A list of puns related to "Thalamo cortico thalamic circuits"
Citation: T. Zhou et al. “History of winning remodels thalamo-PFC circuit to reinforce social dominance”. Science, 14 Jul 2017: Vol. 357, Issue 6347, pp. 162-168
DOI/PMID/ISBN: 10.1126/science.aak9726.
This is an automatic summary, original reduced by 98%.
> Thus, we hypothesized that the phenotype of SPRED2 KOs could be the result of excessive and injurious self-grooming, indicating an OCD-like behavior caused by SPRED2 deficiency in brain regions relevant for the onset of OCD.In SPRED2 KO mice, the Spred2 gene was disrupted by insertion of a gene trap vector between exons 4 and 5 of Spred2.
> Because SPRED2 is a critical inhibitor of Ras/ERK-MAPK signaling, we investigated if SPRED2 deficiency impacts BDNF/TrkB/ERK-MAPK signaling in SPRED2 KO mice.
> SPRED2 is a target of TrkB itself or of a kinase downstream of TrkB. Given the unaltered BDNF levels in the amygdala and the interaction between SPRED2 and TrkB, we further investigated whether the augmented activity of Ras and ERK in SPRED2 KO mice might be a result of specifically increased TrkB activation.
> Increased TrkB/ERK-MAPK signaling caused by SPRED2 deficiency leads to OCD-like grooming in SPRED2 KO mice.
> Changes in thalamo-amygdala synaptic transmission are caused by dysregulated protein expression as a consequence of altered gene transcription, altogether a result of SPRED2 deficiency and the associated upregulation of TrkB/ERK signaling.
> In SPRED2 KO mice, we determined the mechanism how SPRED2 deficiency leads to an increase of active TrkB receptor and signaling, which is mediated downstream by increased Ras activity and ERK-phosporylation and induces OCD-like behavior.
Summary Source | FAQ | Theory | Feedback | Top five keywords: SPRED2^#1 mice^#2 amygdala^#3 expression^#4 protein^#5
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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:
System-Integration models: Consciousness emerges when information from different sources is processed in a closed network.
**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).
**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).
**Postdiction model of Consciousness** (Eagleman, Michel & Doerig): Sensory stimuli arrives to consciousness at different times, but we experience it simultaneously. T
Medium Spiny Neurons
>”Medium spiny neurons (MSNs), also known as spiny projection neurons (SPNs), are a special type of GABAergic inhibitory cell representing 95% of neurons within the human striatum, a basal ganglia structure.[1] Medium spiny neurons have two primary phenotypes (characteristic types): D1-type MSNs of the direct pathway and D2-type MSNs of the indirect pathway.[1][2][3] Most striatal MSNs contain only D1-type or D2-type dopamine receptors, but a subpopulation of MSNs exhibit both phenotypes.” (From Wiki)
>”The firing activity of the main striatal neuron class, the “medium spiny projection neurons,” is highly regulated in adults. Despite exhibiting rich near-threshold activity (“UP states”) driven by excitatory cortical inputs, these neurons are usually silent. It seems likely that medium spiny neurons filter out uncorrelated afferent activity and fire only in response to precisely synchronized inputs.”
THC, D1-D2 Heteromers & MSNs
“This study highlights intriguing discoveries relevant to dopamine receptor signaling and cannabinoid-induced neuroadaptive changes in primate basal ganglia. (1) We provide abundant morphological evidence that dopamine D1 and D2 receptors form complexes in the dorsal striatum and NAc of mammalian species, including mouse, rat, nonhuman primate and human. Evolutionary differences were noted in the expression of dopamine D1-D2 heteromers, with heteromer abundance in the order human > primate > rat > mouse. In all these species, a higher number of MSNs expressing the D1-D2 heteromer was observed in the ventral striatum (i.e., NAc) than in the dorsal striatum. (2) THC increased the number of neurons expressing the D1-D2 heteromer in both regions of the striatum of nonhuman primate brain after chronic administration, from 35% or less, to approximately 80%, together with a 3-fold increase of heteromer density within individual neurons. (3) The chronic low-dose THC regimen led to a phenotypic change in MSNs indicating a reprogramming of these MSNs to co-express the characteristic markers of both striatonigral and striatopallidal neurons together with co-expression of D1 and D2 receptors.”
MSNs & the thalamocortical loop
>”Medium spiny neurons (MSNs) make up as much as 95% of cells within the striatum and send inhibitory projections to s
... keep reading on reddit ➡The title is straightforward. Most atheists also tend to be methodological naturalists and physicalists so the idea of an afterlife is outside of consideration as well. Although the hard problem of consciousness is a contended topic in philosophy of mind and neuroscience (how does qualia arise from matter, why is detection of stimuli accompanied by subjective experience is how I would word it), there are many NCC's that point to it emerging from the brain: cortico-thalamic pathways involved in perception of sensation and processing of stimuli, brainstem regions involved in arousal-control...etc.
No brain = most likely no experience of an afterlife.
However, for the sake of the argument, if you were to empirically test out the possibility of consciousness survival beyond brain death and lack of brain activity, how would you do so? Lots of proponents and disbelievers alike say its beyond the realm of science, but I feel like it may not be the case. I'm thinking of certain ways one could test it out:
I've been trialing Imidazenil as this article mentions and it has definitely been helping with my negative symptoms. I guess it's helping the most by eliminating my ruminating thoughts and giving me clarity in that regard.
It is technically a benzo, however it doesn't cause sedation, amnesia, ataxia or cognitive impairment or tolerance.
>In contrast [to diazepam]... Imidazenil, which fails to allosterically and positively modulate the action of GABA at GABA(A) receptors with alpha(1) subunits that selectively allosterically modulate cortical GABA(A) receptors containing alpha(5) subunits, contribute to the anxiolytic, antipanic, and anticonvulsant actions of these ligands without producing sedation, amnesia, or tolerance.
...
>The remarkably unique features of the pharmacological profile of imidazenil (compared with diazepam or alprazolam) warrant the investigation of this drug as a prospective agent to treat psychotic symptoms in SZ and BP patients with mania. Our interest in the study of imidazenil is justified by the increasing consideration given to the role of GABAergic inhibition in control of the thalamo-cortical afferent and reentrant cortico-thalamic pathways, as well as afferent septal hippocampus and reentrant hippocampal–septal glutamatergicpathways(Mountcastle1998).Thesetwopathways have an important GABAergic component that participates in the regulation of sensory gating and memory acquisition and perhaps in the consolidation of these functions. These cognitive functions are altered in SZ and BP patients with mania(LewisandLieberman2000).Since theexpression of GAD67 is decreased in the PFC and other brain areas of SZ and BP patients with mania (Impagnatiello et al. 1998; Guidotti et al. 2000; Lewis et al. 2004; Woo et al. 2004), one might reason that if imidazenil were used in the treatment of SZ, it could increase cortical GABAergic tone, thereby correcting the symptoms associated with the specific cortical GABAergic downregulation typical of SZ. Imidazenil’s action on the mouse methionine model of SZ To investigate the hypothesis that imidazenil may correct the behavioral consequences of the GABAergic transmission deficit operative in SZ, we studied the effects of imidazenil on the behavioral abnormalities induced in mice by protracted treatment with methionine (Tremolizzo et al. 2002; Tremolizzo et al. 2005 ). These mice exhibit frontal cortex and hippocampal expression deficits o
... keep reading on reddit ➡"The main counter-argument to interpreting VS as a purely ocular phenomenon however, lies in the main criterion for VS, which requires the absence of ophthalmic disorders (Table 1), and also in the normality of basic eye electrophysiology, such as ERG or VEPs, reported in previous VS cohorts (Lauschke et al., 2016; Schankin et al., 2014a). Furthermore, it is unlikely for a whole-field visual disturbance to be caused by a localized disorder of the anterior retino-geniculate visual pathway or of the optic radiations, since these are organized in a monocular or homonymous fashion. These considerations do not exclude that some cases of visual snow might be triggered by eye conditions. In this respect it is interesting to recall that in certain examples, CBS hallucinations are characterized by simple flashes, dots of light, or even palinopsia, an important feature of the VS syndrome (Santhouse et al., 2000)."
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"A second theory on VS pathophysiology could involve a direct thalamic dysfunction. In a process known as thalamo-cortical dysrhythmia, there is a dissociation between the sensory inputs from the thalamus and its projections to the cortex. This 33 mechanism was first described by Llinas in the context of tinnitus (Llinas et al., 1999), and is characterized by an increase in unusual, large-scale and coherent thalamocortical low-frequency oscillations. These delta and theta oscillations are likely caused by a switch from tonic to high-frequency thalamic bursting - due to protracted cell hyperpolarization - and ultimately determine a disintegration of sensory perception at the cortical level. It is certainly possible to hypothesize a role for thalamo-cortical dysrhythmia in visual snow. Potentially, an underlying homeostatic imbalance of the visual pathways, either from altered retinal activity or genetic predisposition, could cause a disinhibition of projections from the posterior visual thalamus to the primary and secondary visual cortices, as well as the parietal cortex, which could in turn affect normal visual perception and at the same time explain both palinopsia and the continuous perception of movement (Lauschke et al., 2016). "
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"**A thir
... keep reading on reddit ➡Medium Spiny Neurons
>”Medium spiny neurons (MSNs), also known as spiny projection neurons (SPNs), are a special type of GABAergic inhibitory cell representing 95% of neurons within the human striatum, a basal ganglia structure.[1] Medium spiny neurons have two primary phenotypes (characteristic types): D1-type MSNs of the direct pathway and D2-type MSNs of the indirect pathway.[1][2][3] Most striatal MSNs contain only D1-type or D2-type dopamine receptors, but a subpopulation of MSNs exhibit both phenotypes.” (From Wiki)
>”The firing activity of the main striatal neuron class, the “medium spiny projection neurons,” is highly regulated in adults. Despite exhibiting rich near-threshold activity (“UP states”) driven by excitatory cortical inputs, these neurons are usually silent. It seems likely that medium spiny neurons filter out uncorrelated afferent activity and fire only in response to precisely synchronized inputs.”
THC, D1-D2 Heteromers & MSNs
>”This study highlights intriguing discoveries relevant to dopamine receptor signaling and cannabinoid-induced neuroadaptive changes in primate basal ganglia. (1) We provide abundant morphological evidence that dopamine D1 and D2 receptors form complexes in the dorsal striatum and NAc of mammalian species, including mouse, rat, nonhuman primate and human. Evolutionary differences were noted in the expression of dopamine D1-D2 heteromers, with heteromer abundance in the order human > primate > rat > mouse. In all these species, a higher number of MSNs expressing the D1-D2 heteromer was observed in the ventral striatum (i.e., NAc) than in the dorsal striatum. (2) THC increased the number of neurons expressing the D1-D2 heteromer in both regions of the striatum of nonhuman primate brain after chronic administration, from 35% or less, to approximately 80%, together with a 3-fold increase of heteromer density within individual neurons. (3) The chronic low-dose THC regimen led to a phenotypic change in MSNs indicating a reprogramming of these MSNs to co-express the characteristic markers of both striatonigral and striatopallidal neurons together with co-expression of D1 and D2 receptors.”
MSNs & the thalamocortical loop
>”Medium spiny neurons (MSNs) make up as much as 95% of cells within the striatum and send inhibitory
... keep reading on reddit ➡Please note that this site uses cookies to personalise content and adverts, to provide social media features, and to analyse web traffic. Click here for more information.