why does it matter.
  • Why this group is a phenomena.
  • Why this group is a powerful tool and why we must protect this group from HF fuckery.

🦍

Let's get to know the brain!

The brain is broken into three parts:

  1. Reptilian or primal brain (Basal Ganglia) - hindbrain
  2. Paleomammalian or emotional brain (Limbic System) - midbrain ➡️ Ape brain!
  3. Neomammalian or rational brain (Neocortex) - forebrain ➡️ Human brain!

🦍

Whats altruism?

Altruism is acting for the welfare of others.

Where does it come from?

The anatomical structures and neural circuits connecting the limbic system and neocortex. In simple words, it comes from the relationship between your Ape brain (yay!) and your Human brain!

Why does this matter?

Because altruism is a key component in group cohesion! From an evolutionary perspective, altruism was about protecting the gene pool, increasing the likelihood of species survival. This is still true today except in this scenario...

🦍

So this subreddit is not about maintaining a gene pool, obviously. It's about bettering ourselves/our situation but to do this we must trust in others, people we have never met, to act in our best interest. WOW. So that's huge, really it is.

Altruism is an elevated form of empathy. Let's dive into this some more because knowledge is power.

Empathy runs on the same circuits as fear and anxiety. What two human attributes do we most often assign to stocks? If you guessed fear and greed then you are right!

This means that this subreddit is a soothing mechanism for the stress caused by the GME saga. Ex. looks at ticker dropping, feels a trickle of FUD, turns to the GME subreddit for empathetic support and affirmation.

Effectively, this subreddit is its own positive feedback loop. As we turn to it for support and receive it, the cohesion tightens and as the cohesion tightens we feel more comfortable giving and receiving support. Being kind matters. It really matters here because for the squeeze to work we need to maintain this altruistic component to the groups cohesion. We can all have different motives, price points and beliefs but it is the community's common goal of self betterment that acts as a force against Wall Street.

🦍

Alright, now why am I calling this group a tool and what the heck do I even mean by that?

Let's compile some important things s

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👤︎ u/Limecandi
📅︎ Mar 29 2021
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Blind Girl Here. Give Me Your Best Blind Jokes!

Do your worst!

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📅︎ Jan 02 2022
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