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Alternatively, separate vasodilator neurons to skin may share the same chemical code as sudomotor neurons.
In vitro, OB TH neurons express NMDA receptors, suggesting that NMDA stimulation is acting directly on TH neurons.
These results provide evidence that kainic acid at appropriate concentrations effectively destroys GABAergic septohippocampal neurons, while sparing cholinergic MSDB neurons.
These results suggest that GABAergic neurons could modulate nitric oxide producing neurons in the dorsal raphe nucleus through direct synaptic relations.
Our results suggest that pedicularioside A has a neuroprotective effect to improve the survival of mesencephalic neurons (dopaminergic neurons and non-dopaminergic neurons).
It also prevents the death of motor neurons and midbrain dopaminergic neurons induced by lesions8,10–12.
These results indicate that nociceptin acts both on neurons precedent to cardiovascular neurons to decrease the activity of GABAergic neurons that synapse upon cardiovascular neurons and directly, inhibiting the postsynaptic currents evoked by GABA.
We also find that bupropion alone reduces GABAergic transmission to DA neurons, thereby diminishing tonic inhibition of these neurons.
Here we demonstrate that cortical neurons directly innervate the brainstem to drive feedforward inhibition of nociceptive neurons.
Open accessJournal ArticleDOI
11 Jan 2011-Science Signaling
28 Citations
These physical changes allow neurons tocommunicate through nonsynaptic signals to adjacent cells, such as other neurons or glia.
Lidocaine helps protect neurons from ischemia by suppressing the direct‐current potential shift, by inhibiting the release of Ca2+ from the intracellular Ca2+ stores, and by inhibiting the influx from the extracellular space.
The death of these neurons supports the hypothesis that outmoded or unused neurons are actively eliminated.

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How does the zona incerta control anxiety?
5 answers
The zona incerta (ZI) plays a crucial role in modulating anxiety through various mechanisms. Studies have shown that silencing ZI blocks the expression of stress-induced social conditioned place aversion (CPA) and enhances anxiety levels in mice subjected to repeated social defeat stress (RSDS). Dysregulation of microglial engulfment capacity in the ventral zona incerta (ZIV) leads to anxiety-like behaviors in acute pain conditions, with chemogenetic activation of ZIVGABA relieving these symptoms. Furthermore, ZI activation suppresses fear generalization, while chemogenetic inhibition of ZI results in fear generalization, indicating its role in regulating fear responses. Additionally, different subpopulations of ZI neurons, such as SOM, CR, and Vglut2-expressing cells, encode and modulate distinct components of anxiety-related behaviors, with specific neuronal activations inducing or reducing anxiety levels. Overall, the ZI exerts control over anxiety through intricate neural circuits and interactions with microglial cells.
How does the levels of nitric oxide in the bloodstream affect the process of citrullination?
5 answers
The levels of nitric oxide (NO) in the bloodstream play a crucial role in the process of citrullination. NO is involved in stimulating the formation of citrulline through the arginine-citrulline transformation. Additionally, NO can modulate the citrullination reaction, which is crucial in the development of autoimmune diseases like rheumatoid arthritis. Furthermore, NO can affect the levels of cGMP, a key signaling molecule in various cellular processes, including erythroid cell differentiation. In patients with liver cirrhosis, elevated levels of NO have been linked to increased citrullination, potentially induced by factors like endotoxin and TNF alpha. Therefore, the presence and regulation of NO in the bloodstream have a significant impact on citrullination processes, influencing various physiological and pathological conditions.
What are the potential uses of red vine in traditional medicine?
5 answers
Red vine, particularly red vine leaf extract, holds significant potential in traditional medicine. Studies have shown that red vine leaf extract, known as AS 195, can effectively alleviate symptoms of chronic venous insufficiency (CVI). Additionally, red vine extracts have been recognized for their antioxidant, anti-inflammatory, anti-edematous, diuretic, and liver protective properties, further highlighting their traditional medicinal value. The extract from red vine leaves has been found to improve cutaneous oxygen supply, microcirculation, and nitric oxide bioavailability, which can benefit individuals with microvascular disorders. Moreover, vine leaves, being rich in polyphenols, have been explored for their therapeutic properties in various biological systems, showcasing their potential in traditional medicine. Overall, red vine and its extracts demonstrate promising uses in addressing various health conditions traditionally.
Is phosphatidil serine useful for seizure?
5 answers
Phosphatidylserine (PS) has therapeutic potential beyond seizures. PS is beneficial for regressive brain diseases, aiding in liposome preparation and dietary therapy. PS receptors play a role in reducing inflammation, treating autoimmune diseases, enhancing tissue graft transplantation, increasing anti-tumor immunity, and inhibiting infections. Additionally, tumor-derived PS affects macrophages, reducing their ability to produce nitric oxide and lyse tumor targets. Interestingly, a parasite, Toxoplasma gondii, predominantly contains phosphatidylthreonine (PtdThr) over PS, showcasing the importance of PtdThr in parasite motility and virulence. While PS may not directly address seizures, its diverse roles in brain health, immunity, and cellular functions highlight its significance in various physiological processes.
How does the vasodilation process affect the perception of warmth in humans?
5 answers
The vasodilation process plays a crucial role in the perception of warmth in humans. When the body temperature rises, vasodilation occurs, leading to an increase in skin blood flow, which helps transfer heat from the body core to the skin surface for cooling. Additionally, vasodilation is associated with sweating, which aids in evaporative cooling of the skin. Studies suggest that the vasodilator response to local heating involves a sensory nerve-dependent peak followed by a slower, nitric oxide-mediated vasodilation, contributing to the sensation of warmth. Furthermore, the use of a vasodilation sleeve over a vascular puncture site traps body heat, causing skin warming and vein dilation, enhancing the perception of warmth. Overall, vasodilation mechanisms, including skin blood flow regulation and sweating, are integral to the perception of warmth in humans.
Can nucleus populsus cells be activated by LPS?
9 answers
Yes, nucleus pulposus (NP) cells can be activated by lipopolysaccharide (LPS), leading to various cellular responses indicative of activation and inflammation. Research has shown that LPS treatment increases TNF receptor 1 (TNFR1) in human nucleus pulposus cells (HNPCs), triggering cell viability loss, apoptosis, and inflammation, which are hallmarks of intervertebral disc degeneration (IDD). Furthermore, LPS has been found to induce the release of inflammatory cytokines such as IL-1β, IL-6, and TNF-α in NP cells, which is a clear sign of cellular activation in response to LPS challenge. Additionally, the study by Zhang et al. demonstrated that LPS treatment simulates intervertebral disc degeneration conditions in NP cells, leading to increased expression of miR-222, which is associated with the promotion of apoptosis and inflammation within these cells. This further supports the notion that LPS can activate NP cells, contributing to degenerative processes. Moreover, LPS has been shown to influence the behavior of various cell types and molecular pathways that could indirectly affect NP cells. For instance, LPS binding protein (LBP) plays a dual role in gram-negative sepsis by mediating LPS-induced cytokine release from mononuclear cells, which could potentially influence the microenvironment of NP cells. The protective effects of moracin against LPS-induced inflammation in NP cells also highlight the responsiveness of these cells to LPS, through mechanisms involving the Nrf2/HO-1 and NF-κB/TGF-β pathways. In summary, evidence from multiple studies confirms that NP cells can indeed be activated by LPS, leading to inflammatory responses, apoptosis, and changes in extracellular matrix composition, which are critical factors in the pathology of IDD.
How does the type and amount of alcohol consumed impact an individual's ability to respond quickly?
5 answers
The type and amount of alcohol consumed can significantly impact an individual's ability to respond quickly. Alcohol consumption affects neurotransmitter levels in the brain, particularly increasing GABAergic signaling and decreasing glutamatergic signaling, which can modulate executive functioning and impair response inhibition. Studies have shown that alcohol-induced response inhibition deficits are influenced by the degree of response automatization, with impairments occurring mainly in automatized responses. Additionally, the amount of consumed alcohol has been found to have a direct correlation with the driver's reaction time, significantly affecting road safety by influencing stopping distances. Chronic, excessive alcohol use is linked to significant cognitive impairment, particularly in older individuals, who may be at a greater risk due to the cognitive decline associated with aging.
How fast synaptogenesis occur?
5 answers
Synaptogenesis occurs at varying speeds depending on the brain region and developmental stage. In the macaque monkey neocortex, the most rapid phase of synaptogenesis lasts around 40 days, centered on birth, with phase 3 being particularly modifiable by stimulation or deprivation. In the hippocampus, synaptogenesis in CA1 occurs within 30 minutes after long-term potentiation induction, with subsequent changes in presynaptic vesicles and axonal boutons observed at 2 hours. Human fetal cortical synaptogenesis initiates between the 6th and 7th gestational week, with a rapid increase in synaptic density by 12-14 weeks. The adult dentate gyrus displays asynchrony in synapse formation, with GABAergic inputs developing early but slowly, while glutamatergic inputs have a late onset and rapid maturation. These findings collectively highlight the dynamic and region-specific nature of synaptogenesis timelines.
What is the relation between amyloid beta and synaptophysin?
4 answers
Amyloid beta (Aβ) and synaptophysin are intricately linked in the context of Alzheimer's disease (AD) pathology. Aβ plays a crucial role in disrupting synaptic function and promoting synaptic toxicity in AD by affecting various mechanisms. Synaptophysin, an abundant protein in synaptic vesicles, is identified as a marker of axonal damage in inflammatory and demyelinating conditions, including AD. Studies have shown that Aβ binds to synaptophysin with high affinity, disrupting the synaptophysin/VAMP2 complex and inhibiting neurotransmitter release and synaptic plasticity. Additionally, Aβ exposure leads to increased intracellular levels of synaptophysin in astrocytes, reducing its release and potentially contributing to the loss of synaptophysin in neurons, further implicating synaptophysin in AD pathology. These findings highlight the intricate relationship between Aβ and synaptophysin in the context of AD.
What is the role of the cholinergic system in neurotransmission and cognition?
4 answers
The cholinergic system plays a crucial role in neurotransmission and cognition. Acetylcholine (ACh) acts as a neurotransmitter with diverse physiological functions, including modulation of the autonomic nervous system, inflammation, cognition, and motor coordination. Cholinergic transmission is essential for memory, learning, attention, and other higher brain functions, with cholinergic synapses being widespread in the human central nervous system. Studies highlight the significance of cholinergic signaling in the prefrontal cortex for signal detection and top-down attentional control, challenging the traditional view of ACh as a slow neuromodulator. Furthermore, deficits in the cholinergic system are implicated in cognitive disorders, emphasizing the importance of cholinergic therapies in conditions like Alzheimer's disease.
How emotional fever affects animal cognition and anxiety?
4 answers
Emotional fever, induced by stressors like exposure to an open field, impacts animal cognition and anxiety. Chronic stress, a significant trigger of emotional responses, can lead to maladaptive behaviors resembling anxiety and depression in animals, affecting cognitive functions. Individual differences in coping with stress influence the development of stress-induced memory alterations, highlighting the interplay between chronic stress and emotional responses in modulating memory performances and brain neurogenesis. High trait anxiety, a risk factor for anxiety disorders, shows marked phenotypic variation in animals, suggesting distinct neural circuits associated with anxiety risk. Understanding how emotional fever influences cognition and anxiety in animals is crucial for elucidating the complex interactions between stress, emotional responses, and cognitive functions.