Heart Conduction System
Potassium Channel Blockers
Refractory Period, Electrophysiological
Potassium Channels, Voltage-Gated
Sodium Channel Blockers
Excitatory Postsynaptic Potentials
Delayed Rectifier Potassium Channels
Calcium Channels, L-Type
Ion Channel Gating
Voltage-Sensitive Dye Imaging
Calcium Channel Blockers
Long QT Syndrome
Ether-A-Go-Go Potassium Channels
Shal Potassium Channels
Cardiac Pacing, Artificial
Sensory Receptor Cells
Nerve Fibers, Unmyelinated
Dose-Response Relationship, Drug
Shaw Potassium Channels
Excitatory Amino Acid Antagonists
NAV1.5 Voltage-Gated Sodium Channel
Organ Culture Techniques
Calcium Channels, T-Type
Nervous System Physiological Phenomena
Torsades de Pointes
Electrophysiologic Techniques, Cardiac
Small-Conductance Calcium-Activated Potassium Channels
Potassium Channels, Inwardly Rectifying
Voltage-Gated Sodium Channels
NAV1.6 Voltage-Gated Sodium Channel
Nerve Fibers, Myelinated
KCNQ Potassium Channels
Optics and Photonics
Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels
Kv1.1 Potassium Channel
Cardiac Complexes, Premature
Further evidence that prostaglandins inhibit the release of noradrenaline from adrenergic nerve terminals by restriction of availability of calcium. (1/21346)1 Guinea-pig vasa deferentia were continuously superfused after labelling the transmitter stores with [3H](-)-noradrenaline. Release of [3H]-(-)-noradrenaline was induced by transmural nerve stimulation. 2 Prostglandin E2 (14 nM) drastically reduced the release of [3H]-(-)-noradrenaline, while tetraethylammonium (2 mM), rubidium (6 mM), phenoxybenzamine (3 muM) each in the presence or absence of Uptake 1 or 2 blockade, and prolonged pulse duration (from 0.5 to 2.0 ms) all significantly increased the release of [3H]-(-)-noradrenaline per nerve impulse. 3 The inhibitory effect of prostaglandin E2 on evoked release of [3H]-(-)-noradrenaline was significantly reduced by tetraethylammonium, rubidium and prolonged pulse duration, whilst it was actually enhanced by phenoxybenzamine. This indicates that increased release of noradrenaline per nerve impulse does not per se counteract the inhibitory effect of prostaglandin E2. 4 It is concluded that tetraethylammonium, rubidium and prolonged pulse duration counteracted the inhibitory effect of prostaglandin E2 on T3H]-(-)-noradrenaline release by promoting calcium influx during the nerve action potential. The results are consistent with, and add more weight to the view that prostaglandins inhibit the release of noradrenaline by restriction of calcium availability. (+info)
Effect of electrotonic potentials on pacemaker activity of canine Purkinje fibers in relation to parasystole. (2/21346)Isolated false tendons excised form dog hearts were mounted in a three-chamber tissue bath. Isotonic sucrose solution was perfused in the central chamber to provide a region of depressed conductivity between the fiber segments in chambers 1 and 3, which were perfused with Tyrode's solution. The electrotonic influence of spontaneous or driven responses evoked in chamber 3 during the first half of the spontaneous cycle of a chamber 1 peacemaker delayed the next spontaneous discharge. This effect changed to acceleration when the chamber 3 segment fired during the second half of the spontaneous cycle. We found that subthreshold depolarizing current pulses 50-300 msec applied across the sucrose gap caused similar degrees of delay or acceleration. Furthermore, hyperpolarizing currents caused the reverse pattern. The results indicate that the discharge pattern of a parasystolic focus may be altered by the electrotonic influence of activity in the surrounding tissue. The significance of these findings is considered in relation to the mechanism of production of parasystolic rhythms. (+info)
Low resting potential and postnatal upregulation of NMDA receptors may cause Cajal-Retzius cell death. (3/21346)Using in situ patch-clamp techniques in rat telencephalic slices, we have followed resting potential (RP) properties and the functional expression of NMDA receptors in neocortical Cajal-Retzius (CR) cells from embryonic day 18 to postnatal day 13, the time around which these cells normally disappear. We find that throughout their lives CR cells have a relatively depolarized RP (approximately -50 mV), which can be made more hyperpolarized (approximately -70 mV) by stimulation of the Na/K pump with intracellular ATP. The NMDA receptors of CR cells are subjected to intense postnatal upregulation, but their similar properties (EC50, Hill number, sensitivity to antagonists, conductance, and kinetics) throughout development suggest that their subunit composition remains relatively homogeneous. The low RP of CR cells is within a range that allows for the relief of NMDA channels from Mg2+ blockade. Our findings are consistent with the hypothesis that CR cells may degenerate and die subsequent to uncontrolled overload of intracellular Ca2+ via NMDA receptor activation by ambient glutamate. In support of this hypothesis we have obtained evidence showing the protection of CR cells via in vivo blockade of NMDA receptors with dizocilpine. (+info)
Activity-dependent metaplasticity of inhibitory and excitatory synaptic transmission in the lamprey spinal cord locomotor network. (4/21346)Paired intracellular recordings have been used to examine the activity-dependent plasticity and neuromodulator-induced metaplasticity of synaptic inputs from identified inhibitory and excitatory interneurons in the lamprey spinal cord. Trains of spikes at 5-20 Hz were used to mimic the frequency of spiking that occurs in network interneurons during NMDA or brainstem-evoked locomotor activity. Inputs from inhibitory and excitatory interneurons exhibited similar activity-dependent changes, with synaptic depression developing during the spike train. The level of depression reached was greater with lower stimulation frequencies. Significant activity-dependent depression of inputs from excitatory interneurons and inhibitory crossed caudal interneurons, which are central elements in the patterning of network activity, usually developed between the fifth and tenth spikes in the train. Because these interneurons typically fire bursts of up to five spikes during locomotor activity, this activity-dependent plasticity will presumably not contribute to the patterning of network activity. However, in the presence of the neuromodulators substance P and 5-HT, significant activity-dependent metaplasticity of these inputs developed over the first five spikes in the train. Substance P induced significant activity-dependent depression of inhibitory but potentiation of excitatory interneuron inputs, whereas 5-HT induced significant activity-dependent potentiation of both inhibitory and excitatory interneuron inputs. Because these metaplastic effects are consistent with the substance P and 5-HT-induced modulation of the network output, activity-dependent metaplasticity could be a potential mechanism underlying the coordination and modulation of rhythmic network activity. (+info)
Ionic currents underlying spontaneous action potentials in isolated cerebellar Purkinje neurons. (5/21346)Acutely dissociated cell bodies of mouse Purkinje neurons spontaneously fired action potentials at approximately 50 Hz (25 degrees C). To directly measure the ionic currents underlying spontaneous activity, we voltage-clamped the cells using prerecorded spontaneous action potentials (spike trains) as voltage commands and used ionic substitution and selective blockers to isolate individual currents. The largest current flowing during the interspike interval was tetrodotoxin-sensitive sodium current (approximately -50 pA between -65 and -60 mV). Although the neurons had large voltage-dependent calcium currents, the net current blocked by cobalt substitution for calcium was outward at all times during spike trains. Thus, the electrical effect of calcium current is apparently dominated by rapidly activated calcium-dependent potassium currents. Under current clamp, all cells continued firing spontaneously (though approximately 30% more slowly) after block of T-type calcium current by mibefradil, and most cells continued to fire after block of all calcium current by cobalt substitution. Although the neurons possessed hyperpolarization-activated cation current (Ih), little current flowed during spike trains, and block by 1 mM cesium had no effect on firing frequency. The outward potassium currents underlying the repolarization of the spikes were completely blocked by 1 mM TEA. These currents deactivated quickly (<1 msec) after each spike. We conclude that the spontaneous firing of Purkinje neuron cell bodies depends mainly on tetrodotoxin-sensitive sodium current flowing between spikes. The high firing rate is promoted by large potassium currents that repolarize the cell rapidly and deactivate quickly, thus preventing strong hyperpolarization and restoring a high input resistance for subsequent depolarization. (+info)
Somatic recording of GABAergic autoreceptor current in cerebellar stellate and basket cells. (6/21346)Patch-clamp recordings were performed from stellate and basket cells in rat cerebellar slices. Under somatic voltage clamp, short depolarizing pulses were applied to elicit action potentials in the axon. After the action potential, a bicuculline- and Cd2+-sensitive current transient was observed. A similar response was obtained when eliciting axonal firing by extracellular stimulation. With an isotonic internal Cl- solution, the peak amplitude of this current varied linearly with the holding potential, yielding an extrapolated reversal potential of -20 to 0 mV. Unlike synaptic or autaptic GABAergic currents obtained in the same preparation, the current transient had a slow rise-time and a low variability between trials. This current was blocked when 10 mM BAPTA was included in the recording solution. In some experiments, the current transient elicited axonal action potentials. The current transient was reliably observed in animals aged 12-15 d, with a mean amplitude of 82 pA at -70 mV, but was small and rare in the age group 29-49 d. Numerical simulations could account for all properties of the current transient by assuming that an action potential activates a distributed GABAergic conductance in the axon. The actual conductance is probably restricted to release sites, with an estimated mean presynaptic current response of 10 pA per site (-70 mV, age 12-15 d). We conclude that in developing rats, stellate and basket cell axons have a high density of GABAergic autoreceptors and that a sizable fraction of the corresponding current can be measured from the soma. (+info)
Inducible genetic suppression of neuronal excitability. (7/21346)Graded, reversible suppression of neuronal excitability represents a logical goal of therapy for epilepsy and intractable pain. To achieve such suppression, we have developed the means to transfer "electrical silencing" genes into neurons with sensitive control of transgene expression. An ecdysone-inducible promoter drives the expression of inwardly rectifying potassium channels in polycistronic adenoviral vectors. Infection of superior cervical ganglion neurons did not affect normal electrical activity but suppressed excitability after the induction of gene expression. These experiments demonstrate the feasibility of controlled ion channel expression after somatic gene transfer into neurons and serve as the prototype for a novel generalizable approach to modulate excitability. (+info)
Cerebellar Purkinje cell simple spike discharge encodes movement velocity in primates during visuomotor arm tracking. (8/21346)Pathophysiological, lesion, and electrophysiological studies suggest that the cerebellar cortex is important for controlling the direction and speed of movement. The relationship of cerebellar Purkinje cell discharge to the control of arm movement parameters, however, remains unclear. The goal of this study was to examine how movement direction and speed and their interaction-velocity-modulate Purkinje cell simple spike discharge in an arm movement task in which direction and speed were independently controlled. The simple spike discharge of 154 Purkinje cells was recorded in two monkeys during the performance of two visuomotor tasks that required the animals to track targets that moved in one of eight directions and at one of four speeds. Single-parameter regression analyses revealed that a large proportion of cells had discharge modulation related to movement direction and speed. Most cells with significant directional tuning, however, were modulated at one speed, and most cells with speed-related discharge were modulated along one direction; this suggested that the patterns of simple spike discharge were not adequately described by single-parameter models. Therefore, a regression surface was fitted to the data, which showed that the discharge could be tuned to specific direction-speed combinations (preferred velocities). The overall variability in simple spike discharge was well described by the surface model, and the velocities corresponding to maximal and minimal discharge rates were distributed uniformly throughout the workspace. Simple spike discharge therefore appears to integrate information about both the direction and speed of arm movements, thereby encoding movement velocity. (+info)
There are many different types of cardiac arrhythmias, including:
1. Tachycardias: These are fast heart rhythms that can be too fast for the body's needs. Examples include atrial fibrillation and ventricular tachycardia.
2. Bradycardias: These are slow heart rhythms that can cause symptoms like fatigue, dizziness, and fainting. Examples include sinus bradycardia and heart block.
3. Premature beats: These are extra beats that occur before the next regular beat should come in. They can be benign but can also indicate an underlying arrhythmia.
4. Supraventricular arrhythmias: These are arrhythmias that originate above the ventricles, such as atrial fibrillation and paroxysmal atrial tachycardia.
5. Ventricular arrhythmias: These are arrhythmias that originate in the ventricles, such as ventricular tachycardia and ventricular fibrillation.
Cardiac arrhythmias can be diagnosed through a variety of tests including electrocardiograms (ECGs), stress tests, and holter monitors. Treatment options for cardiac arrhythmias vary depending on the type and severity of the condition and may include medications, cardioversion, catheter ablation, or implantable devices like pacemakers or defibrillators.
The QT interval is a measure of the time it takes for the ventricles to recover from each heartbeat and prepare for the next one. In people with LQTS, this recovery time is prolonged, which can disrupt the normal rhythm of the heart and increase the risk of arrhythmias.
LQTS is caused by mutations in genes that encode proteins involved in the cardiac ion channels, which regulate the flow of ions into and out of the heart muscle cells. These mutations can affect the normal functioning of the ion channels, leading to abnormalities in the electrical activity of the heart.
Symptoms of LQTS can include palpitations, fainting spells, and seizures. In some cases, LQTS can be diagnosed based on a family history of the condition or after a sudden death in an otherwise healthy individual. Other tests, such as an electrocardiogram (ECG), echocardiogram, and stress test, may also be used to confirm the diagnosis.
Treatment for LQTS typically involves medications that regulate the heart's rhythm and reduce the risk of arrhythmias. In some cases, an implantable cardioverter-defibrillator (ICD) may be recommended to monitor the heart's activity and deliver an electric shock if a potentially life-threatening arrhythmia is detected. Lifestyle modifications, such as avoiding stimuli that trigger symptoms and taking precautions during exercise and stress, may also be recommended.
In summary, Long QT syndrome is a rare inherited disorder that affects the electrical activity of the heart, leading to an abnormal prolongation of the QT interval and an increased risk of irregular and potentially life-threatening heart rhythms. It is important for individuals with LQTS to be closely monitored by a healthcare provider and to take precautions to manage their condition and reduce the risk of complications.
In Vfib, the electrical activity of the heart becomes disorganized, leading to a fibrillatory pattern of contraction. This means that the ventricles are contracting in a rapid, unsynchronized manner, rather than the coordinated, synchronized contractions that occur in normal heart function.
Vfib can be caused by a variety of factors, including coronary artery disease, heart attack, cardiomyopathy, and electrolyte imbalances. It can also be triggered by certain medications, such as digoxin, or by electrical shocks to the heart.
Symptoms of Vfib include palpitations, shortness of breath, chest pain, and loss of consciousness. If not treated promptly, Vfib can lead to cardiac arrest and death.
Treatment of Vfib typically involves electrical cardioversion, which involves delivering an electric shock to the heart to restore a normal heart rhythm. In some cases, medications may also be used to help regulate the heart rhythm. In more severe cases, surgery or other interventions may be necessary to address any underlying causes of Vfib.
Overall, ventricular fibrillation is a serious medical condition that requires prompt treatment to prevent complications and ensure effective cardiac function.
Torsades de pointes is often associated with certain medications, such as antiarrhythmics, beta blockers, and cardiac glycosides, as well as with underlying heart conditions, such as coronary artery disease, hypertension, and heart failure. The condition can cause the heart to beat in an irregular and disorganized manner, which can lead to ineffective pumping of blood and can ultimately result in cardiac arrest and death.
Torsades de pointes is typically diagnosed based on the patient's medical history, physical examination, and results of electrocardiogram (ECG) tests. Treatment for the condition may involve stopping any medications that may be contributing to the arrhythmia, administering anti-arrhythmic drugs, and in some cases, implanting a cardioverter-defibrillator (ICD) to regulate the heart's rhythm.
In summary, torsades de pointes is a serious and potentially life-threatening arrhythmia that can be caused by various medications and underlying heart conditions. It is important for healthcare providers to be aware of this condition and to take appropriate measures to diagnose and treat it promptly in order to prevent complications and improve patient outcomes.
There are several types of premature complexes, including:
1. Premature atrial complex (PAC): An extra heartbeat that originates in the atria, usually due to a rapid or irregular heart rate.
2. Premature ventricular complex (PVC): An extra heartbeat that originates in the ventricles, which can be more serious than PACs and may require further evaluation.
3. Premature nodal rhythm: A condition where the AV node (the electrical pathway between the atria and ventricles) fires prematurely, causing a rapid heart rate.
PCCs can be diagnosed using electrocardiography (ECG), which records the electrical activity of the heart. Treatment options for PCCs depend on the underlying cause and may include medications to regulate the heart rhythm, cardioversion (a procedure that restores a normal heart rhythm using electrical shock), or catheter ablation (a minimally invasive procedure that destroys the abnormal electrical pathway).
Tachycardia, ventricular can be classified into several types based on its duration and the presence of other symptoms. These include:
1. Paroxysmal ventricular tachycardia (PVT): This is a rapid heart rate that occurs in episodes lasting less than 30 seconds and may be accompanied by palpitations, shortness of breath, or dizziness.
2. Sustained ventricular tachycardia: This is a rapid heart rate that persists for more than 30 seconds and may require medical intervention to return the heart to normal rhythm.
3. Ventricular fibrillation (VF): This is a life-threatening condition in which the ventricles are unable to pump blood effectively due to rapid, disorganized electrical activity.
Symptoms of tachycardia, ventricular may include:
* Palpitations or rapid heartbeat
* Shortness of breath
* Dizziness or lightheadedness
* Chest pain or discomfort
* Fatigue or weakness
Diagnosis of tachycardia, ventricular is typically made based on a physical examination, medical history, and results of diagnostic tests such as electrocardiogram (ECG), echocardiogram, or stress test. Treatment options may include medications to regulate heart rhythm, cardioversion to restore normal heart rhythm, and in some cases, implantation of a cardioverter-defibrillator (ICD) to prevent sudden death.
In summary, tachycardia, ventricular is a rapid heart rate that originates in the ventricles and can be caused by a variety of conditions. It is important to seek medical attention if symptoms persist or worsen over time. With proper diagnosis and treatment, it is possible to manage the condition and improve quality of life.
There are several risk factors for developing AF, including:
1. Age: The risk of developing AF increases with age, with the majority of cases occurring in people over the age of 65.
2. Hypertension (high blood pressure): High blood pressure can damage the heart and increase the risk of developing AF.
3. Heart disease: People with heart disease, such as coronary artery disease or heart failure, are at higher risk of developing AF.
4. Diabetes mellitus: Diabetes can increase the risk of developing AF.
5. Sleep apnea: Sleep apnea can increase the risk of developing AF.
6. Certain medications: Certain medications, such as thyroid medications and asthma medications, can increase the risk of developing AF.
7. Alcohol consumption: Excessive alcohol consumption has been linked to an increased risk of developing AF.
8. Smoking: Smoking is a risk factor for many cardiovascular conditions, including AF.
9. Obesity: Obesity is a risk factor for many cardiovascular conditions, including AF.
Symptoms of AF can include:
1. Palpitations (rapid or irregular heartbeat)
2. Shortness of breath
4. Dizziness or lightheadedness
5. Chest pain or discomfort
AF can be diagnosed with the help of several tests, including:
1. Electrocardiogram (ECG): This is a non-invasive test that measures the electrical activity of the heart.
2. Holter monitor: This is a portable device that records the heart's rhythm over a 24-hour period.
3. Event monitor: This is a portable device that records the heart's rhythm over a longer period of time, usually 1-2 weeks.
4. Echocardiogram: This is an imaging test that uses sound waves to create pictures of the heart.
5. Cardiac MRI: This is an imaging test that uses magnetic fields and radio waves to create detailed pictures of the heart.
Treatment for AF depends on the underlying cause and may include medications, such as:
1. Beta blockers: These medications slow the heart rate and reduce the force of the heart's contractions.
2. Antiarrhythmics: These medications help regulate the heart's rhythm.
3. Blood thinners: These medications prevent blood clots from forming and can help reduce the risk of stroke.
4. Calcium channel blockers: These medications slow the entry of calcium into the heart muscle cells, which can help slow the heart rate and reduce the force of the heart's contractions.
In some cases, catheter ablation may be recommended to destroy the abnormal electrical pathway causing AF. This is a minimally invasive procedure that involves inserting a catheter through a vein in the leg and guiding it to the heart using x-ray imaging. Once the catheter is in place, energy is applied to the abnormal electrical pathway to destroy it and restore a normal heart rhythm.
It's important to note that AF can increase the risk of stroke, so anticoagulation therapy may be recommended to reduce this risk. This can include medications such as warfarin or aspirin, or in some cases, implantable devices such as a left atrial appendage closure device.
In conclusion, atrial fibrillation is a common heart rhythm disorder that can increase the risk of stroke and heart failure. Treatment options depend on the underlying cause and may include medications, cardioversion, catheter ablation, or anticoagulation therapy. It's important to work closely with a healthcare provider to determine the best course of treatment for AF.
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.
Peripheral Nervous System Diseases can result from a variety of causes, including:
1. Trauma or injury
2. Infections such as Lyme disease or HIV
3. Autoimmune disorders such as Guillain-Barré syndrome
4. Genetic mutations
5. Tumors or cysts
6. Toxins or poisoning
7. Vitamin deficiencies
8. Chronic diseases such as diabetes or alcoholism
Some common Peripheral Nervous System Diseases include:
1. Neuropathy - damage to the nerves that can cause pain, numbness, and weakness in the affected areas.
2. Multiple Sclerosis (MS) - an autoimmune disease that affects the CNS and PNS, causing a range of symptoms including numbness, weakness, and vision problems.
3. Peripheral Neuropathy - damage to the nerves that can cause pain, numbness, and weakness in the affected areas.
4. Guillain-Barré syndrome - an autoimmune disorder that causes muscle weakness and paralysis.
5. Charcot-Marie-Tooth disease - a group of inherited disorders that affect the nerves in the feet and legs, leading to muscle weakness and wasting.
6. Friedreich's ataxia - an inherited disorder that affects the nerves in the spine and limbs, leading to coordination problems and muscle weakness.
7. Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) - an autoimmune disorder that causes inflammation of the nerves, leading to pain, numbness, and weakness in the affected areas.
8. Amyotrophic Lateral Sclerosis (ALS) - a progressive neurological disease that affects the nerve cells responsible for controlling voluntary muscle movement, leading to muscle weakness, atrophy, and paralysis.
9. Spinal Muscular Atrophy - an inherited disorder that affects the nerve cells responsible for controlling voluntary muscle movement, leading to muscle weakness and wasting.
10. Muscular Dystrophy - a group of inherited disorders that affect the nerve cells responsible for controlling voluntary muscle movement, leading to muscle weakness and wasting.
It's important to note that this is not an exhaustive list and there may be other causes of muscle weakness. If you are experiencing persistent or severe muscle weakness, it is important to see a healthcare professional for proper evaluation and diagnosis.
There are several types of channelopathies, including:
1. Long QT syndrome: This is a condition that affects the ion channels in the heart, leading to abnormal heart rhythms and increased risk of sudden death.
2. Short QT syndrome: This is a rare condition that has the opposite effect of long QT syndrome, causing the heart to beat too quickly.
3. Catecholaminergic polymorphic ventricular tachycardia (CPVT): This is a rare disorder that affects the ion channels in the heart, leading to abnormal heart rhythms and increased risk of sudden death.
4. Brugada syndrome: This is a condition that affects the ion channels in the heart, leading to abnormal heart rhythms and increased risk of sudden death.
5. Wolff-Parkinson-White (WPW) syndrome: This is a condition that affects the ion channels in the heart, leading to abnormal heart rhythms and increased risk of sudden death.
6. Neuromuscular disorders: These are disorders that affect the nerve-muscle junction, leading to muscle weakness and wasting. Examples include muscular dystrophy and myasthenia gravis.
7. Dystrophinopathies: These are a group of disorders that affect the structure of muscle cells, leading to muscle weakness and wasting. Examples include Duchenne muscular dystrophy and Becker muscular dystrophy.
8. Myotonia: This is a condition that affects the muscles, causing them to become stiff and rigid.
9. Hyperkalemic periodic paralysis: This is a rare condition that causes muscle weakness and paralysis due to abnormal potassium levels in the body.
10. Hypokalemic periodic paralysis: This is a rare condition that causes muscle weakness and paralysis due to low potassium levels in the body.
11. Thyrotoxic periodic paralysis: This is a rare condition that causes muscle weakness and paralysis due to an overactive thyroid gland.
12. Hyperthyroidism: This is a condition where the thyroid gland becomes overactive, leading to increased heart rate, weight loss, and muscle weakness.
13. Hypothyroidism: This is a condition where the thyroid gland becomes underactive, leading to fatigue, weight gain, and muscle weakness.
14. Pituitary tumors: These are tumors that affect the pituitary gland, which regulates hormone production in the body.
15. Adrenal tumors: These are tumors that affect the adrenal glands, which produce hormones such as cortisol and aldosterone.
16. Carcinoid syndrome: This is a condition where cancer cells in the digestive system produce hormones that can cause muscle weakness and wasting.
17. Multiple endocrine neoplasia (MEN): This is a genetic disorder that affects the endocrine system and can cause tumors to grow in the thyroid, adrenal, and parathyroid glands.
These are just some of the many potential causes of muscle weakness. It's important to see a healthcare professional for an accurate diagnosis and appropriate treatment.
Atrial action potential
Pacemaker action potential
Action potential pulse
Ventricular action potential
Cardiac action potential
Compound muscle action potential
Quantitative models of the action potential
Inhibitory postsynaptic potential
Transient receptor potential channel
Subthreshold membrane potential oscillations
Local field potential
Plant perception (physiology)
Lateralized readiness potential
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- In neurons, the rapid rise in potential, depolarization, is an all-or-nothing event that is initiated by the opening of sodium ion channels within the plasma membrane. (theburningofrome.com)
- What happens during depolarization in an action potential? (theburningofrome.com)
- During an action potential, the depolarization is so large that the potential difference across the cell membrane briefly reverses polarity, with the inside of the cell becoming positively charged. (theburningofrome.com)
- An action potential is generated in the following steps: depolarization, repolarization, hyperpolarization and a refactory period. (theburningofrome.com)
- First, action potentials are generated by the depolarization of the cell membrane, which causes a change in voltage across the membrane. (theclassicwanderer.com)
- An action potential is a rapid rise and subsequent fall in voltage or membrane potential across a cellular membrane with a characteristic pattern. (theburningofrome.com)
- When the membrane potential of the axon hillock of a neuron reaches threshold, a rapid change in membrane potential occurs in the form of an action potential. (theburningofrome.com)
- This moving change in membrane potential has three phases. (theburningofrome.com)
- During the rising phase the membrane potential depolarizes (becomes more positive). (theburningofrome.com)
- The reason for this is that the action potential is caused by a change in the membrane potential. (theclassicwanderer.com)
- The ions will flow until the membrane potential is restored to its original state. (theclassicwanderer.com)
- The restoration of the membrane potential is called the repolarization. (theclassicwanderer.com)
- An action potential (or nerve impulse ) is a transient alteration of the transmembrane voltage (or membrane potential ) across an excitable membrane generated by the activity of voltage-gated ion channels embedded in the membrane. (phys.org)
- Abrupt changes in the membrane potential that sweep along the CELL MEMBRANE of excitable cells in response to excitation stimuli. (bvsalud.org)
- One reason action potentials cannot travel backwards is because they are generated by the opening of voltage-gated sodium channels. (theclassicwanderer.com)
- If action potentials could travel backwards, the cell would never reach its threshold voltage and the sodium channels would never open. (theclassicwanderer.com)
- This is why we can see action potentials generated by very weak stimuli, such as when we first touch something. (theclassicwanderer.com)
- If action potentials could travel backwards, then we would not see this all-or-none behavior, and action potentials would be generated only by very strong stimuli. (theclassicwanderer.com)
- Evoked potentials are the electrical signals generated by the nervous system in response to sensory stimuli. (medscape.com)
- Auditory, visual, and somatosensory stimuli are used commonly for clinical evoked potential studies. (medscape.com)
- Subtraction of the masked AP waveform from the unmasked AP yields a derived potential, provided the continuous tone is above the threshold of cochlear sensitivity. (wustl.edu)
- This relation between the loss in compound action potential (CAP) sensitivity and the noise duty cycle (or rest period) was abolished by the presence of CO. The cochlear microphonic (CM) amplitude revealed similar results to those seen using the CAP. (cdc.gov)
- Action potentials play multiple roles in several types of excitable cells such as neurons, myocytes, and electrocytes. (phys.org)
- This model entry recreates figures 2 and 4 from the paper illustrating how conductance densities of voltage gated channels (fig 2) and the timing of synaptic input with backpropagating action potentials (fig 4) affects membrane voltage trajectories. (yale.edu)
- An association has been curated linking Rnf207 and positive regulation of voltage-gated potassium channel activity involved in ventricular cardiac muscle cell action potential repolarization in Rattus norvegicus. (mcw.edu)
- An action potential is a rapid sequence of changes in the voltage across a membrane. (theburningofrome.com)
- This change in voltage is called an action potential.The action potential travels down the axon to the axon terminal. (theclassicwanderer.com)
- The best known action potentials are pulse-like waves of voltage that travel along axons of neurons. (phys.org)
- Action potentials are caused when different ions cross the neuron membrane. (theburningofrome.com)
- What is an action potential in a neuron? (theburningofrome.com)
- These neurotransmitters cross the synapse and bind to receptors on the dendrites of the next neuron, initiating a new action potential.In this way, action potentials can travel long distances, from the brain to the toes, and allow us to interact with our environment. (theclassicwanderer.com)
- Why is action potential propagation is one way in its movement along a neuron? (theclassicwanderer.com)
- Comparative epidemiology of two potential hazards: threshold for public health action. (cdc.gov)
- At the axon terminal, the action potential triggers the release of chemical signals, called neurotransmitters. (theclassicwanderer.com)
- The study of motor unit action potential (MUAP) activity from electromyographic signals is an important stage on neurological investigations that aim to understand the state of the neuromuscular system. (actapress.com)
- Somatosensory evoked potentials (SEPs) consist of a series of waves that reflect sequential activation of neural structures along the somatosensory pathways. (medscape.com)
- In May 2018, Mr and Mrs Ross commenced a funded class action on behalf of the 3,000 customers who settled with Southern Response following the Canterbury earthquakes (the Ross class action ). (bellgully.com)
- A single action potential evoked a transient increase of intradendritic calcium concentration ([Ca2+]i) that was reduced in size and prolonged when the Fura-2 concentration was increased from 20 to 250 microM. (nih.gov)
- Francis N. Intermittent Fasting and Brain Health: Efficacy and Potential Mechanisms of Action. (lidsen.com)
- The experimental results of the analysis of a data set consisting of MUAPs measured from the surface of the First Dorsal Interosseous, a hand muscle, indicate that the MUAP features corresponding to the hyperpolarization period in the physisiological process of generation of muscle fibre action potentials are consistently estimated as the most relevant and, therefore, as those that should be paid preferential attention for the interpretation of the MUAP groupings. (actapress.com)
- When an insect visits the trap and tilts the mechanosensors on the inner surface, action potentials (APs) are fired. (edu.au)
- Particle penetration through intact skin and a method for determining potential exposure through surface contamination. (cdc.gov)
- In November 2020, the Supreme Court ruled that the Ross class action could be brought on an opt-out basis (see our update on that decision here ). (bellgully.com)
- Meanwhile, in a separate claim brought against Southern Response by Mr and Mrs Dodds, the Court of Appeal ruled in September 2020 that Southern Response misled customers about their earthquake insurance entitlements, in the same way as that alleged in the Ross class action. (bellgully.com)
- We will give strong preference to papers that emphasize an alteration (or a potential alteration) in the fundamental disease course of Alzheimer's disease, vascular aging diseases, osteoarthritis, osteoporosis, skin aging, immune senescence, and other age-related diseases. (lidsen.com)
- Examples of cells that signal via action potentials are neurons and muscle cells. (theburningofrome.com)
- Each muscle fiber that contracts will produce an action potential. (medlineplus.gov)
- The presence, size, and shape of the wave form of the action potential produced on the oscilloscope, provides information about the ability of the muscle to respond to nervous stimulation. (medlineplus.gov)
- NYSDOH have determined that current and potential future exposures to arsenic in shallow residential soil arsenic exposure? (cdc.gov)
- Wash hands after outdoor activities to help reduce the ATSDR will coordinate with state and federal partners potential for exposure. (cdc.gov)
- contaminants of concerns in soil), evaluate the public health implications of additional sampling results, and · Properly maintain water treatment systems in recommend public health actions to reduce exposure, as accordance with the manufacturer's specification. (cdc.gov)
- Public health officials and project managers concerned with appropriate actions to take at hazardous waste sites may want information on levels of exposure associated with more subtle effects in humans or animals (LOAEL) or exposure levels below which no adverse effects (NOAEL) have been observed. (cdc.gov)
- This is the latest study involving the University of Plymouth to examine the potential ecological impacts of both the construction and adaptation of coastal and ocean structures. (plymouth.ac.uk)
- The technique involves recording the cochlear action potential (AP) response to a suprathreshold probe tone, first in the absence and then in the presence of a continuous masking tone at the same frequency. (wustl.edu)
- abstract = "An evoked-potential technique has been evaluated which detects whether the cochlea responds to a continuous, low level tone. (wustl.edu)
- This side event showcased the potential for stepping up implementation of NbS across multiple policy sectors and saw the launch of a new UN Environmental Programme (UNEP) report , and a new initiative to coordinate global efforts to advance NbS. (iisd.org)
- Moderator Inka Gnittke, BMUV , Germany, introduced the event by highlighting the new Enhancing Nature-based Solutions for an Accelerated Climate Transformation (ENACT) initiative to coordinate action on biodiversity and NbS, which was launched by Germany, the Egyptian COP 27 Presidency, and International Union for Conservation of Nature (IUCN). (iisd.org)
- The Action Fund engages in educational, advocacy and electoral activity, including grassroots organizing, legislative advocacy, and voter education. (plannedparenthoodaction.org)
- Among my responsibilities as the president of Sarah Lawrence College is that of monitoring federal and state policy debates and resulting regulatory and legislative actions that could have substantial consequences for the College. (sarahlawrence.edu)
- Two Congressional actions currently under consideration raise significant concerns. (sarahlawrence.edu)
- 1984. The reversal potential of excitatory amino acid action on granule cells of the rat dentate gyrus. (cdc.gov)
- Washington - Planned Parenthood Action Fund President Alexis McGill Johnson released the following statement after President Donald Trump announced he intends to nominate someone to fill Justice Ruth Bader Ginsburg's seat on the Supreme Court on Saturday. (plannedparenthoodaction.org)
- The High Court recently released four related judgments in the class action brought against Southern Response by two of its customers, Mr and Mrs Ross. (bellgully.com)
- The Court rejected the plaintiffs' request that Southern Response be restrained from communicating with potential class members while the plaintiffs sought to build their class by spending opt-out notices. (bellgully.com)
- Finally, action potential propagation is one way because it is an all-or-none response. (theclassicwanderer.com)
- The Planned Parenthood Action Fund works to advance access to sexual health care and defend reproductive rights. (plannedparenthoodaction.org)
- Recent data suggests that this input consists largely of bursts of action potentials (APs). (edu.au)
- The niques and consumption mores, African cas ava - imported from Brazil by the potential health impact of phytocomplexes fo d has some common basic features.3 Portuguese) are very common. (who.int)
- The purpose of this Health Alert Network (HAN) Health Update is to inform clinicians and public health agencies about the potential for new clusters or outbreaks of mpox cases and to provide resources on clinical evaluation, treatment, vaccination, and testing. (cdc.gov)
- The aim of the grant is to promote health research as a tool for national development programming, and to increase the use of evidence-based action and health planning for provision of equitable health care. (who.int)
- Health for All and the Global Plan of Action for Workers' Health. (who.int)
- To counter that, scientists have called for urgent global action so that the construction of future artificial structures - or the decommissioning of existing ones - doesn't create an additional ecological burden on areas of the planet already being severely impacted by the effects of climate change. (plymouth.ac.uk)
- another reason is that action potentials are all-or-none events. (theclassicwanderer.com)
- Lemke highlighted Germany's pledge to increase financing for international action on biodiversity by EUR 1.5 billion and urged reflecting NbS in Nationally Determined Contributions (NDCs) and in the closing declaration of COP 27. (iisd.org)
- Following the Supreme Court's decision, the next step in the class action is for class members notices to be issued, advising class members of the class action and how to opt out. (bellgully.com)
- A combined case seeking class action status would include anyone who purchased or sold futures contracts or an option on NYMEX platinum or palladium or COMEX silver or gold between (at least) January 1, 2009, and December 31, 2015. (bmg-group.com)
- Edmonds admitted that he and other co-conspirators at JPM fraudulently manipulated the precious metals market from 2009 to 2015, the same timeframe covered in the class action suits. (bmg-group.com)
- The action potential is unidirectional because it is an all-or-none event. (theclassicwanderer.com)
- This food price crisis could be worse than in 2011… what are the potential action areas? (foodnavigator.com)
- 2000. Mode of action of liver tumor induction by trichloroethylene and its metabolites, trichloroacetate and dichloroacetate. (cdc.gov)
- But wheat and mil et) - often the main dish at vegetal microRNAs and synergistic action even though each region of Africa has its lunch, is prevalent in the Sahara.Along the of plant bioactive components on endoge- own distinctive dishes, preparation tech- Ivory Coast ro t crops, (primarily yam and nous human microRNA regulation. (who.int)
- "This crisis has the potential to be far more disruptive than the 2010/11 food price hike because the food, fertilizer and energy disruptions are potentially much bigger," warned Professor Tim Benton, Director of the Environment and Society Programme at Chatham House. (foodnavigator.com)