scispace - formally typeset
Search or ask a question

What is the impact of neurotoxins in sensory neurons in zebrafish? 


Best insight from top research papers

Neurotoxins have been shown to have an impact on sensory neurons in zebrafish. Bisphenol F (BPF) exposure led to inhibited locomotion, reduced moving distance, and central nervous system (CNS) cell apoptosis, indicating neurotoxicity . MPTP, MPP+, and rotenone exposure caused dopaminergic (DAnergic) cell loss in the ventral diencephalon (vDC) region, resulting in motor deficits . Diisopropylfluorophosphate (DFP) exposure caused CNS neuron hyperactivation, increased neuronal apoptosis, and altered glutamatergic/GABAergic synaptic activity . However, zebrafish did not show neurological abnormalities or changes in phosphatidylcholines (PCs), lysophosphatidylcholines (LPCs), and glycerolphosphocholine (GPC) profiles after exposure to neuropathic organophosphorus compounds (OPs) . Additionally, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) exposure induced mitochondrial fragmentation in dopaminergic neurons and activated the pink1/parkin pathway involved in mitophagy .

Answers from top 5 papers

More filters
Papers (5)Insight
The provided paper does not specifically mention the impact of neurotoxins on sensory neurons in zebrafish.
The paper does not specifically mention the impact of neurotoxins on sensory neurons in zebrafish. The paper focuses on the impact of the neurotoxin MPTP on dopaminergic neurons, mitochondrial fragmentation, and sensorimotor impairments in adult zebrafish.
The provided paper does not specifically mention the impact of neurotoxins on sensory neurons in zebrafish.
The provided paper does not mention the impact of neurotoxins on sensory neurons in zebrafish.
The provided paper does not mention the impact of neurotoxins on sensory neurons in zebrafish.

Related Questions

What are the affects of neurotoxins on elders?5 answersNeurotoxins can have significant impacts on elderly individuals due to various factors such as decreased hepatic metabolizing capacity, renal clearance, and changes in the central nervous system. Exposure to neurotoxicants can lead to neuronal loss, altered neurotransmitter levels, and decreased adaptability to xenobiotics, making the elderly more susceptible to neurologic dysfunction. A diagnostic blood test panel can help assess neurotoxin levels in the blood, including aluminum, arsenic, lead, mercury, and manganese, which can damage the brain, while selenium within a certain range acts protectively. Additionally, certain dietary neurotoxins can contribute to neurotoxicity in humans, affecting the nervous system's function and structure, with over a thousand chemicals reported to have neurotoxic effects. Despite lacking Phase III clinical trial data, a notable percentage of neurotoxin treatments for esthetic purposes in older individuals were observed internationally in 2020.
What alterations do zebrafish models with Parkinsonism present?4 answersZebrafish models with Parkinsonism present several alterations. Chronic exposure to manganese chloride (MnCl2) leads to non-motor and motor PD-like symptoms, including reduced locomotory activity, anxiety, depression-like behavior, and olfactory dysfunction. Rotenone treatment in zebrafish results in decreased dopamine release and uptake, impaired latent learning, and diminished locomotor activity. In a zebrafish PD model induced by 6-hydroxydopamine (6-OHDA), a reduction in electric-induced locomotor activity and tyrosine hydroxylase (TH) expression levels was observed. Another study using rotenone exposure in zebrafish found dysregulated dopamine-related gene expression, reduced dopamine levels, and upregulation of genes involved in T cell receptor signaling, microgliosis regulation, cellular response to IL-1, and apoptotic signaling pathways. These alterations in zebrafish models provide insights into the pathogenesis of Parkinson's disease and can be used for studying experimental parkinsonism and screening potential therapies.
Has aversive stimuli been studied on zebrafish?5 answersAversive stimuli have been studied on zebrafish. One study assessed the repeatability of aversive learning in zebrafish by conditioning them to avoid a color cue associated with a mild electric shock. The results showed that zebrafish did not display consistent individual differences in aversive learning across different color conditions. Another study designed a fear-conditioning paradigm in which zebrafish were familiarized with a fear-eliciting stimulus represented by robotic zebrafish replicas. The zebrafish displayed a marked avoidance of the stimulus-paired compartment, indicating fear conditioning. Ethanol administration was found to abolish the conditioned avoidance response. Additionally, another study found that larval zebrafish exhibited a form of behavioral sensitization in response to an aversive chemical stimulus, resulting in enhanced locomotion and elevated heart rate. This sensitization persisted for at least 30 minutes and was associated with enhanced neural activity in a specific brain area.
How many neurons are in a zebrafish brain?2 answers
What are neuron poisons called?4 answers
What will happen if your motor neurons are exposed to Dendrotoxin?7 answers

See what other people are reading

Downregulated mitophagy and persistent dysfunctional mitochondria
5 answers
Persistent dysfunctional mitochondria due to downregulated mitophagy can lead to cellular dysfunction and disease progression. Mitophagy, a selective autophagy process, is crucial for removing damaged mitochondria to maintain cellular homeostasis. In conditions like prion diseases, where mitophagy is impaired, there is an accumulation of damaged mitochondria due to deficiencies in PINK1-parkin-mediated mitophagy. Additionally, factors like increased reactive oxygen species levels can induce Parkin-dependent mitophagy, but downregulation of mitophagy-associated proteins like OPTN, NDP52, and MFN2 can hinder this process, leading to the persistence of dysfunctional mitochondria. Therefore, restoring proper mitophagy mechanisms through interventions that stimulate mitophagy may offer therapeutic potential for conditions associated with downregulated mitophagy and the accumulation of dysfunctional mitochondria.
What are different bacteria tha cause botulism?
5 answers
Clostridium botulinum is the primary bacterium responsible for causing botulism, producing eight serotypes of botulinum neurotoxin (BoNT) labeled A-H. Additionally, Clostridium baratii and Clostridium butyricum can also produce botulinum neurotoxins. A comparative genomic study revealed that Clostridium botulinum Group I and Clostridium sporogenes are closely related bacteria that contribute to foodborne, infant, and wound botulism. Furthermore, a multiplex PCR assay was developed to differentiate between Clostridium botulinum Group I, C. sporogenes, and two major subgroups within Clostridium botulinum Group II, aiding in the identification of these botulism-causing bacteria. Therefore, Clostridium botulinum, along with related species like Clostridium baratii and Clostridium butyricum, are the key bacteria associated with botulism cases in both humans and animals.
Are there health benefits of eating lions mane mushrooms?
5 answers
Eating Lion's Mane mushrooms, scientifically known as Hericium erinaceus, offers various health benefits supported by research. These mushrooms are rich in bioactive compounds like hericenones, erinacines, and polysaccharides, which have neuroprotective, antioxidant, and immunomodulating properties. Studies suggest that Lion's Mane mushrooms can aid in improving memory, modulating stress responses, and potentially treating neurological disorders like Alzheimer's disease and post-traumatic brain injury. Additionally, Lion's Mane mushrooms have shown antimicrobial effects against various pathogens, including Staphylococcus aureus, Escherichia coli, and Candida albicans, indicating potential benefits in combating infections. Overall, incorporating Lion's Mane mushrooms into the diet may offer a range of health advantages, particularly in supporting brain health, immunity, and overall well-being.
Dose GSK3368715 been treated on neuronal cells
5 answers
GSK3368715 has not been specifically mentioned in the provided contexts. However, related compounds like GSK2606414, GSK3β inhibitors, and GSK2981710 have been studied in neuronal cells. GSK2606414, a PERK inhibitor, showed neuroprotective effects against high glucose-induced neurotoxicity in neuroblastoma cells. GSK3β inhibition affected organoid development, influencing cell survival, proliferation, and differentiation in cerebral organoids. Additionally, GSK-3beta inhibition was found to protect against MPP(+)-induced neurotoxicity by regulating mitochondrial functions in neuronal cell models. On the other hand, GSK2981710, a medium-chain triglyceride, did not significantly impact cognitive function or neuronal activity in healthy older adults. Although GSK3368715 specifically was not studied, these related compounds provide insights into the effects of similar compounds on neuronal cells.
How does dendritic spine density change following treatment with various factors?
5 answers
Following treatment with different factors, dendritic spine density undergoes distinct changes. Chronic cocaine exposure leads to a shift from smaller to larger diameter spines. In Parkinson's disease models induced by MPTP, a reduction in dendritic spine density of striatal medium spiny neurons is observed, associated with altered expression of serum-induced kinase (SNK) and spine-associated Rap guanosine triphosphatase (SPAR). Chronic corticosterone exposure decreases spine density in the hippocampus, correlating with the onset of depression, while fluoxetine treatment reverses this decrease. Olfactory bulbectomy reduces spine density in hippocampal regions, which can be reversed by antidepressant treatment, while neonatal clomipramine administration and maternal deprivation do not affect spine density. In a parkinsonism model, significant changes in spine density and perisomatic GABAergic boutons density are observed in medium spiny neurons, indicating structural modifications after nigrostriatal denervation and l-DOPA treatment.
What is the oral dose of carbon monoxide for therapy?
7 answers
The therapeutic application of carbon monoxide (CO) via oral administration has been explored in various research contexts, demonstrating its potential across a range of diseases, including inflammatory conditions, sickle cell disease (SCD), ulcerative colitis (UC), acute kidney injury (AKI), and Parkinson's disease (PD), as well as in cancer therapy. The dosing regimens and formulations have varied depending on the specific therapeutic target and delivery method being investigated. For instance, in the context of treating SCD, a liquid CO formulation named HBI-002 was administered by gavage at a dose of 10 ml/kg once daily to transgenic mouse models of SCD, showing significant anti-inflammatory effects and improvement in hemoglobin levels and red blood cell counts. Similarly, in PD models, an oral CO drug product, also referred to as HBI-002, was administered at the same dose of 10 ml/kg daily by gavage, demonstrating neuroprotective effects by reducing cell death and pathology associated with PD. In the development of oral CO delivery systems, various strategies have been employed to ensure safety and efficacy. One approach involved designing an oral CO releasing system (OCORS) that allows for tunable CO release into the gastrointestinal tract while preventing systemic exposure and ensuring that only the therapeutic CO is released. Another strategy involved immobilizing organic CO prodrugs to silica microparticles, aiming to minimize systemic exposure to the prodrug and its carrier portion while still delivering CO therapeutically. For UC treatment, a dextran-functionalized PLGA nanocarrier was developed for the co-delivery of CO and andrographolide, a compound with anti-inflammatory properties, demonstrating synergistic anti-inflammatory and pro-resolving effects in a colitis model. In the context of AKI, the therapeutic potential of CO was highlighted without specifying a particular dose, emphasizing its cytoprotective and immunomodulatory effects. Research into CO's role in cancer therapy has also been explored, focusing on its physiological regulatory function and the development of CO-related nano-drugs, without detailing specific oral dosages. Emerging delivery strategies based on nanomaterials for CO therapy have been proposed to overcome challenges related to target selectivity and toxicity at high concentrations, suggesting a promising future for CO's therapeutic applications. Additionally, there are indications of dosing regimens for CO administration in various treatments and methods for enhancing organ function post-transplant, although specific dosages are not detailed. In summary, while the specific oral dose of CO for therapy can vary depending on the disease model and delivery system, a dose of 10 ml/kg daily by gavage has been utilized in research for treating SCD and PD, with other studies employing different strategies for CO delivery and dosing regimens tailored to their respective therapeutic goals.
What is the current understanding of the molecular mechanisms underlying facial palsy botulinum toxin?
5 answers
The current understanding of the molecular mechanisms underlying facial palsy caused by botulinum toxin involves its unique mode of action at peripheral nerve terminals. Botulinum neurotoxins (BoNTs) are highly potent toxins that inhibit neurotransmitter release, leading to paralysis. They enter nerve terminals, cleave SNARE proteins, and block acetylcholine release, causing muscle weakness. BoNTs exhibit specificity in binding, limiting their action to targeted areas, making them valuable for treating conditions like facial palsy. Molecular dynamics simulations have shown that BoNT/F1 interacts with glycosylated human synaptic vesicle glycoprotein A (SV2A) through N-glycan moieties, unlike BoNT/A1, which interacts with protein content. Understanding these mechanisms is crucial for developing therapeutic interventions and inhibitors.
Dopamine transporter glycosylation correlates with the vulnerability of midbrain dopaminergic cells in Parkinson's disease
5 answers
Glycosylation of the dopamine transporter (DAT) is not directly addressed in the provided contexts. However, the studies highlight the significance of DAT activity in the vulnerability of midbrain dopaminergic cells in Parkinson's disease. The expression levels of DAT mRNA and protein are closely related to the susceptibility of these cells to neurotoxins. Additionally, alterations in protein glycation have been linked to neuronal dysfunction in synucleinopathies, impacting motor and cognitive functions. While glycation-induced dysfunction is explored, the direct correlation between DAT glycosylation and vulnerability of midbrain dopaminergic cells in Parkinson's disease is not explicitly discussed in the provided research.
What effect is HDAC6 deficiency on brain?
5 answers
HDAC6 deficiency has diverse effects on the brain. Studies show that HDAC6 knockout mice exhibit hyperactivity and anxiety, along with moderate alterations in Parkinson's disease pathology, such as slight alleviation of motor injury. Additionally, HDAC6 inhibition in the context of intracerebral hemorrhage (ICH) leads to resistance against oxidative stress and neuronal apoptosis, with a mechanism involving the acetylation of Malate dehydrogenase 1 (MDH1). Furthermore, dysfunction of HDAC6 contributes to deficits in neurogenesis post-stroke, affecting dendritic maturation of newly generated neurons and hindering functional recovery, which can be improved through HDAC6 suppression. In Alzheimer's disease models, reducing HDAC6 levels restores learning and memory by rendering neurons resistant to amyloid-β-mediated impairment of mitochondrial trafficking. These findings collectively highlight the significant impact of HDAC6 deficiency on various brain functions and pathologies.
What are the specific mechanisms by which morphine affects the development and survival of larvae?
4 answers
Morphine affects the development and survival of larvae through various mechanisms. In zebrafish embryos, morphine treatment improved mortality rates, hatching rates, locomotor activity, and antioxidant enzyme activities altered by 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) exposure. Additionally, morphine presence in rabbit tissues was found to retard larval development rate but accelerate puparial development rate in Chrysomya albiceps, affecting the postmortem interval estimation. Furthermore, oral morphine consumption by parents in Drosophila Melanogaster led to changes in larvae, pupae, and imago development stages, indicating an impact on the overall life cycle of the species. These findings collectively highlight the diverse ways in which morphine influences larval development and survival across different species and experimental setups.
How does morphine affect the development and survival of larvae at a molecular level?
4 answers
Morphine has varying effects on larvae at a molecular level. Studies on zebrafish embryos exposed to morphine show that it can regulate the survival and death of neurons, impacting developmental parameters, locomotor activity, and gene expressions related to neuronal health. In Drosophila Melanogaster, oral morphine consumption by parents affects larval development, pupation, and imago stages, indicating a disruption in the development process. Additionally, chronic exposure to morphine in zebrafish CNS leads to altered gene expressions related to neuronal development, neurotransmission, and CNS patterning, suggesting potential impacts on neuronal differentiation and function. These findings collectively highlight the complex molecular mechanisms through which morphine influences the development and survival of larvae.