Old astrocyte dump is below the pre-load so I can’t search of it easily – being lazy and making a new dump.
Astrocytic modulation of central pattern generating motor circuits – Was wondering if valence reciprocally modulated salience, answer is looking yep!
Experience-dependent structural plasticity in the adult brain: How the learning brain grows – The more I think about this paper the more HOLY SHITBALLS I keep spurting. So prior to this, I still had NO IDEA how the hell we actually stored information, I think my assumption was what has been offered frequently recently, that SVZ cells just have amazingly fast reorganizational ability of their local environment. Instead, what appears to be happening is that astrocytes record the data internally, then over time manipulate the local environment to store it.
If we take a step back from thinking “brain” and think nervous system, so many nervous system artifacts derive from the literal swelling/inflammation effect of astrocytes. This effect moves the experience of “pain” from being entirely in the head to a local affect, centered around the nodes of ranvier. “Pain” is a high stimulation state, and the local glial populations are relaying this state because they are overstimulated.
AHHHHAHSAHFAKSHDKASHDKJHSADKJHASD. WHY DO WE SLEEP?!? Feed forward systems are always on, meaning astrocytes won’t get the opportunity to “decompress” unless for most organisms without sleep. Interestingly, sleep itself is not necessary – only periodic shutdown to allow astrocytes (and microglia to some extent) time to decompress.
For the traditional view of the cerebral cortex being a critical requirement of “consciousness”, dolphins represent a HUGE problem. One look at their cortexes and most of our beliefs about the complexity of our cortical structures are challenged pretty succinctly IMO. One of the rationalizations for this is that dolphins need to replicate their entire set of cognitive processes across both hemispheres because they never “sleep”, instead shutting down half of their brain at a time.
This rationalization hits (IMO) on the primary function of “sleep” in all multicellular life, allowing a return to equilibrium. For astrocytes, organisms must sleep because if they don’t they can’t learn if astrocytes never get a chance to “unswell” and modify their local environment.
The Na+/K+ pump dominates control of glycolysis in hippocampal dentate granule cells
Dynamics of a sleep homeostat observed in glia during behavior
Astrocytes regulate locomotion by orchestrating neuronal rhythmicity in the spinal network via potassium clearance – All according to keikaku. The entire nervous system is brain.
Glial ER and GAP junction mediated Ca 2+ waves are crucial to maintain normal brain excitability
Enhancing GAT-3 in thalamic astrocytes promotes resilience to brain injury in rodents
Noncanonical activation of GLI signaling in SOX2+ cells drives medulloblastoma relapse
Insulin regulates neurovascular coupling through astrocytes – And with that, “Alzheimer’s” is well defined.
Therapeutic functions of astrocytes to treat α-synuclein pathology in Parkinson’s disease
Targets for astrocyte-based treatments of Parkinson’s disease (PD)
Tropism of SARS-CoV-2 for human cortical astrocytes
Transient Astrocytic Gq Signaling Underlies Remote Memory Enhancement
Dopamine Activates Astrocytes in Prefrontal Cortex via α1-Adrenergic Receptors
Astrocyte-neuron metabolic cooperation shapes brain activity – Neurons normalize signal between local astrocyte groups.
HepaCAM controls astrocyte self-organization and coupling – Astrocyte “dysfunction”/lack of function as causal to epilepsy?
Astrocyte Ca2+-evoked ATP release regulates myelinated axon excitability and conduction speed – All signal properties of neurons are controlled by astrocytes.
Astrocyte-neuron signaling in the mesolimbic dopamine system: the hidden stars of dopamine signaling – If I see a variation on the word star used in an astrocyte article title 17 or 20 more times, I shall be slightly disinterested.
Microglia and astrocyte involvement in neurodegeneration and brain cancer – Beating cancer natively is pretty much dumb fucking luck (b cells), but the brain doesn’t have the big nukes the rest of the body has.
Inhibition of astrocytic DRD2 suppresses CNS inflammation in an animal model of multiple sclerosis
Isolation and Direct Neuronal Reprogramming of Mouse Astrocytes – Hopefully this replicates, usually they have to roll back the cell to an endothelial or PSC.
The Effects of Optogenetic Activation of Astrocytes on Spike-and-Wave Discharges in Genetic Absence Epileptic Rats – Okay this needs to be a formal topic.
Emerging role of astrocytes in oxytocin-mediated control of neural circuits and brain functions – Eh, but yeah.
Advances in quantitative analysis of astrocytes using machine learning – Didn’t realize we were this far behind on automatic processing
Neurotoxic reactive astrocytes induce cell death via saturated lipids – Lol, smothers the channels in fat.
Distribution Patterns of Astrocyte Populations in the Human Cortex – So is GFAP specifically a cortical marker? This is a pretty big oof if so. Aquaporin seems to be involved in a lot more interactions than is readily apparent. Is it because water is wet or some other mechanic?
ATP indirectly stimulates hippocampal CA1 and CA3 pyramidal neurons via the activation of neighboring P2X7 receptor-bearing astrocytes and NG2 glial cells, respectively – This is a really long way of saying “astrocytes directly stimulate neurons”.
Establishment of autaptic culture with human-induced pluripotent stem cell-derived astrocytes – And evidence for the model keeps falling into place in directions I hadn’t even considered. This fills in the mechanic for astrocytes accessing other astrocyte local environments as well as feeding back their own local/internal environment.
A single cell death is disruptive to spontaneous Ca2+ activity in astrocytes – Astrocytes signal in an interdependent manner.
Foundations and implications of astrocyte heterogeneity during brain development and disease