alpha7 Nicotinic Acetylcholine Receptor
Bicyclo Compounds, Heterocyclic
Cobra Neurotoxin Proteins
Dose-Response Relationship, Drug
Molecular Sequence Data
Amino Acid Sequence
Vesicular Acetylcholine Transport Proteins
Drug Partial Agonism
Tobacco Use Disorder
Ion Channel Gating
Receptor, Muscarinic M1
Receptors, Serotonin, 5-HT3
Myasthenic Syndromes, Congenital
Receptor, Muscarinic M3
Receptor, Muscarinic M2
Quaternary Ammonium Compounds
Epilepsy, Frontal Lobe
Protein Structure, Tertiary
Myasthenia Gravis, Autoimmune, Experimental
Receptor, Muscarinic M4
Ventral Tegmental Area
Substance Withdrawal Syndrome
Protein Structure, Secondary
Gene Expression Regulation
Parasympathetic Nervous System
Neuromuscular Blocking Agents
Recombinant Fusion Proteins
Sequence Homology, Amino Acid
Receptor, Muscarinic M5
Neuromuscular Nondepolarizing Agents
Selective effects of a 4-oxystilbene derivative on wild and mutant neuronal chick alpha7 nicotinic receptor. (1/725)1. We assessed the pharmacological activity of triethyl-(beta-4-stilbenoxy-ethyl) ammonium (MG624), a drug that is active on neuronal nicotinic receptors (nicotinic AChR). Experiments on the major nicotinic AChR subtypes present in chick brain, showed that it inhibits the binding of [125I]-alphaBungarotoxin (alphaBgtx) to the alpha7 subtype, and that of [3H]-epibatidine (Epi) to the alpha4beta2 subtype, with Ki values of respectively 106 nM and 84 microM. 2. MG624 also inhibited ACh elicited currents (I(ACh)) in the oocyte-expressed alpha7 and alpha4beta2 chick subtypes with half-inhibitory concentrations (IC50) of respectively 109 nM and 3.2 microM. 3. When tested on muscle-type AChR, it inhibited [125I]-alphaBgtx binding with a Ki of 32 microM and ACh elicited currents (I(ACh)) in the oocyte-expressed alpha1beta1gammadelta chick subtype with an IC50 of 2.9 microM. 4. The interaction of MG624 with the alpha7 subtype was investigated using an alpha7 homomeric mutant receptor with a threonine-for-leucine 247 substitution (L247T alpha7). MG624 did not induce any current in oocytes expressing the wild type alpha7 receptor, but did induce large currents in the oocyte-expressed L247T alpha7 receptor. The MG624 elicited current (I(MG62)) has an EC50 of 0.2 nM and a Hill coefficient nH of 1.9, and is blocked by the nicotinic receptor antagonist methyllycaconitine (MLA). 5. These binding and electrophysiological studies show that MG624 is a potent antagonist of neuronal chick alpha7 nicotinic AChR, and becomes a competitive agonist following the mutation of the highly conserved leucine residue 247 located in the M2 channel domain. (+info)
Pairwise interactions between neuronal alpha7 acetylcholine receptors and alpha-conotoxin ImI. (2/725)The present work uses alpha-conotoxin ImI (CTx ImI) to probe the neurotransmitter binding site of neuronal alpha7 acetylcholine receptors. We identify key residues in alpha7 that contribute to CTx ImI affinity, and use mutant cycles analysis to identify pairs of residues that stabilize the receptor-conotoxin complex. We first mutated key residues in the seven known loops of alpha7 that converge at the subunit interface to form the ligand binding site. The mutant subunits were expressed in 293 HEK cells, and CTx ImI binding was measured by competition against the initial rate of 125I-alpha-bungarotoxin binding. The results reveal a predominant contribution by Tyr-195 in alpha7, accompanied by smaller contributions by Thr-77, Tyr-93, Asn-111, Gln-117, and Trp-149. Based upon our previous identification of bioactive residues in CTx ImI, we measured binding of receptor and toxin mutations and analyzed the results using thermodynamic mutant cycles. The results reveal a single dominant interaction between Arg-7 of CTx ImI and Tyr-195 of alpha7 that anchors the toxin to the binding site. We also find multiple weak interactions between Asp-5 of CTx ImI and Trp-149, Tyr-151, and Gly-153 of alpha7, and between Trp-10 of CTx ImI and Thr-77 and Asn-111 of alpha7. The overall results establish the orientation of CTx ImI as it bridges the subunit interface and demonstrate close approach of residues on opposing faces of the alpha7 binding site. (+info)
alpha-bungarotoxin receptors contain alpha7 subunits in two different disulfide-bonded conformations. (3/725)Neuronal nicotinic alpha7 subunits assemble into cell-surface complexes that neither function nor bind alpha-bungarotoxin when expressed in tsA201 cells. Functional alpha-bungarotoxin receptors are expressed if the membrane-spanning and cytoplasmic domains of the alpha7 subunit are replaced by the homologous regions of the serotonin-3 receptor subunit. Bgt-binding surface receptors assembled from chimeric alpha7/serotonin-3 subunits contain subunits in two different conformations as shown by differences in redox state and other features of the subunits. In contrast, alpha7 subunit complexes in the same cell line contain subunits in a single conformation. The appearance of a second alpha7/serotonin-3 subunit conformation coincides with the formation of alpha-bungarotoxin-binding sites and intrasubunit disulfide bonding, apparently within the alpha7 domain of the alpha7/serotonin-3 chimera. In cell lines of neuronal origin that produce functional alpha7 receptors, alpha7 subunits undergo a conformational change similar to alpha7/serotonin-3 subunits. alpha7 subunits, thus, can fold and assemble by two different pathways. Subunits in a single conformation assemble into nonfunctional receptors, or subunits expressed in specialized cells undergo additional processing to produce functional, alpha-bungarotoxin-binding receptors with two alpha7 conformations. Our results suggest that alpha7 subunit diversity can be achieved postranslationally and is required for functional homomeric receptors. (+info)
Minimal conformation of the alpha-conotoxin ImI for the alpha7 neuronal nicotinic acetylcholine receptor recognition: correlated CD, NMR and binding studies. (4/725)The alpha-ImI conotoxin, a selective potent inhibitor of the mammalian neuronal alpha7 nicotinic acetylcholine receptor (n-AchR), was shown by point mutation or by L-alanine scanning to display two regions essential for bioactivity: the active site Asp5-Pro6-Arg7 in the first loop and Trp10 in the second loop. The deletion of the Cys3,Cys12 disulfide bond in the alpha-ImI scaffold, e.g. peptide II, had no effect on its binding affinity. CD spectra, NMR studies and structure calculations were carried out on the wild type alpha-ImI, the weakest analog (R7A) and peptide II (equipotent to alpha-ImI) in order to point out the conformational differences between these compounds. Then, an attempt to correlate the conformational data and the affinity results was proposed. CD and NMR data were identical for the R7A analog and alpha-ImI, revealing the crucial functional role of the Arg7 side chain. On the other hand, the scaffold of the first loop in peptide II was shown by NMR to represent the minimal conformation for the optimal interaction of the toxin with the neuronal alpha7 n-AchR. Last, the beta-turn forming property of the 6th residue (Pro) in the active site of the alpha-ImI can be correlated with its affinity. (+info)
Alpha7 nicotinic receptor subunits are not necessary for hippocampal-dependent learning or sensorimotor gating: a behavioral characterization of Acra7-deficient mice. (5/725)The alpha7 nicotinic acetylcholine receptor (nAChR) subunit is abundantly expressed in the hippocampus and contributes to hippocampal cholinergic synaptic transmission suggesting that it may contribute to learning and memory. There is also evidence for an association between levels of alpha7 nAChR and in sensorimotor gating impairments. To examine the role of alpha7 nAChRs in learning and memory and sensorimotor gating, Acra7 homozygous mutant mice and their wild-type littermates were tested in a Pavlovian conditioned fear test, for spatial learning in the Morris water task, and in the prepulse inhibition paradigm. Exploratory activity, motor coordination, and startle habituation were also evaluated. Acra7 mutant mice displayed the same levels of contextual and auditory-cue condition fear as wild-type mice. Similarly, there were no differences in spatial learning performance between mutant and wild-type mice. Finally, Acra7 mutant and wild-type mice displayed similar levels of prepulse inhibition. Other behavioral responses in Acra7 mutant mice were also normal, except for an anxiety-related behavior in the open-field test. The results of this study show that the absence of alpha7 nAChRs has little impact on normal, base-line behavioral responses. Future studies will examine the contribution of alpha7 nAChR to the enhancement of learning and sensorimotor gating following nicotine treatments. (+info)
Cell-free expression and functional reconstitution of homo-oligomeric alpha7 nicotinic acetylcholine receptors into planar lipid bilayers. (6/725)The alpha7 nicotinic acetylcholine receptor (nAChR) is a ligand-gated ion channel that modulates neurotransmitter release in the central nervous system. We show here that functional, homo-oligomeric alpha7 nAChRs can be synthesized in vitro with a rabbit reticulocyte lysate translation system supplemented with endoplasmic reticulum microsomes, reconstituted into planar lipid bilayers, and evaluated using single-channel recording techniques. Because wild-type alpha7 nAChRs desensitize rapidly, we used a nondesensitizing form of the alpha7 receptor with mutations in the second transmembrane domain (S2'T and L9'T) to record channel activity in the continuous presence of agonist. Endoglycosidase H treatment of microsomes containing nascent alpha7 S2'T/L9'T nAChRs indicated that the receptors were glycosylated. A proteinase K protection assay revealed a 36-kDa fragment in the ER lumen, consistent with a large extracellular domain predicted by most topological models, indicating that the protein was folded integrally through the ER membrane. alpha7 S2'T/L9'T receptors reconstituted into planar lipid bilayers had a unitary conductance of approximately 50 pS, were highly selective for monovalent cations over Cl(-), were nonselective between K(+) and Na(+), and were blocked by alpha-bungarotoxin. This is the first demonstration that a functional ligand-gated ion channel can be synthesized using an in vitro expression system. (+info)
Strychnine activates neuronal alpha7 nicotinic receptors after mutations in the leucine ring and transmitter binding site domains. (7/725)Recent work has shown that strychnine, the potent and selective antagonist of glycine receptors, is also an antagonist of nicotinic acetylcholine (AcCho) receptors including neuronal homomeric alpha7 receptors, and that mutating Leu-247 of the alpha7 nicotinic AcCho receptor-channel domain (L247Talpha7; mut1) converts some nicotinic antagonists into agonists. Therefore, a study was made of the effects of strychnine on Xenopus oocytes expressing the chick wild-type alpha7 or L247Talpha7 receptors. In these oocytes, strychnine itself did not elicit appreciable membrane currents but reduced the currents elicited by AcCho in a reversible and dose-dependent manner. In sharp contrast, in oocytes expressing L247Talpha(7) receptors with additional mutations at Cys-189 and Cys-190, in the extracellular N-terminal domain (L247T/C189-190Salpha7; mut2), micromolar concentrations of strychnine elicited inward currents that were reversibly inhibited by the nicotinic receptor blocker alpha-bungarotoxin. Single-channel recordings showed that strychnine gated mut2-channels with two conductance levels, 56 pS and 42 pS, and with kinetic properties similar to AcCho-activated channels. We conclude that strychnine is a modulator, as well as an activator, of some homomeric nicotinic alpha7 receptors. After injecting oocytes with mixtures of cDNAs encoding mut1 and mut2 subunits, the expressed hybrid receptors were activated by strychnine, similar to the mut2, and had a high affinity to AcCho like the mut1. A pentameric symmetrical model yields the striking conclusion that two identical alpha7 subunits may be sufficient to determine the functional properties of alpha7 receptors. (+info)
Nicotinic receptor activation in human cerebral cortical interneurons: a mechanism for inhibition and disinhibition of neuronal networks. (8/725)Cholinergic control of the activity of human cerebral cortical circuits has long been thought to be accounted for by the interaction of acetylcholine (ACh) with muscarinic receptors. Here we report the discovery of functional nicotinic receptors (nAChRs) in interneurons of the human cerebral cortex and discuss the physiological and clinical implications of these findings. The whole-cell mode of the patch-clamp technique was used to record responses triggered by U-tube application of the nonselective agonist ACh and of the alpha7-nAChR-selective agonist choline to interneurons visualized by means of infrared-assisted videomicroscopy in slices of the human cerebral cortex. Choline induced rapidly desensitizing whole-cell currents that, being sensitive to blockade by methyllycaconitine (MLA; 50 nM), were most likely subserved by an alpha7-like nAChR. In contrast, ACh evoked slowly decaying whole-cell currents that, being sensitive to blockade by dihydro-beta-erythroidine (DHbetaE; 10 microM), were most likely subserved by an alpha4beta2-like nAChR. Application of ACh (but not choline) to the slices also triggered GABAergic postsynaptic currents (PSCs). Evidence is provided that ACh-evoked PSCs are the result of activation of alpha4beta2-like nAChRs present in preterminal axon segments and/or in presynaptic terminals of interneurons. Thus, nAChRs can relay inhibitory and/or disinhibitory signals to pyramidal neurons and thereby modulate the activity of neuronal circuits in the human cerebral cortex. These mechanisms, which appear to be retained across species, can account for the involvement of nAChRs in cognitive functions and in certain neuropathological conditions. (+info)
The symptoms of myasthenia gravis can vary in severity and may include:
* Weakness in the arms and legs
* Fatigue and muscle tiredness
* Difficulty swallowing (dysphagia)
* Difficulty speaking or slurred speech (dysarthria)
* Drooping eyelids (ptosis)
* Double vision (diplopia)
* Weakness in the muscles of the face, arms, and legs
The exact cause of myasthenia gravis is not known, but it is believed to be an autoimmune disorder, meaning that the body's immune system mistakenly attacks healthy tissues. It can also be caused by other medical conditions such as thyroid disease, vitamin deficiencies, or infections.
There is no cure for myasthenia gravis, but there are various treatments available to manage the symptoms and improve quality of life. These include:
* Medications such as corticosteroids, immunosuppressants, and cholinesterase inhibitors
* Plasmapheresis, a procedure that removes harmful antibodies from the blood
* Intravenous immunoglobulin (IVIG), which contains antibodies that can help block the immune system's attack on the nerve-muscle junction
* Surgery to remove the thymus gland, which is believed to play a role in the development of myasthenia gravis
It is important for individuals with myasthenia gravis to work closely with their healthcare provider to manage their symptoms and prevent complications. With proper treatment and self-care, many people with myasthenia gravis are able to lead active and fulfilling lives.
Tobacco use disorder refers to a condition where an individual engages in the excessive and compulsive consumption of tobacco products, despite the negative consequences it may have on their health and well-being. Tobacco use disorder is a common condition that affects millions of people worldwide, and it is characterized by a pattern of continued tobacco use despite harmful effects, as well as an increased tolerance to tobacco and withdrawal symptoms when trying to stop.
The Diagnostic and Statistical Manual of Mental Disorders (DSM-5) defines tobacco use disorder as a chronic condition that can manifest in different forms, including nicotine dependence and tobacco abuse. The criteria for diagnosing tobacco use disorder include:
1. Tolerance: A need to use more tobacco to achieve the desired effect.
2. Withdrawal: Experiencing symptoms such as irritability, anxiety, or depression when trying to stop using tobacco.
3. Loss of control: Consuming more tobacco than intended or for longer periods than intended.
4. Negative consequences: Continuing to use tobacco despite social, physical, or psychological problems caused by its use.
5. Increased time and effort spent on using tobacco.
6. Craving or a strong desire to use tobacco.
7. Failure to control or reduce tobacco use.
Tobacco use disorder can have severe consequences, including lung cancer, heart disease, respiratory problems, and other health issues. It can also lead to social and economic problems, such as lost productivity and strained relationships with family and friends. Treatment for tobacco use disorder includes behavioral therapies, medications, and support groups, and it is important for individuals struggling with this condition to seek professional help to quit using tobacco and improve their overall health and well-being.
There are several different types of congenital myasthenic syndromes, each with its own unique set of symptoms and characteristics. Some of the most common include:
* Congenital myasthenic syndrome type 1 (CMS1): This is the most common type of CMS and is caused by a mutation in the CHRNA1 gene. It is characterized by muscle weakness, poor feeding, and delays in development.
* Congenital myasthenic syndrome type 2 (CMS2): This type is caused by a mutation in the CHRNB1 gene and is characterized by muscle weakness, cognitive impairment, and seizures.
* Congenital myasthenic syndrome type 3 (CMS3): This type is caused by a mutation in the MAP2 gene and is characterized by muscle weakness, developmental delays, and intellectual disability.
There is currently no cure for congenital myasthenic syndromes, but various treatments can help manage the symptoms. These may include physical therapy, occupational therapy, speech therapy, and medications such as acetylcholinesterase inhibitors and steroids. In some cases, a bone marrow transplant may be necessary.
The prognosis for individuals with congenital myasthenic syndromes varies depending on the specific type and severity of the disorder. Some individuals may have mild symptoms and lead relatively normal lives, while others may have more severe symptoms and require ongoing medical care and support. With appropriate treatment and management, many individuals with CMS can lead fulfilling lives.
The frontal lobe is responsible for several higher-level cognitive functions, including decision-making, planning, and problem-solving. Therefore, FLE can significantly impact an individual's quality of life, particularly in terms of cognitive and behavioral functioning.
There are two main types of FLE:
1. Localization-related FLE: This type of epilepsy is characterized by seizures that arise from a specific location within the frontal lobe. The seizures may be limited to one side of the brain or may involve both sides.
2. Non-localization related FLE: This type of epilepsy is characterized by seizures that do not have a specific localization within the frontal lobe. Instead, the seizures may involve multiple areas of the frontal lobe or may be widespread throughout the brain.
The symptoms of FLE can vary depending on the location and extent of the seizure activity in the frontal lobe. Some common symptoms include:
* Confusion and disorientation
* Memory loss or difficulty with memory formation
* Difficulty with attention and concentration
* Slowing down of mental processing
* Impaired decision-making and problem-solving abilities
* Changes in mood or behavior, such as irritability or apathy
* Muscle weakness or stiffness
* Involuntary movements or tremors
FLE can be diagnosed using a variety of imaging techniques, such as electroencephalography (EEG), magnetic resonance imaging (MRI), and positron emission tomography (PET). Treatment options for FLE include medications, such as anticonvulsants and mood stabilizers, and surgical interventions, such as cortical resection or temporal lobectomy.
In summary, frontal lobe epilepsy is a complex condition that can have a significant impact on an individual's quality of life. It is important for individuals with FLE to work closely with their healthcare providers to develop a treatment plan that addresses their specific needs and helps to manage their symptoms. With appropriate treatment, many individuals with FLE are able to lead fulfilling lives.
Experimental myasthenia gravis refers to a type of myasthenia gravis that is caused by experimental or artificial means, such as through the use of drugs or other substances that mimic or trigger an immune response. This type of myasthenia gravis is often used in research settings to study the underlying mechanisms of the disease and to test new treatments.
Autoimmune myasthenia gravis, on the other hand, refers to a type of myasthenia gravis that is caused by an abnormal immune response, where the immune system mistakenly attacks the acetylcholine receptors at the neuromuscular junction. This type of myasthenia gravis is more common than experimental myasthenia gravis and can be caused by a variety of factors, such as genetic predisposition, infections, or environmental triggers.
Overall, myasthenia gravis, autoimmune, and experimental refer to different aspects of the disease, with each term having its own specific meaning and application in the medical field.
* Muscle and bone pain
* Nausea and vomiting
* Seizures (in severe cases)
The specific symptoms of substance withdrawal syndrome can vary depending on the substance being withdrawn from, but some common symptoms include:
* Alcohol: tremors, anxiety, insomnia, nausea and vomiting, headaches, and seizures
* Opioids: withdrawal symptoms can include anxiety, muscle aches, sweating, nausea and vomiting, diarrhea, and depression
* Benzodiazepines: withdrawal symptoms can include anxiety, insomnia, tremors, and seizures
The diagnosis of substance withdrawal syndrome is typically made based on the patient's history of substance use and the presence of withdrawal symptoms. A healthcare provider may also order laboratory tests to rule out other conditions that may be causing the symptoms. Treatment for substance withdrawal syndrome usually involves supportive care, such as rest, hydration, and pain management, as well as medication to manage withdrawal symptoms. In some cases, medical professionals may also recommend a gradual tapering of the substance over a period of time to minimize withdrawal symptoms.
It is important for individuals who are experiencing withdrawal symptoms to seek medical attention as soon as possible, as untreated withdrawal can lead to serious complications, such as seizures and dehydration. With appropriate treatment, most individuals with substance withdrawal syndrome can recover fully and successfully overcome their addiction.
1. Difficulty regulating body temperature, leading to episodes of hyperthermia (elevated body temperature) or hypothermia (low body temperature).
2. Abnormal heart rate and rhythm, including bradycardia (slow heart rate) or tachycardia (fast heart rate).
3. Poor digestion and gastrointestinal problems such as constipation, diarrhea, nausea, and vomiting.
4. Difficulty swallowing, which can lead to respiratory problems.
5. Orthostatic intolerance, which can cause dizziness, lightheadedness, or fainting when standing up.
6. Seizures and other neurological symptoms such as tremors, muscle weakness, and loss of coordination.
7. Cognitive impairment, including developmental delays, intellectual disability, and learning disabilities.
8. Sleep disturbances, including insomnia and sleep apnea.
9. Emotional difficulties such as anxiety, depression, and mood swings.
10. Vision problems, including blurred vision, double vision, and light sensitivity.
Primary dysautonomias are caused by genetic mutations that affect the development or function of the autonomic nervous system. There are several subtypes of primary dysautonomias, each with distinct symptoms and characteristics. These conditions are rare and can be difficult to diagnose, as they often resemble other more common conditions such as anxiety disorders or attention deficit hyperactivity disorder (ADHD). Treatment for primary dysautonomias typically involves a combination of medication and lifestyle modifications, such as reducing stress, increasing fluid intake, and avoiding overexertion. In some cases, surgery may be necessary to correct anatomical abnormalities or to implant medical devices that help regulate the autonomic nervous system.
Some common autoimmune diseases of the nervous system include:
1. Multiple sclerosis (MS): A chronic condition that affects the brain, spinal cord, and optic nerves, causing a range of symptoms including numbness, weakness, and vision problems.
2. Neuromyelitis optica (NMO): A rare condition that causes inflammation in the optic nerves and spinal cord, leading to vision loss and muscle weakness.
3. Guillain-Barré syndrome: A rare autoimmune disorder that causes muscle weakness and paralysis, often after a viral infection.
4. Chronic inflammatory demyelinating polyneuropathy (CIDP): A chronic condition that affects the peripheral nerves, causing numbness, weakness, and pain in the hands and feet.
5. Acute disseminated encephalomyelitis (ADEM): A rare condition that causes inflammation in the brain and spinal cord, leading to a range of symptoms including fever, headache, and muscle weakness.
The exact cause of autoimmune diseases of the nervous system is not fully understood, but they are believed to be triggered by a combination of genetic and environmental factors. Treatment options vary depending on the specific condition, but may include medications to reduce inflammation and modulate the immune system, as well as physical therapy and lifestyle modifications.
1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.
2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.
3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.
4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.
5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.
6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.
7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.
8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.
9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.
10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.
Mydriasis is a condition where the pupil remains dilated for an extended period, even in low light conditions. It can be caused by various factors such as injury to the head or eye, stroke, brain tumors, multiple sclerosis, and certain medications. Mydriasis can cause problems with vision, including blurred vision, double vision, and sensitivity to light. Treatment options for mydriasis depend on the underlying cause, but may include glasses or contact lenses to correct refractive errors, prism lenses to align images properly, or medications to reduce inflammation or treat underlying conditions.
Causes of Mydriasis
Mydriasis can be caused by a variety of factors, including:
1. Trauma to the head or eye: A blow to the head or a penetrating eye injury can cause mydriasis due to damage to the nerves that control pupil size.
2. Stroke or cerebral vasculature disorders: A stroke or other conditions that affect blood flow to the brain can cause mydriasis due to damage to the nerves that control pupillary constriction.
3. Brain tumors: Tumors in the brain, such as melanoma, can cause mydriasis by compressing or damaging the nerves that control pupil size.
4. Multiple sclerosis: This autoimmune disease can damage the nerves that control pupillary constriction, leading to mydriasis.
5. Medications: Certain medications, such as anticholinergic drugs and certain antihistamines, can cause mydriasis as a side effect.
Symptoms of Mydriasis
The symptoms of mydriasis may include:
1. Dilated pupils that do not constrict in response to light
2. Blurred vision or double vision
3. Sensitivity to light
4. Headaches or eye strain
5. Seeing halos around lights
6. Difficulty seeing at night or in low light conditions
7. Nausea and vomiting
Diagnosis of Mydriasis
To diagnose mydriasis, a comprehensive eye exam is necessary to rule out other causes of dilated pupils. The doctor may perform a series of tests to evaluate the function of the nervous system and the muscles that control pupillary constriction. These tests may include:
1. Pupillometry: This test measures the size of the pupils and their reaction to light.
2. Ophthalmoscopy: This test allows the doctor to visualize the inside of the eye and assess the function of the retina and optic nerve.
3. Eye movement testing: This test evaluates the muscles that control eye movement and their coordination with the pupillary constriction reflex.
4. Neurological exam: A neurological exam may be performed to rule out other conditions that can cause dilated pupils, such as brain tumors or multiple sclerosis.
Treatment of Mydriasis
The treatment of mydriasis depends on the underlying cause of the condition. In some cases, treating the underlying condition can resolve the mydriasis. Other treatments that may be used to manage mydriasis include:
1. Pupillary constriction medications: These medications can help reduce the size of dilated pupils and improve vision.
2. Prism glasses: In some cases, prism glasses may be prescribed to help align the visual fields and improve binocular vision.
3. Eye exercises: Eye exercises may be recommended to strengthen the muscles that control eye movement and improve coordination between the pupils.
4. Surgery: In rare cases, surgery may be necessary to treat mydriasis caused by a physical obstruction or other abnormality in the eye.
Prognosis of Mydriasis
The prognosis for mydriasis is generally good if the underlying cause is treated promptly and effectively. However, if the condition is left untreated, it can lead to complications such as:
1. Vision loss: Prolonged dilated pupils can lead to vision loss due to retinal damage or optic nerve damage.
2. Eye strain: Dilated pupils can cause eye strain and fatigue, which can lead to headaches and other symptoms.
3. Increased risk of eye injuries: Dilated pupils may increase the risk of eye injuries, as the pupil is more vulnerable to trauma when it is dilated.
4. Increased risk of infection: Dilated pupils may increase the risk of infection, as the pupil is more exposed to foreign substances and bacteria.
Prevention of Mydriasis
There are several steps you can take to help prevent mydriasis:
1. Get regular eye exams: Regular eye exams can help detect any underlying conditions that may be causing dilated pupils, such as cataracts or glaucoma.
2. Wear protective eyewear: Wearing protective eyewear, such as goggles or safety glasses, can help prevent eye injuries and reduce the risk of mydriasis.
3. Avoid exposure to bright lights: Bright lights can cause dilated pupils, so it is best to avoid exposure to bright lights, especially during the day.
4. Use artificial tears: Artificial tears can help keep the eyes moist and reduce the risk of mydriasis.
5. Get enough sleep: Getting enough sleep can help prevent eye strain and fatigue, which can lead to mydriasis.
6. Take breaks when working on a computer: Taking breaks when working on a computer can help reduce eye strain and fatigue, which can lead to mydriasis.
7. Use good lighting: Good lighting can help reduce eye strain and fatigue, which can lead to mydriasis.
8. Avoid smoking: Smoking can increase the risk of mydriasis, so it is best to avoid smoking.
9. Maintain good hygiene: Maintaining good hygiene, such as washing your hands frequently and avoiding sharing makeup or other products, can help prevent infection and reduce the risk of mydriasis.
Mydriasis is a common condition that can cause eye strain and fatigue, as well as increase the risk of eye injuries and infection. There are several steps you can take to prevent mydriasis, including avoiding smoking, getting enough sleep, using artificial tears, and taking breaks when working on a computer. Additionally, maintaining good hygiene and using good lighting can help reduce the risk of mydriasis. If you experience any symptoms of mydriasis, it is important to seek medical attention as soon as possible to prevent complications.
The term "schizophrenia" was first used by the Swiss psychiatrist Eugen Bleuler in 1908 to describe the splitting of mental functions, which he believed was a key feature of the disorder. The word is derived from the Greek words "schizein," meaning "to split," and "phrenos," meaning "mind."
There are several subtypes of schizophrenia, including:
1. Paranoid Schizophrenia: Characterized by delusions of persecution and suspicion, and a tendency to be hostile and defensive.
2. Hallucinatory Schizophrenia: Characterized by hearing voices or seeing things that are not there.
3. Disorganized Schizophrenia: Characterized by disorganized thinking and behavior, and a lack of motivation or interest in activities.
4. Catatonic Schizophrenia: Characterized by immobility, mutism, and other unusual movements or postures.
5. Undifferentiated Schizophrenia: Characterized by a combination of symptoms from the above subtypes.
The exact cause of schizophrenia is still not fully understood, but it is believed to involve a combination of genetic, environmental, and neurochemical factors. It is important to note that schizophrenia is not caused by poor parenting or a person's upbringing.
There are several risk factors for developing schizophrenia, including:
1. Genetics: A person with a family history of schizophrenia is more likely to develop the disorder.
2. Brain chemistry: Imbalances in neurotransmitters such as dopamine and serotonin have been linked to schizophrenia.
3. Prenatal factors: Factors such as maternal malnutrition or exposure to certain viruses during pregnancy may increase the risk of schizophrenia in offspring.
4. Childhood trauma: Traumatic events during childhood, such as abuse or neglect, have been linked to an increased risk of developing schizophrenia.
5. Substance use: Substance use has been linked to an increased risk of developing schizophrenia, particularly cannabis and other psychotic substances.
There is no cure for schizophrenia, but treatment can help manage symptoms and improve quality of life. Treatment options include:
1. Medications: Antipsychotic medications are the primary treatment for schizophrenia. They can help reduce positive symptoms such as hallucinations and delusions, and negative symptoms such as a lack of motivation or interest in activities.
2. Therapy: Cognitive-behavioral therapy (CBT) and other forms of talk therapy can help individuals with schizophrenia manage their symptoms and improve their quality of life.
3. Social support: Support from family, friends, and support groups can be an important part of the treatment plan for individuals with schizophrenia.
4. Self-care: Engaging in activities that bring pleasure and fulfillment, such as hobbies or exercise, can help individuals with schizophrenia improve their overall well-being.
It is important to note that schizophrenia is a complex condition, and treatment should be tailored to the individual's specific needs and circumstances. With appropriate treatment and support, many people with schizophrenia are able to lead fulfilling lives and achieve their goals.
Types of NMJ Diseases:
1. Myasthenia Gravis (MG): An autoimmune disorder that causes muscle weakness and fatigue due to the immune system attacking the NMJs.
2. Lambert-Eaton Myasthenic Syndrome (LEMS): A rare autoimmune disorder that affects the NMJ and can cause muscle weakness, fatigue, and other symptoms.
3. Congenital Myasthenic Syndromes (CMS): A group of rare genetic disorders that affect the development and function of the NMJ, leading to muscle weakness and other symptoms.
4. Neuronal Ceroid Lipofuscinosis (NCL): A group of rare genetic disorders that affect the nervous system and can cause muscle weakness, seizures, and vision loss.
5. Inflammatory Myopathies: A group of muscle disorders caused by inflammation, such as polymyositis or dermatomyositis, which can affect the NMJ and cause muscle weakness.
Symptoms of NMJ Diseases:
1. Muscle weakness or paralysis
2. Fatigue and exhaustion
3. Difficulty swallowing or breathing (in severe cases)
4. Droopy eyelids or double vision
5. Slurred speech or difficulty speaking
6. Weakness in the arms and legs
7. Muscle wasting and loss of muscle mass
8. Seizures or fits
9. Vision loss or blurred vision
10. Cramps or spasms
Diagnosis of NMJ Diseases:
1. Medical history and physical examination
2. Electromyography (EMG) to test muscle activity and strength
3. Nerve conduction studies (NCS) to test nerve function
4. Imaging tests such as MRI or CT scans to rule out other conditions
5. Blood tests to check for autoantibodies or other signs of inflammation
6. Genetic testing to diagnose inherited forms of NMJ diseases
Treatment of NMJ Diseases:
1. Medications such as steroids, immunosuppressants, and anticonvulsants to reduce inflammation and muscle weakness
2. Physical therapy to improve muscle strength and function
3. Occupational therapy to improve daily living skills
4. Speech therapy to improve communication and swallowing difficulties
5. Surgery to relieve compression or repair damaged nerves or muscles
6. Plasmapheresis (plasma exchange) to remove harmful antibodies from the blood
7. Intravenous immunoglobulin (IVIG) therapy to reduce inflammation and modulate the immune system
8. Immunoadsorption therapy to remove antibodies from the blood and restore immune balance
9. Stem cell transplantation to replace damaged cells with healthy ones
10. Gene therapy to repair genetic defects causing NMJ diseases.
It's important to note that the treatment of NMJ diseases is highly individualized and may vary depending on the specific diagnosis, severity of symptoms, and overall health of the patient. A multidisciplinary approach involving neurologists, physical therapists, occupational therapists, speech therapists, and other specialists may be necessary to provide comprehensive care.
There are many different types of ANS diseases, including:
1. Dysautonomia: a general term that refers to dysfunction of the autonomic nervous system.
2. Postural orthostatic tachycardia syndrome (POTS): a condition characterized by rapid heart rate and other symptoms that occur upon standing.
3. Neurocardiogenic syncope: a form of fainting caused by a sudden drop in blood pressure.
4. Multiple system atrophy (MSA): a progressive neurodegenerative disorder that affects the autonomic nervous system and other parts of the brain.
5. Parkinson's disease: a neurodegenerative disorder that can cause autonomic dysfunction, including constipation, urinary incontinence, and erectile dysfunction.
6. Dopamine deficiency: a condition characterized by low levels of the neurotransmitter dopamine, which can affect the ANS and other body systems.
7. Autonomic nervous system disorders associated with autoimmune diseases, such as Guillain-Barré syndrome and lupus.
8. Trauma: physical or emotional trauma can sometimes cause dysfunction of the autonomic nervous system.
9. Infections: certain infections, such as Lyme disease, can affect the autonomic nervous system.
10. Genetic mutations: some genetic mutations can affect the functioning of the autonomic nervous system.
Treatment for ANS diseases depends on the specific condition and its underlying cause. In some cases, medication may be prescribed to regulate heart rate, blood pressure, or other bodily functions. Lifestyle changes, such as regular exercise and stress management techniques, can also be helpful in managing symptoms. In severe cases, surgery may be necessary to correct anatomical abnormalities or repair damaged nerves.
The symptoms of catatonia can vary widely and may include:
1. Immobility: The patient may remain in a fixed position for extended periods of time, even when asked to move or perform tasks.
2. Mutism: The patient may be unable to speak, or may speak very little, despite being able to understand speech and communicate non-verbally.
3. Negativism: The patient may resist instructions or commands given by others, often in a passive-aggressive manner.
4. Perseveration: The patient may persist in performing a task or action that is no longer appropriate or relevant.
5. Stereotypy: The patient may exhibit repetitive and purposeless movements, such as rocking or pacing.
6. Posturing: The patient may assume and maintain abnormal postures, such as holding their arms or legs in unusual positions.
7. Oculogyric crisis: A sudden, sustained upward deviation of the eyes, often accompanied by neck stiffness and resistance to movement.
8. Echolalia: The patient may repeat words or phrases spoken by others, often in a echoing or parrot-like manner.
9. Echopraxia: The patient may imitate the movements of others, such as facial expressions or gestures.
The exact cause of catatonia is not fully understood, but it is thought to be related to dysfunction in certain areas of the brain, including the basal ganglia and the cortex. It can be triggered by a variety of factors, such as stress, trauma, infections, or certain medications.
Treatment for catatonia usually involves a combination of pharmacological and behavioral interventions. Benzodiazepines, such as lorazepam, are often used to help manage agitation and psychomotor agitation, while antipsychotic medications, such as haloperidol, can be effective in reducing positive symptoms. Electroconvulsive therapy (ECT) may also be considered in severe cases that do not respond to other treatments. Behavioral interventions, such as cognitive-behavioral therapy and behavioral activation, can help patients with catatonia to develop more adaptive coping strategies and improve their overall functioning.
Neuroblastoma is caused by a genetic mutation that affects the development and growth of nerve cells. The cancerous cells are often sensitive to chemotherapy, but they can be difficult to remove surgically because they are deeply embedded in the nervous system.
There are several different types of neuroblastoma, including:
1. Infantile neuroblastoma: This type of neuroblastoma occurs in children under the age of one and is often more aggressive than other types of the cancer.
2. Juvenile neuroblastoma: This type of neuroblastoma occurs in children between the ages of one and five and tends to be less aggressive than infantile neuroblastoma.
3. Adult neuroblastoma: This type of neuroblastoma occurs in adults and is rare.
4. Metastatic neuroblastoma: This type of neuroblastoma has spread to other parts of the body, such as the bones or liver.
Symptoms of neuroblastoma can vary depending on the location and size of the tumor, but they may include:
* Abdominal pain
* Loss of appetite
* Weight loss
* Bone pain
* Swelling in the abdomen or neck
* Increased heart rate
Diagnosis of neuroblastoma typically involves a combination of imaging tests, such as CT scans and MRI scans, and biopsies to confirm the presence of cancerous cells. Treatment for neuroblastoma usually involves a combination of chemotherapy, surgery, and radiation therapy. The prognosis for neuroblastoma varies depending on the type of cancer, the age of the child, and the stage of the disease. In general, the younger the child and the more aggressive the treatment, the better the prognosis.
Nicotinic acetylcholine receptor
Brain-derived neurotrophic factor
Mir-590 microRNA precursor family
Innate immune system
Alpha-7 nicotinic receptor
Muscarinic acetylcholine receptor M5
Alpha-3 beta-2 nicotinic receptor
Alpha-4 beta-2 nicotinic receptor
David S. Bredt
Differential Signalling Induced by alpha7 Nicotinic Acetylcholine Receptors in Hippocampal Dentate Gyrus in Vitro and in Vivo
Targeting alpha7 nicotinic acetylcholine receptors in the treatment of schizophrenia - PubMed
In vivo pharmacological characterization of a novel selective alpha7 neuronal nicotinic acetylcholine receptor agonist ABT-107:...
In vivo pharmacological characterization of a novel selective alpha7 neuronal nicotinic acetylcholine receptor agonist ABT-107:...
Nicotine withdrawal in the rat: role of alpha7 nicotinic receptors in the ventral tegmental area
Effect of CHRFAM7A Δ2bp gene variant on secondary inflammation after spinal cord injury - PubMed
Molecules | Free Full-Text | Striatal Cholinergic Signaling in Time and Space
SLURP1 gene: MedlinePlus Genetics
Person Details: Frederic J. Seidler (Superfund Research Program)
The vagal innervation of the gut and immune homeostasis | Gut
Climb Aboard! Neuroimmunology Is Leaving the Station
PA-13-193: Mechanisms of Alcohol and Nicotine Co-Addiction (R21)
Santosh Helekar - Research output - Houston Methodist Scholars
morphine News Research Articles - Page 2 of 2
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Nicotinic alpha 7 receptor clusters on hippocampal GABAergic neurons: regulation by synaptic activity and neurotrophins
Yung-Ho Hsu - Research output - Taipei Medical University
NDF-RT Code NDF-RT Name
Alpha7 Nicotinic Receptors and MAP Kinase in AD Models | BrightFocus Foundation
Benzethonium. Medical search
Alpha-7 nicotinic agonists for cognitive deficits in neuropsychiatric disorders: A translational meta-analysis of rodent and...
- The most abundant homomeric nicotinic acetylcholine receptors (nAChRs) in the mammalian brain are the pentameric alpha7 nAChRs which consist of five alpha7 subunits, and each subunit provides an orthosteric low affinity binding site for its endogenous ligand, acetylcholine. (nih.gov)
- Since genetic linkage studies implicated the alpha7 nAChRs subunit gene CHRNA7 in schizophrenia, there is a considerable interest for developing drug therapies targeting alpha7 nAChRs. (nih.gov)
- 5. Expression of nicotinic acetylcholine receptor subunit genes in non-small-cell lung cancer reveals differences between smokers and nonsmokers. (nih.gov)
- SLURP-1 specifically interacts with the alpha7 (α7) subunit, which is a piece of some nAChRs. (medlineplus.gov)
- We have studied the effects of pure racemic ketamine, the preservative BCl and the Ketalar mixture on human neuronal nicotinic acetylcholine receptors (nAChRs) composed of the alpha7 subunit or alpha4 and beta2 subunits expressed in Xenopus laevis oocytes. (lookformedical.com)
- Association between a genetic variant of the alpha-7 nicotinic acetylcholine receptor subunit and four types of dementia. (cdc.gov)
- We previously reported that alpha7 nicotinic acetylcholine receptor (nAChR) agonism produces efficacy in preclinical cognition models correlating with activation of cognitive and neuroprotective signaling pathways associated with Alzheimer's disease (AD) pathology. (nih.gov)
- In the present studies, the selective and potent alpha7 nAChR agonist 5-(6-[(3R)-1-azabicyclo[2.2.2]oct-3-yloxy] pyridazin-3-yl)-1H-indole (ABT-107) was evaluated in behavioral assays representing distinct cognitive domains. (nih.gov)
- Studies were also conducted to address potential issues that may be associated with the clinical development of an alpha7 nAChR agonist. (nih.gov)
- Inhibition of the alpha7 nAChRs occurred within a clinically relevant concentration range, while inhibition of the alpha4beta2 nAChR was observed only at higher concentrations. (lookformedical.com)
- 3. Ketamine is a noncompetitive inhibitor at both the alpha7 and alpha4beta2 nAChR. (lookformedical.com)
- In contrast, BCl causes a parallel shift in the ACh dose-response curve at the alpha7 nAChR suggesting competitive inhibition. (lookformedical.com)
- Animal models of cognitive dysfunction relevant to both disorders suggest the α7 nicotinic acetylcholine receptor (nAChR) may be a promising drug development target, with multiple clinical trials subsequently testing this hypothesis in individuals with SCZ and AD. (vumc.org)
- In brain slices, alpha7 nAChR activation increased levels of the signaling molecules Ca2+ and cAMP in granule cells but not in GABAergic neurons. (nih.gov)
- Taken together, the results shed new light on the action of alpha7 nAChR on brain circuitry. (nih.gov)
- Distribution and high level expression of alpha7 nAChRs within the limbic circuitry, including the hippocampus and prefrontal cortical areas are in line with their involvement in various cognitive functions. (nih.gov)
- Activation of alpha7 nAChRs generates a conformational change of sub-unit proteins, making the channel permeable to cations, in particular calcium, leading to change in neuronal activity and excitability, and via increased intracellular calcium, modulating transmitter release and neuronal network activity. (nih.gov)
- In this review recent development of selective agonists and positive allosteric modulators of alpha7 nAChRs are discussed. (nih.gov)
- In addition to summarizing medicinal chemistry efforts, both cellular and neuronal network pharmacology of alpha7 nAChRs are covered. (nih.gov)
- The association between CHRNA7 gene and impaired P50 auditory gating has provided an attractive endophenotype, and its use as a potential translational biomarker for alpha7 nAChRs drug discovery is discussed. (nih.gov)
- Laboratory studies show that SLURP-1 can bind to nicotinic acetylcholine receptors (nAChRs). (medlineplus.gov)
- 2. Ketamine inhibited responses to 1 mM acetylcholine (ACh) in both the human alpha7 and alpha4beta2 nAChRs, with IC(50) values of 20 and 50 microM respectively. (lookformedical.com)
- The surprising increased inhibitory potency of Ketalar compared with pure ketamine appeared to be due to the activity of BCl, which inhibited both alpha7 (IC(50) value of 122 nM) and alpha4beta2 (IC(50) value of 49 nM) nAChRs at concentrations present in the clinical formulation of Ketalar. (lookformedical.com)
- 4. Since alpha7 nAChRs are likely to be inhibited during clinical use of Ketalar, the actions of ketamine and BCl on this receptor subtype may play a role in the profound analgesia, amnesia, immobility and/or autonomic modulation produced by this anaesthetic. (lookformedical.com)
- the function may involve the proposed role as modulator of nicotinic acetylcholine receptors (nAChRs) activity. (nih.gov)
- Activation of alpha7 nicotinic acetylcholine receptors (nAChRs) has distinct effects on the responses of different types of neurons in a brain region called the hippocampus, according to NIEHS researchers and their collaborators. (nih.gov)
- Stimulation of alpha7 nAChRs enhances learning and memory and promotes the maturation of adult-born neurons. (nih.gov)
- Specifically, it has not been clear whether alpha7 nAChRs mobilize different signaling pathways in distinct neuronal populations. (nih.gov)
- To address this question, the researchers studied how stimulation of alpha7 nAChRs affects the responses of granule cells and GABAergic neurons in the hippocampus, which plays a critical role in learning and memory. (nih.gov)
- HN - 2014 FX - Transplantation, Homologous MH - alpha7 Nicotinic Acetylcholine Receptor UI - D064569 MN - D12.776.157.530.400.400.100.500.500 MN - D12.776.543.550.425.500.100.500.500 MN - D12.776.543.585.400.500.100.500.500 MN - D12.776.543.750.51.687.500 MN - D12.776.543.750.720.360.550.500 MS - A member of the NICOTINIC ACETYLCHOLINE RECEPTOR subfamily of the LIGAND-GATED ION CHANNEL family. (nih.gov)
- and AQW051, a Phase II alpha-7 nicotinic acetylcholine receptor partial agonist. (broadstreetalerts.com)
- Genetic Association Study of the Alpha 7 Nicotinic Receptor (CHRNA7) with the Development of Schizophrenia and Bipolar Disorder in Korean Population. (cdc.gov)
- Alpha-7 nicotinic agonists for cognitive deficits in neuropsychiatric disorders: A translational meta-analysis of rodent and human studies. (vumc.org)
- Bilateral intrategmental injections of the selective alpha7 nicotinic receptor antagonist methyllycaconitine reduced locomotion in the nicotine-treated rats, but not in control animals. (nih.gov)
- Peng C, Han Y, Sanders T, Chew G, Liu J, Hawrot E, Chi C, Wang C. "alpha4/7-conotoxin Lp1.1 is a novel antagonist of neuronal nicotinic acetylcholine receptors. (brown.edu)
- Like other Ly6/uPAR-related proteins, SLURP-1 folds into a particular shape and is thought to attach (bind) to other proteins called receptors to carry out signaling within cells. (medlineplus.gov)
- Proteomic Investigation of Murine Neuronal α7-Nicotinic Acetylcholine Receptor Interacting Proteins. (brown.edu)
- Hawrot E. "Connecting the dots between G proteins, G protein coupled receptors, and neuronal nicotinic acetylcholine receptors (Comment on DOI 10.1002/bies.201300082). (brown.edu)
- 9. The expression and pharmacological characterization of nicotinic acetylcholine receptor subunits in HBE16 airway epithelial cells. (nih.gov)
- Moreover, treatments targeting these receptors improve cognitive deficits associated with Alzheimer's disease, schizophrenia, and Down's syndrome. (nih.gov)
- 17. Nicotinic Receptor Subunits Atlas in the Adult Human Lung. (nih.gov)
- We have used fluorescently labeled alpha-bungarotoxin to image alpha7-containing receptors on hippocampal neurons and to examine their regulation in culture. (indexindex.com)
- A 3 d blockade of electrical activity with tetrodotoxin or NMDA receptors with APV dramatically reduced the proportion of GABAergic neurons expressing high levels of receptor staining and reduced the mean number of distinguishable receptor clusters on individual neurons. (indexindex.com)
- Anti-BDNF and anti-NGF antibodies produced decrements equivalent to those of tetrodotoxin and APV, whereas addition of BDNF and NGF each increased staining levels and increased the number of distinguishable receptor clusters on GABAergic neurons. (indexindex.com)
- The results indicate that both NMDA receptor activation and the neurotrophins BDNF and NGF are necessary to sustain the distribution patterns of alpha7-containing nicotinic receptors on GABAergic hippocampal neurons. (indexindex.com)
- Preliminary results suggest that a receptor for amyloid beta peptide on the cell surface of neurons is the alpha7 nicotinic acetylcholine receptor. (brightfocus.org)
- Similarly, recordings in mice revealed that nicotine injection increased alpha7 receptor-dependent activity of granule cells but did not increase the firing rate of GABAergic neurons. (nih.gov)
- Paulo JA, Hawrot E. "Effect of homologous serotonin receptor loop substitutions on the heterologous expression in Pichia of a chimeric acetylcholine-binding protein with alpha-bungarotoxin-binding activity. (brown.edu)
- Caffery PM, Krishnaswamy A, Sanders T, Liu J, Hartlaub H, Klysik J, Cooper E, Hawrot E. "Engineering neuronal nicotinic acetylcholine receptors with functional sensitivity to alpha-bungarotoxin: a novel alpha3-knock-in mouse. (brown.edu)
- Dr. Sweatt will use genetic approaches to examine whether deletion of the alpha7 receptor gene leads to amelioration of memory deficits exhibited in transgenic mice with AD and decreases in biochemical markers. (brightfocus.org)
- Mulcahy MJ, Blattman SB, Barrantes FJ, Lukas RJ, Hawrot E. "Resistance to Inhibitors of Cholinesterase 3 (Ric-3) Expression Promotes Selective Protein Associations with the Human α7-Nicotinic Acetylcholine Receptor Interactome. (brown.edu)
- 10. Functional properties of homomeric, human alpha 7-nicotinic acetylcholine receptors heterologously expressed in the SH-EP1 human epithelial cell line. (nih.gov)
- Previous data show that nicotinic receptors in the ventral tegmental area are of importance for the nicotine withdrawal syndrome. (nih.gov)
- Here we have investigated the specific role of alpha7 nicotinic receptors in the ventral tegmental area for the neurobiological and behavioral consequences of nicotine withdrawal. (nih.gov)
- Our results indicate that alpha7 nicotinic receptors in the ventral tegmental area are involved in the nicotine withdrawal syndrome. (nih.gov)
- 1. Nicotine signals through muscle-type and neuronal nicotinic acetylcholine receptors in both human bronchial epithelial cells and airway fibroblasts. (nih.gov)
- 2. Nicotine activates cell-signaling pathways through muscle-type and neuronal nicotinic acetylcholine receptors in non-small cell lung cancer cells. (nih.gov)
- 3. Nicotine enhances expression of the alpha 3, alpha 4, alpha 5, and alpha 7 nicotinic receptors modulating calcium metabolism and regulating adhesion and motility of respiratory epithelial cells. (nih.gov)
- 12. Nicotine induces fibrogenic changes in human liver via nicotinic acetylcholine receptors expressed on hepatic stellate cells. (nih.gov)
- 16. Effects of chronic nicotine treatment on expression of diverse nicotinic acetylcholine receptor subtypes. (nih.gov)
- Blockade of either GABA(A) receptors with bicuculline or nicotinic receptors with d-tubocurarine had no effect, although exposure to nicotine could increase the level of receptor staining. (indexindex.com)
- The cholinergic interneurons of the striatum account for a small fraction of all striatal cell types but due to their extensive axonal arborization give the striatum the highest content of acetylcholine of almost any nucleus in the brain. (mdpi.com)
- Because of their specific locations and their high relative calcium permeability, the receptors not only mediate cholinergic transmission in the hippocampus but also influence signaling at noncholinergic synapses. (indexindex.com)
- The aim of this study was to investigate the antiinflammatory benefits of SNS in colitis rats and explore the roles of the cholinergic antiinflammatory pathway, macrophage autophagy, and nucleotide oligomerization domain-like receptor thermal protein domain associated protein 3 (NLRP3) inflammatory bodies. (neuromodulationjournal.org)
- 11. Overexpression and activation of the alpha9-nicotinic receptor during tumorigenesis in human breast epithelial cells. (nih.gov)
- The VN, through release of acetylcholine, dampens immune cell activation by interacting with α-7 nicotinic acetylcholine receptors. (bmj.com)
- Many point to regulation of adaptive immunity, including ptpn22 (protein tyrosine phosphatase, non-receptor type 22 which regulates lymphocyte activation), ctla4 and cd40 (both implicated in co-stimulation of T cells). (bmj.com)
- ABT-107 increased extracellular cortical acetylcholine in rats, whereas acute administration increased cortical extracellular signal-regulated kinase and cAMP response element- binding protein phosphorylation in mice, neurochemical and biochemical events germane to cognitive function. (nih.gov)
- We review the evidence for this theory and use a mathematical model to integrate the measurements reported in the literature, from which we estimate the temporospatial distribution of acetylcholine after release from a synaptic vesicle and from multiple vesicles during tonic firing and pauses. (mdpi.com)
- Ketamine and its preservative, benzethonium chloride, both inhibit human recombinant alpha7 and alpha4beta2 neuronal nicotinic acetylcholine receptors in Xenopus oocytes. (lookformedical.com)
- Association study of the human partially duplicated alpha7 nicotinic acetylcholine receptor genetic variant with bipolar disorder. (cdc.gov)
- 2019. Perinatal diazinon exposure compromises the development of acetylcholine and serotonin systems. (nih.gov)
- Central role of alpha7 nicotinic receptor in differentiation of the stratified squamous epithelium. (medlineplus.gov)
- 8. Nicotinic acetylcholine receptor expression in human airway correlates with lung function. (nih.gov)
- 13. Regulated expression of the IL-31 receptor in bronchial and alveolar epithelial cells, pulmonary fibroblasts, and pulmonary macrophages. (nih.gov)
- 14. Functional expression of alpha 7 nicotinic acetylcholine receptors in human periodontal ligament fibroblasts and rat periodontal tissues. (nih.gov)
- As a past Established Investigator of the American Heart Association and Upjohn Professor of Pharmacology, my research interests include the understanding of the structure and function of nicotinic acetylcholine receptors and of the neurotoxins that target these important receptors. (brown.edu)
- Proteomic investigation of human α7-nicotinic acetylcholine receptor signaling mechanisms. (brown.edu)
- Nicotinic acetylcholine receptors containing the alpha7 gene product are expressed at substantial levels in the hippocampus. (indexindex.com)
- Se compone en su totalidad de subunidades a7 pentaméricas expresadas en el sistema nervioso central, sistema nervioso autónomo, sistema vascular, linfocitos y bazo. (bvsalud.org)
- Nicotinic acetylcholine receptors are best known for their role in chemical signaling between nerve cells, but they are also found in other tissues. (medlineplus.gov)
- The function may implicate a possible role as a scavenger receptor for PLAU thereby blocking PLAU-dependent functions of PLAUR such as in cell migration and proliferation (PubMed:25168896). (nih.gov)
- The identification of the alpha 7 receptor involvement in AD allows for the future study of agents that block the receptor as potential therapeutics for AD. (brightfocus.org)
- Association with alpha7 nicotinic acetylcholine receptors. (nih.gov)
- Through its interaction with these receptors, SLURP-1 may be involved in skin growth and development. (medlineplus.gov)