Calcium Channel Blockers
Calcium Channels, L-Type
Calcium Channels, N-Type
Calcium Channels, T-Type
Calcium Channel Agonists
Ion Channel Gating
Potassium Channels, Inwardly Rectifying
Calcium Channels, P-Type
Calcium Channels, R-Type
Potassium Channel Blockers
Potassium Channels, Voltage-Gated
Potassium Channels, Calcium-Activated
Sodium Channel Blockers
TRPC Cation Channels
Shaker Superfamily of Potassium Channels
Large-Conductance Calcium-Activated Potassium Channels
Cyclic Nucleotide-Gated Cation Channels
Molecular Sequence Data
TRPV Cation Channels
Dose-Response Relationship, Drug
Amino Acid Sequence
Ryanodine Receptor Calcium Release Channel
TRPM Cation Channels
Acid Sensing Ion Channels
Epithelial Sodium Channels
Kv1.3 Potassium Channel
Ether-A-Go-Go Potassium Channels
Kv1.2 Potassium Channel
Kv1.1 Potassium Channel
Kv1.5 Potassium Channel
Small-Conductance Calcium-Activated Potassium Channels
Transient Receptor Potential Channels
KCNQ Potassium Channels
Shab Potassium Channels
Shaw Potassium Channels
Kv1.4 Potassium Channel
Protein Structure, Tertiary
G Protein-Coupled Inwardly-Rectifying Potassium Channels
Shal Potassium Channels
KCNQ2 Potassium Channel
Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels
NAV1.5 Voltage-Gated Sodium Channel
Intermediate-Conductance Calcium-Activated Potassium Channels
KCNQ3 Potassium Channel
Large-Conductance Calcium-Activated Potassium Channel alpha Subunits
Inositol 1,4,5-Trisphosphate Receptors
Delayed Rectifier Potassium Channels
NAV1.2 Voltage-Gated Sodium Channel
Voltage-Gated Sodium Channels
Cell Membrane Permeability
Protein Kinase C
Cyclic AMP-Dependent Protein Kinases
Sequence Homology, Amino Acid
NAV1.4 Voltage-Gated Sodium Channel
Voltage-Dependent Anion Channels
Functional consequences of mutations in the human alpha1A calcium channel subunit linked to familial hemiplegic migraine. (1/8682)Mutations in alpha1A, the pore-forming subunit of P/Q-type calcium channels, are linked to several human diseases, including familial hemiplegic migraine (FHM). We introduced the four missense mutations linked to FHM into human alpha1A-2 subunits and investigated their functional consequences after expression in human embryonic kidney 293 cells. By combining single-channel and whole-cell patch-clamp recordings, we show that all four mutations affect both the biophysical properties and the density of functional channels. Mutation R192Q in the S4 segment of domain I increased the density of functional P/Q-type channels and their open probability. Mutation T666M in the pore loop of domain II decreased both the density of functional channels and their unitary conductance (from 20 to 11 pS). Mutations V714A and I1815L in the S6 segments of domains II and IV shifted the voltage range of activation toward more negative voltages, increased both the open probability and the rate of recovery from inactivation, and decreased the density of functional channels. Mutation V714A decreased the single-channel conductance to 16 pS. Strikingly, the reduction in single-channel conductance induced by mutations T666M and V714A was not observed in some patches or periods of activity, suggesting that the abnormal channel may switch on and off, perhaps depending on some unknown factor. Our data show that the FHM mutations can lead to both gain- and loss-of-function of human P/Q-type calcium channels. (+info)
Ionic currents underlying spontaneous action potentials in isolated cerebellar Purkinje neurons. (2/8682)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. (3/8682)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)
Activation of human D3 dopamine receptor inhibits P/Q-type calcium channels and secretory activity in AtT-20 cells. (4/8682)The D3 dopamine receptor is postulated to play an important role in the regulation of neurotransmitter secretion at both pre- and postsynaptic terminals. However, this hypothesis and the underlying mechanisms remain untested because of the lack of D3-selective ligands, paucity of appropriate model secretory systems, and the weak and inconsistent coupling of D3 receptors to classical signal transduction pathways. The absence of ligands that selectively discriminate between D3 and D2 receptors in vivo precludes the study of D3 receptor function in the brain and necessitates the use of heterologous expression systems. In this report we demonstrate that activation of the human D3 dopamine receptor expressed in the AtT-20 neuroendocrine cell line causes robust inhibition of P/Q-type calcium channels via pertussis toxin-sensitive G-proteins. In addition, using the vesicle trafficking dye FM1-43, we show that D3 receptor activation significantly inhibits spontaneous secretory activity in these cells. Our results not only support the hypothesis that the D3 receptor can regulate secretory activity but also provide insight into the underlying signaling mechanisms. We propose a functional model in which the D3 receptor tightly regulates neurotransmitter release at a synapse by only allowing the propagation of spikes above a certain frequency or burst-duration threshold. (+info)
Voltage and calcium use the same molecular determinants to inactivate calcium channels. (5/8682)During sustained depolarization, voltage-gated Ca2+ channels progressively undergo a transition to a nonconducting, inactivated state, preventing Ca2+ overload of the cell. This transition can be triggered either by the membrane potential (voltage-dependent inactivation) or by the consecutive entry of Ca2+ (Ca2+-dependent inactivation), depending on the type of Ca2+ channel. These two types of inactivation are suspected to arise from distinct underlying mechanisms, relying on specific molecular sequences of the different pore-forming Ca2+ channel subunits. Here we report that the voltage-dependent inactivation (of the alpha1A Ca2+ channel) and the Ca2+-dependent inactivation (of the alpha1C Ca2+ channel) are similarly influenced by Ca2+ channel beta subunits. The same molecular determinants of the beta subunit, and therefore the same subunit interactions, influence both types of inactivation. These results strongly suggest that the voltage and the Ca2+-dependent transitions leading to channel inactivation use homologous structures of the different alpha1 subunits and occur through the same molecular process. A model of inactivation taking into account these new data is presented. (+info)
Calmodulin mediates calcium-dependent activation of the intermediate conductance KCa channel, IKCa1. (6/8682)Small and intermediate conductance Ca2+-activated K+ channels play a crucial role in hyperpolarizing the membrane potential of excitable and nonexcitable cells. These channels are exquisitely sensitive to cytoplasmic Ca2+, yet their protein-coding regions do not contain consensus Ca2+-binding motifs. We investigated the involvement of an accessory protein in the Ca2+-dependent gating of hIKCa1, a human intermediate conductance channel expressed in peripheral tissues. Cal- modulin was found to interact strongly with the cytoplasmic carboxyl (C)-tail of hIKCa1 in a yeast two-hybrid system. Deletion analyses defined a requirement for the first 62 amino acids of the C-tail, and the binding of calmodulin to this region did not require Ca2+. The C-tail of hSKCa3, a human neuronal small conductance channel, also bound calmodulin, whereas that of a voltage-gated K+ channel, mKv1.3, did not. Calmodulin co-precipitated with the channel in cell lines transfected with hIKCa1, but not with mKv1. 3-transfected lines. A mutant calmodulin, defective in Ca2+ sensing but retaining binding to the channel, dramatically reduced current amplitudes when co-expressed with hIKCa1 in mammalian cells. Co-expression with varying amounts of wild-type and mutant calmodulin resulted in a dominant-negative suppression of current, consistent with four calmodulin molecules being associated with the channel. Taken together, our results suggest that Ca2+-calmodulin-induced conformational changes in all four subunits are necessary for the channel to open. (+info)
Characterization of elementary Ca2+ release signals in NGF-differentiated PC12 cells and hippocampal neurons. (7/8682)Elementary Ca2+ release signals in nerve growth factor- (NGF-) differentiated PC12 cells and hippocampal neurons, functionally analogous to the "Ca2+ sparks" and "Ca2+ puffs" identified in other cell types, were characterized by confocal microscopy. They either occurred spontaneously or could be activated by caffeine and metabotropic agonists. The release events were dissimilar to the sparks and puffs described so far, as many arose from clusters of both ryanodine receptors (RyRs) and inositol 1,4,5-trisphosphate receptors (InsP3Rs). Increasing either the stimulus strength or loading of the intracellular stores enhanced the frequency of and coupling between elementary release sites and evoked global Ca2+ signals. In the PC12 cells, the elementary Ca2+ release preferentially occurred around the branch points. Spatio-temporal recruitment of such elementary release events may regulate neuronal activities. (+info)
Control and assessment of the uterus and cervix during pregnancy and labour. (8/8682)Preterm labour and resultant preterm birth are the most important problems in perinatology. Countless efforts have failed to establish a single effective treatment of preterm labour, partly because the mechanisms regulating the uterus and cervix during pregnancy are not well understood. New knowledge is needed to inhibit early progression of labour (uterine contractility and cervical ripening), and adequate quantitative tools to evaluate the uterus and cervix during pregnancy are lacking. In this review, we outline studies showing that the uterus (myometrium) and cervix pass through a conditioning step in preparation for labour. This step is not easily identifiable with present methods to assess the uterus or cervix. In the uterus, this seemingly irreversible step consists of changes in the electrical properties to make muscle more excitable and responsive to produce forceful contractions. In the cervix, the step consists of softening of the connective tissue components. Progesterone appears to have a dominant role in controlling both the uterus and cervix, as antiprogestins induce early, preterm conditioning leading to preterm labour. Apparently, nitric oxide (NO) also controls conditioning of the uterus and cervix. In the uterus, NO, in concert with progesterone, inhibits uterine contractility. At term, NO production by the uterus and placenta are decreased and allow labour to progress. In contrast, NO in the cervix increases at the end of pregnancy and it may be the final pathway for stimulating cervical ripening by activation of metalloenzymes. The progress of labour can be assessed non-invasively using electromyographic (EMG) signals from the uterus (the driving force for contractility) recorded from the abdominal surface. Uterine EMG bursts detected in this manner characterize uterine contractile events during human and animal pregnancy. A low uterine EMG activity, measured transabdominally throughout most of pregnancy, rises dramatically during labour. EMG activity also increases substantially during preterm labour in humans and rats. This method may be used one day to predict impending preterm labour and identify control steps and treatments. A quantitative method also assesses the cervix, using an optical device which measures collagen fluorescence in the cervix. The collascope estimates cervical collagen content from a fluorescent signal generated when collagen cross-links are illuminated with excitation light of about 340 nm. The system has proved useful in rats and humans at various stages of pregnancy, and indicates that cervical softening occurs progressively in the last one-third of pregnancy. In rats, collascope readings correlate with resistance measurements made in the isolated cervix, which may help to assess cervical function during pregnancy, and indicate control and treatments. (+info)
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.
There are two types of hypertension:
1. Primary Hypertension: This type of hypertension has no identifiable cause and is also known as essential hypertension. It accounts for about 90% of all cases of hypertension.
2. Secondary Hypertension: This type of hypertension is caused by an underlying medical condition or medication. It accounts for about 10% of all cases of hypertension.
Some common causes of secondary hypertension include:
* Kidney disease
* Adrenal gland disorders
* Hormonal imbalances
* Certain medications
* Sleep apnea
* Cocaine use
There are also several risk factors for hypertension, including:
* Age (the risk increases with age)
* Family history of hypertension
* Lack of exercise
* High sodium intake
* Low potassium intake
Hypertension is often asymptomatic, and it can cause damage to the blood vessels and organs over time. Some potential complications of hypertension include:
* Heart disease (e.g., heart attacks, heart failure)
* Kidney disease (e.g., chronic kidney disease, end-stage renal disease)
* Vision loss (e.g., retinopathy)
* Peripheral artery disease
Hypertension is typically diagnosed through blood pressure readings taken over a period of time. Treatment for hypertension may include lifestyle changes (e.g., diet, exercise, stress management), medications, or a combination of both. The goal of treatment is to reduce the risk of complications and improve quality of life.
The symptoms of LEMS typically develop gradually over time and may include:
1. Muscle weakness that worsens with activity and improves with rest.
2. Weakness in the legs, hips, and shoulders.
3. Fatigue and muscle cramps.
4. Difficulty walking or standing upright.
5. Double vision or other eye problems.
6. Dry mouth and difficulty swallowing.
7. Increased heart rate and blood pressure.
8. Impaired reflexes.
9. Decreased sweating.
10. Weight loss.
The exact cause of LEMS is not known, but it is believed to be an autoimmune disorder in which the immune system mistakenly attacks the VGCCs in the neuromuscular junction. The condition is often associated with other autoimmune disorders such as thyroiditis, vitiligo, and adrenal insufficiency.
There is no cure for LEMS, but treatment options are available to manage the symptoms. These may include:
1. Immunosuppressive medications such as prednisone to reduce inflammation and suppress the immune system.
2. Intracranial pressure-lowering medications such as acetazolamide to reduce the pressure in the brain.
3. Muscle strengthening exercises to improve muscle function.
4. Physical therapy to maintain muscle strength and flexibility.
5. Orthostatic hypotension medications to manage orthostatic hypotension (a drop in blood pressure when standing).
6. Pain management medications to relieve muscle cramps, spasms, or pain.
7. Nutritional support to ensure adequate nutrition and prevent weight loss.
8. Respiratory support as needed to manage respiratory muscle weakness.
9. Speech therapy to improve communication skills.
10. Psychological support to cope with the emotional and social challenges of the condition.
It is important for individuals with LEMS to work closely with their healthcare team to manage their symptoms and prevent complications. With proper treatment, many people with LEMS can lead active and fulfilling lives.
The diagnosis of absence epilepsy is typically made based on a combination of clinical findings, including:
-A history of recurrent brief loss of awareness or staring spells
-Normal neurological examination between episodes
-Abnormal EEG activity during seizures (spikes or sharp waves)
Treatment for absence epilepsy usually involves medication, such as ethosuximide, valproic acid, or lamotrigine. In some cases, surgery may be considered if medications are ineffective or have significant side effects.
It is important to note that absence epilepsy can be a challenging condition to diagnose and treat, as the spells can be difficult to distinguish from other conditions such as daydreaming or attention deficit hyperactivity disorder (ADHD).
Some common types of calcium metabolism disorders include:
1. Hypocalcemia (low calcium levels): This can be caused by a deficiency in dietary calcium intake, malabsorption of calcium, or excessive urinary excretion of calcium. Symptoms can include muscle cramps, tremors, and tingling sensations in the fingers and toes.
2. Hypercalcemia (high calcium levels): This can be caused by an overactive parathyroid gland, cancer, or excessive intake of vitamin D. Symptoms can include fatigue, nausea, constipation, and kidney stones.
3. Osteoporosis: This is a condition characterized by weak and brittle bones that can lead to fractures. It is often associated with hormonal imbalances, vitamin D deficiency, or other factors that disrupt calcium metabolism.
4. Hyperparathyroidism (overactive parathyroid gland): This is a condition in which the parathyroid glands produce too much parathyroid hormone (PTH), leading to elevated calcium levels and potential complications such as kidney stones, bone loss, and cardiovascular disease.
5. Vitamin D-dependent rickets type 1: This is a rare genetic disorder that affects the body's ability to absorb vitamin D and maintain normal calcium levels. It can lead to softening of the bones and other skeletal deformities.
6. Familial hypophosphatemic rickets type 1: This is a rare genetic disorder that affects the body's ability to regulate phosphate levels, leading to softening of the bones and other skeletal deformities.
7. Tumor-induced osteomalacia: This is a condition in which cancerous tumors, typically found in the lung or breast, produce high levels of proteins that interfere with the body's ability to absorb vitamin D and maintain normal calcium levels. It can lead to softening of the bones and other skeletal deformities.
8. Chronic kidney disease: This is a condition in which the kidneys are not functioning properly, leading to elevated levels of phosphate and other waste products in the blood. It can lead to softening of the bones and other complications such as heart disease.
9. Paget's disease of bone: This is a condition that affects the way bones grow and repair themselves, leading to deformities and pain. It is often associated with inflammation and elevated levels of calcium in the blood.
10. Chronic alcoholism: Prolonged heavy drinking can lead to deficiencies in vitamin D and calcium, as well as other nutrients that are essential for bone health. It can increase the risk of osteoporosis and fractures.
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.
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.
There are several types of kidney calculi, including:
1. Calcium oxalate calculi: These are the most common type of calculus and are often associated with conditions such as hyperparathyroidism or excessive intake of calcium supplements.
2. Uric acid calculi: These are more common in people with gout or a diet high in meat and sugar.
3. Cystine calculi: These are rare and usually associated with a genetic disorder called cystinuria.
4. Struvite calculi: These are often seen in women with urinary tract infections (UTIs).
Symptoms of kidney calculi may include:
1. Flank pain (pain in the side or back)
2. Pain while urinating
3. Blood in the urine
4. Cloudy or strong-smelling urine
5. Fever and chills
6. Nausea and vomiting
Kidney calculi are diagnosed through a combination of physical examination, medical history, and diagnostic tests such as X-rays, CT scans, or ultrasound. Treatment options for kidney calculi depend on the size and location of the calculus, as well as the severity of any underlying conditions. Small calculi may be treated with conservative measures such as fluid intake and medication to help flush out the crystals, while larger calculi may require surgical intervention to remove them.
Preventive measures for kidney calculi include staying hydrated to help flush out excess minerals in the urine, maintaining a balanced diet low in oxalate and animal protein, and avoiding certain medications that can increase the risk of calculus formation. Early detection and treatment of underlying conditions such as hyperparathyroidism or gout can also help prevent the development of kidney calculi.
Overall, kidney calculi are a common condition that can be managed with proper diagnosis and treatment. However, they can cause significant discomfort and potentially lead to complications if left untreated, so it is important to seek medical attention if symptoms persist or worsen over time.
The symptoms of hypokalemic periodic paralysis can vary in severity and may include:
* Muscle weakness or paralysis, typically affecting the legs but sometimes affecting the arms or face as well
* Muscle cramps and twitching
* Abnormal heart rhythms
* Weakness or paralysis of the respiratory muscles, which can lead to breathing difficulties
* Vision problems, such as blurred vision or double vision
* Dizziness and fainting
The exact cause of hypokalemic periodic paralysis is not known, but it is thought to be related to mutations in certain genes that affect the way potassium ions are regulated in the body. The disorder is usually diagnosed through a combination of clinical evaluation, laboratory tests, and genetic analysis.
There is no cure for hypokalemic periodic paralysis, but treatment options may include:
* Potassium supplements to maintain normal potassium levels in the blood
* Medications to regulate heart rhythms and prevent abnormal heartbeats
* Physical therapy to improve muscle strength and function
* Avoiding triggers such as stress, certain medications, or changes in potassium levels
* In severe cases, a pacemaker may be implanted to regulate the heartbeat.
It is important to note that hypokalemic periodic paralysis can be a challenging disorder to manage and may have a significant impact on quality of life. However, with proper treatment and management, many individuals with this condition are able to lead active and fulfilling lives.
Some common causes of hypocalcemia include:
1. Vitamin D deficiency: Vitamin D is essential for the absorption of calcium from the diet. A lack of vitamin D can lead to low levels of calcium in the blood.
2. Parathyroid gland disorders: The parathyroid glands are located in the neck and regulate calcium levels in the blood. Disorders such as hypoparathyroidism (underactive parathyroid glands) or hyperparathyroidism (overactive parathyroid glands) can cause hypocalcemia.
3. Malabsorption: Certain conditions, such as celiac disease or Crohn's disease, can lead to malabsorption of nutrients, including calcium.
4. Kidney problems: Kidney failure can cause hypocalcemia by reducing the amount of calcium that is excreted in the urine.
5. Hypomagnesemia (low levels of magnesium): Magnesium is important for calcium metabolism, and low levels of magnesium can contribute to hypocalcemia.
Symptoms of hypocalcemia can include:
1. Muscle cramps
3. Twitching or tremors
5. Tingling or numbness in the fingers and toes
6. Difficulty swallowing
Treatment for hypocalcemia usually involves addressing the underlying cause of the condition. For example, if the condition is caused by a vitamin D deficiency, supplements may be prescribed. If the condition is caused by a parathyroid gland disorder, surgery may be necessary to remove the affected gland or glands. In some cases, calcium supplements may be prescribed to help restore normal calcium levels.
It's important to note that hypocalcemia can be a sign of an underlying condition, and it should be treated promptly to prevent complications. If you suspect you or someone you know may have hypocalcemia, it is important to seek medical attention as soon as possible. A healthcare professional can diagnose the condition and recommend appropriate treatment.
* Genetic mutations or deletions
* Infections such as meningitis or encephalitis
* Stroke or bleeding in the brain
* Traumatic head injury
* Multiple sclerosis or other demyelinating diseases
* Brain tumors
* Cerebellar degeneration due to aging
* Coordination difficulties, such as stumbling or poor balance
* Tremors or shaky movements
* Slurred speech and difficulty with fine motor skills
* Nystagmus (involuntary eye movements)
* Difficulty with gait and walking
* Fatigue, weakness, and muscle wasting
* Physical examination and medical history
* Neurological examination to test coordination, balance, and reflexes
* Imaging studies such as MRI or CT scans to rule out other conditions
* Genetic testing to identify inherited forms of cerebellar ataxia
* Electromyography (EMG) to test muscle activity and nerve function
* Physical therapy to improve balance, coordination, and gait
* Occupational therapy to help with daily activities and fine motor skills
* Speech therapy to address slurred speech and communication difficulties
* Medications to manage symptoms such as tremors or spasticity
* Assistive devices such as canes or walkers to improve mobility
* The prognosis for cerebellar ataxia varies depending on the underlying cause. In some cases, the condition may be slowly progressive and lead to significant disability over time. In other cases, the condition may remain stable or even improve with treatment.
Living with cerebellar ataxia can be challenging, but there are many resources available to help individuals with the condition manage their symptoms and maintain their quality of life. These resources may include:
* Physical therapy to improve balance and coordination
* Occupational therapy to assist with daily activities
* Speech therapy to address communication difficulties
* Assistive devices such as canes or walkers to improve mobility
* Medications to manage symptoms such as tremors or spasticity
* Support groups for individuals with cerebellar ataxia and their families
Overall, the key to managing cerebellar ataxia is early diagnosis and aggressive treatment. With proper management, individuals with this condition can lead active and fulfilling lives despite the challenges they face.
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 symptoms of hypercalcemia may include:
* Nausea and vomiting
* Abdominal pain
* Kidney stones
* Bone pain or fractures
If left untreated, hypercalcemia can lead to complications such as kidney damage, heart problems, and an increased risk of osteoporosis. Treatment options may include medications to reduce calcium levels, surgery to remove a tumor or overactive parathyroid gland, or dialysis if the patient has kidney failure.
Early diagnosis and treatment are important to prevent long-term complications and improve the patient's quality of life.
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.
Neuralgia is often difficult to diagnose and treat, as the underlying cause can be challenging to identify. However, various medications and therapies can help manage the pain and other symptoms associated with this condition. These may include pain relievers, anticonvulsants, antidepressants, and muscle relaxants, as well as alternative therapies such as acupuncture or physical therapy.
Some common forms of neuralgia include:
1. Trigeminal neuralgia: This is a condition that affects the trigeminal nerve, which carries sensation from the face to the brain. It is characterized by sudden, intense pain in the face, typically on one side.
2. Postherpetic neuralgia (PHN): This is a condition that occurs after a shingles infection, and is characterized by persistent pain in the affected area.
3. Occipital neuralgia: This is a condition that affects the nerves in the back of the head and neck, and can cause pain in the back of the head, neck, and face.
4. Geniculate neuralgia: This is a rare condition that affects the nerves in the jaw and ear, and can cause pain in the jaw, face, and ear.
Overall, neuralgia is a complex and debilitating condition that can significantly impact an individual's quality of life. It is important for individuals experiencing symptoms of neuralgia to seek medical attention to determine the underlying cause and develop an appropriate treatment plan.
There are several types of ataxia, each with different symptoms and causes. Some common forms of ataxia include:
1. Spinocerebellar ataxia (SCA): This is the most common form of ataxia and is caused by a degeneration of the cerebellum and spinal cord. It can cause progressive weakness, loss of coordination, and difficulty with speaking and swallowing.
2. Friedreich's ataxia: This is the second most common form of ataxia and is caused by a deficiency of vitamin E in the body. It can cause weakness in the legs, difficulty walking, and problems with speech and language.
3. Ataxia-telangiectasia (AT): This is a rare form of ataxia that is caused by a gene mutation. It can cause progressive weakness, loss of coordination, and an increased risk of developing cancer.
4. Acute cerebellar ataxia: This is a sudden and temporary form of ataxia that can be caused by a variety of factors such as infections, injuries, or certain medications.
5. Drug-induced ataxia: Certain medications can cause ataxia as a side effect.
6. Vitamin deficiency ataxia: Deficiencies in vitamins such as vitamin B12 or folate can cause ataxia.
7. Metabolic disorders: Certain metabolic disorders such as hypothyroidism, hyperthyroidism, and hypoglycemia can cause ataxia.
8. Stroke or brain injury: Ataxia can be a result of a stroke or brain injury.
9. Multiple system atrophy (MSA): This is a rare progressive neurodegenerative disorder that can cause ataxia, parkinsonism, and autonomic dysfunction.
10. Spinocerebellar ataxia (SCA): This is a group of rare genetic disorders that can cause progressive cerebellar ataxia, muscle wasting, and other signs and symptoms.
It's important to note that this is not an exhaustive list and there may be other causes of ataxia not mentioned here. If you suspect you or someone you know may have ataxia, it is important to consult a healthcare professional for proper diagnosis and treatment.
There are several different types of pain, including:
1. Acute pain: This type of pain is sudden and severe, and it usually lasts for a short period of time. It can be caused by injuries, surgery, or other forms of tissue damage.
2. Chronic pain: This type of pain persists over a long period of time, often lasting more than 3 months. It can be caused by conditions such as arthritis, fibromyalgia, or nerve damage.
3. Neuropathic pain: This type of pain results from damage to the nervous system, and it can be characterized by burning, shooting, or stabbing sensations.
4. Visceral pain: This type of pain originates in the internal organs, and it can be difficult to localize.
5. Psychogenic pain: This type of pain is caused by psychological factors such as stress, anxiety, or depression.
The medical field uses a range of methods to assess and manage pain, including:
1. Pain rating scales: These are numerical scales that patients use to rate the intensity of their pain.
2. Pain diaries: These are records that patients keep to track their pain over time.
3. Clinical interviews: Healthcare providers use these to gather information about the patient's pain experience and other relevant symptoms.
4. Physical examination: This can help healthcare providers identify any underlying causes of pain, such as injuries or inflammation.
5. Imaging studies: These can be used to visualize the body and identify any structural abnormalities that may be contributing to the patient's pain.
6. Medications: There are a wide range of medications available to treat pain, including analgesics, nonsteroidal anti-inflammatory drugs (NSAIDs), and muscle relaxants.
7. Alternative therapies: These can include acupuncture, massage, and physical therapy.
8. Interventional procedures: These are minimally invasive procedures that can be used to treat pain, such as nerve blocks and spinal cord stimulation.
It is important for healthcare providers to approach pain management with a multi-modal approach, using a combination of these methods to address the physical, emotional, and social aspects of pain. By doing so, they can help improve the patient's quality of life and reduce their suffering.
There are several different types of calcinosis, each with its own unique causes and symptoms. Some common forms of calcinosis include:
1. Dystrophic calcinosis: This type of calcinosis occurs in people with muscular dystrophy, a group of genetic disorders that affect muscle strength and function. Dystrophic calcinosis can cause calcium deposits to form in the muscles, leading to muscle weakness and wasting.
2. Metastatic calcinosis: This type of calcinosis occurs when cancer cells spread to other parts of the body and cause calcium deposits to form. Metastatic calcinosis can occur in people with a variety of different types of cancer, including breast, lung, and prostate cancer.
3. Idiopathic calcinosis: This type of calcinosis occurs for no apparent reason, and the exact cause is not known. Idiopathic calcinosis can affect people of all ages and can cause calcium deposits to form in a variety of different tissues.
4. Secondary calcinosis: This type of calcidosis occurs as a result of an underlying medical condition or injury. For example, secondary calcinosis can occur in people with kidney disease, hyperparathyroidism (a condition in which the parathyroid glands produce too much parathyroid hormone), or traumatic injuries.
Treatment for calcinosis depends on the underlying cause and the severity of the condition. In some cases, treatment may involve managing the underlying disease or condition that is causing the calcium deposits to form. Other treatments may include medications to reduce inflammation and pain, physical therapy to improve mobility and strength, and surgery to remove the calcium deposits.
Causes: There are several causes of night blindness, including:
1. Vitamin A deficiency: Vitamin A is essential for the health of the retina, and a deficiency can lead to night blindness.
2. Retinitis pigmentosa: This is a group of inherited conditions that can cause progressive damage to the retina and result in night blindness.
3. Cataracts: A cataract can cause a person to become night blind by blocking the light that enters the eye.
4. Glaucoma: This is a group of eye conditions that can damage the optic nerve and lead to vision loss, including night blindness.
5. Other medical conditions: Certain medical conditions such as diabetes, multiple sclerosis, and stroke can cause night blindness.
Symptoms: The symptoms of night blindness can vary depending on the underlying cause, but common symptoms include:
1. Difficulty seeing in low light environments
2. Blind spots or missing areas of vision
3. Sensitivity to light
4. Glare or halos around lights
5. Difficulty adjusting to changes in light levels
Diagnosis: Night blindness is typically diagnosed through a comprehensive eye exam, which may include a visual acuity test, refraction test, and retinal examination. Imaging tests such as an OCT scan or retinal photography may also be used to evaluate the retina and optic nerve.
Treatment: The treatment of night blindness depends on the underlying cause. For example, vitamin A supplements may be prescribed for a vitamin A deficiency, while cataract surgery may be recommended for cataracts. In some cases, no treatment may be necessary, and the condition may resolve on its own over time.
Prevention: While some cases of night blindness are unavoidable, there are steps you can take to reduce your risk of developing the condition. These include:
1. Maintaining a healthy diet that includes foods rich in vitamin A and other essential nutrients for eye health.
2. Wearing sunglasses with UV protection to protect your eyes from excessive sunlight.
3. Avoiding smoking and excessive alcohol consumption, which can damage the optic nerve and retina.
4. Getting regular eye exams to detect any underlying eye problems early on.
5. Wearing protective eyewear when engaging in activities that could potentially harm your eyes, such as sports or working with hazardous materials.
Migraine with aura is considered to be a more severe form of migraine than migraine without aura, which does not have the same neurological symptoms before the headache. Migraine with aura is also associated with a higher risk of other health problems, such as stroke and dementia.
There are several treatments available for migraine with aura, including medications that can help to reduce the frequency and severity of the headaches, as well as lifestyle changes such as avoiding triggers and getting regular exercise. It is important for people who experience migraine with aura to work closely with their healthcare provider to develop an effective treatment plan.
* Type 1: Hypokalemic Periodic Paralysis (Hyperkalemia-induced muscle weakness)
* Type 2: Hyperkalemic Periodic Paralysis (K+ channels dysfunction, leading to muscle weakness)
* Type 3: Peripheral nerve damage causing FPPA
* Type 4: Central nervous system damage causing FPPA
Slide 3: Causes of Familial Periodic Paralysis (FPPA)
* Genetic mutations in SCN4A, KCNA1, and other genes involved in ion channel function
* Abnormalities in the expression and function of ion channels
* Autosomal dominant or recessive inheritance pattern
Slide 4: Symptoms of Familial Periodic Paralysis (FPPA)
* Muscle weakness or paralysis, often triggered by changes in diet, physical activity, or other environmental factors
* Weakness of the lower extremities more pronounced than the upper extremities
* Muscle cramps and twitching
* Abdominal pain
* Nausea and vomiting
Slide 5: Diagnosis of Familial Periodal Paralysis (FPPA)
* Clinical evaluation, including patient history and physical examination
* Electromyography (EMG) to assess muscle activity and diagnose FPPA
* Genetic testing to identify genetic mutations associated with FPPA
* Blood tests to measure potassium levels and rule out other conditions
Slide 6: Treatment of Familial Periodic Paralysis (FPPA)
* Potassium supplements to maintain normal potassium levels
* Avoiding triggers such as stress, cold temperature, and certain medications
* Physical therapy to improve muscle strength and function
* Pain management with analgesics and other medications as needed
Slide 7: Prognosis of Familial Periodic Paralysis (FPPA)
* FPPA is a chronic condition with no cure, but with proper management, patients can lead relatively normal lives
* The prognosis varies depending on the severity and frequency of attacks, as well as the presence of any complications
* Early diagnosis and treatment can improve the quality of life for patients with FPPA
Slide 8: Current Research in Familial Periodic Paralysis (FPPA)
* Genetic research to better understand the underlying causes of FPPA and develop new treatments
* Studies on the effectiveness of new medications and therapies for FPPA
* Investigation into the potential use of stem cells for treating FPPA
Slide 9: Current Challenges in Familial Periodic Paralysis (FPPA)
* Limited awareness and understanding of FPPA among healthcare professionals and the general public
* Lack of effective treatments for severe cases of FPPA
* Limited availability of specialized care and support for patients with FPPA
Slide 10: Conclusion
* Familial periodic paralysis (FPPA) is a rare and complex condition that affects both children and adults
* Early diagnosis and proper management are critical to improving the quality of life for patients with FPPA
* Ongoing research offers hope for new treatments and therapies, but more work needs to be done to increase awareness and understanding of this condition.
Insulinoma is a rare type of pancreatic tumor that produces excess insulin, leading to low blood sugar levels. These tumors are typically benign and can be treated with surgery or medication.
Insulinomas account for only about 5% of all pancreatic neuroendocrine tumors. They usually occur in the head of the pancreas and can cause a variety of symptoms, including:
1. Hypoglycemia (low blood sugar): The excess insulin produced by the tumor can cause blood sugar levels to drop too low, leading to symptoms such as shakiness, dizziness, confusion, and rapid heartbeat.
2. Hyperinsulinism (elevated insulin levels): In addition to hypoglycemia, insulinomas can also cause elevated insulin levels in the blood.
3. Abdominal pain: Insulinomas can cause abdominal pain and discomfort.
4. Weight loss: Patients with insulinomas may experience unexplained weight loss.
5. Nausea and vomiting: Some patients may experience nausea and vomiting due to the hypoglycemia or other symptoms caused by the tumor.
Insulinomas are usually diagnosed through a combination of imaging tests such as CT scans, MRI scans, and PET scans, and by measuring insulin and C-peptide levels in the blood. Treatment options for insulinomas include surgery to remove the tumor, medications to control hypoglycemia and hyperinsulinism, and somatostatin analogs to reduce hormone secretion.
Insulinoma is a rare and complex condition that requires careful management by a multidisciplinary team of healthcare professionals, including endocrinologists, surgeons, and radiologists. With appropriate treatment, most patients with insulinomas can experience long-term remission and improved quality of life.
Hyperalgesia is often seen in people with chronic pain conditions, such as fibromyalgia, and it can also be a side effect of certain medications or medical procedures. Treatment options for hyperalgesia depend on the underlying cause of the condition, but may include pain management techniques, physical therapy, and medication adjustments.
In clinical settings, hyperalgesia is often assessed using a pinprick test or other pain tolerance tests to determine the patient's sensitivity to different types of stimuli. The goal of treatment is to reduce the patient's pain and improve their quality of life.
There are different types of anoxia, including:
1. Cerebral anoxia: This occurs when the brain does not receive enough oxygen, leading to cognitive impairment, confusion, and loss of consciousness.
2. Pulmonary anoxia: This occurs when the lungs do not receive enough oxygen, leading to shortness of breath, coughing, and chest pain.
3. Cardiac anoxia: This occurs when the heart does not receive enough oxygen, leading to cardiac arrest and potentially death.
4. Global anoxia: This is a complete lack of oxygen to the entire body, leading to widespread tissue damage and death.
Treatment for anoxia depends on the underlying cause and the severity of the condition. In some cases, hospitalization may be necessary to provide oxygen therapy, pain management, and other supportive care. In severe cases, anoxia can lead to long-term disability or death.
Prevention of anoxia is important, and this includes managing underlying medical conditions such as heart disease, diabetes, and respiratory problems. It also involves avoiding activities that can lead to oxygen deprivation, such as scuba diving or high-altitude climbing, without proper training and equipment.
In summary, anoxia is a serious medical condition that occurs when there is a lack of oxygen in the body or specific tissues or organs. It can cause cell death and tissue damage, leading to serious health complications and even death if left untreated. Early diagnosis and treatment are crucial to prevent long-term disability or death.
There are two main types of myotonia:
1. Thomsen's disease: This is an inherited form of myotonia that affects the muscles of the face, neck, and limbs. It is caused by mutations in the CLCN1 gene and can be severe, causing difficulty with speaking, swallowing, and breathing.
2. Becker's muscular dystrophy: This is a form of muscular dystrophy that affects both the skeletal and cardiac muscles. It is caused by mutations in the DMPK gene and can cause myotonia, muscle weakness, and heart problems.
The symptoms of myotonia can vary depending on the severity of the condition and may include:
* Muscle stiffness and rigidity
* Spasms or twitches
* Difficulty with movement and mobility
* Fatigue and weakness
* Muscle wasting
Myotonia can be diagnosed through a combination of physical examination, medical history, and diagnostic tests such as electromyography (EMG) and muscle biopsy. There is no cure for myotonia, but treatment options may include:
* Physical therapy to improve movement and mobility
* Medications to relax muscles and reduce spasms
* Lifestyle modifications such as avoiding triggers and taking regular breaks to rest
* Surgery in severe cases to release or lengthen affected muscles.
It is important to note that myotonia can be a symptom of other underlying conditions, so proper diagnosis and management by a healthcare professional is essential to determine the best course of treatment.
There are many different types of seizures, each with its own unique set of symptoms. Some common types of seizures include:
1. Generalized seizures: These seizures affect both sides of the brain and can cause a range of symptoms, including convulsions, loss of consciousness, and muscle stiffness.
2. Focal seizures: These seizures affect only one part of the brain and can cause more specific symptoms, such as weakness or numbness in a limb, or changes in sensation or vision.
3. Tonic-clonic seizures: These seizures are also known as grand mal seizures and can cause convulsions, loss of consciousness, and muscle stiffness.
4. Absence seizures: These seizures are also known as petit mal seizures and can cause a brief loss of consciousness or staring spell.
5. Myoclonic seizures: These seizures can cause sudden, brief muscle jerks or twitches.
6. Atonic seizures: These seizures can cause a sudden loss of muscle tone, which can lead to falls or drops.
7. Lennox-Gastaut syndrome: This is a rare and severe form of epilepsy that can cause multiple types of seizures, including tonic, atonic, and myoclonic seizures.
Seizures can be diagnosed through a combination of medical history, physical examination, and diagnostic tests such as electroencephalography (EEG) or imaging studies. Treatment for seizures usually involves anticonvulsant medications, but in some cases, surgery or other interventions may be necessary.
Overall, seizures are a complex and multifaceted symptom that can have a significant impact on an individual's quality of life. It is important to seek medical attention if you or someone you know is experiencing seizures, as early diagnosis and treatment can help to improve outcomes and reduce the risk of complications.
The exact cause of malignant hyperthermia is not fully understood, but it is believed to be related to a genetic predisposition and exposure to certain anesthetic agents. The condition can be triggered by a variety of factors, including the use of certain anesthetics, stimulation of the sympathetic nervous system, and changes in blood sugar levels.
Symptoms of malignant hyperthermia can include:
* Elevated body temperature (usually above 104°F/40°C)
* Muscle rigidity and stiffness
* Heart arrhythmias and palpitations
* Shivering or tremors
* Confusion, agitation, or other neurological symptoms
* Shortness of breath or respiratory failure
If left untreated, malignant hyperthermia can lead to serious complications such as seizures, brain damage, and even death. Treatment typically involves the immediate discontinuation of any triggering anesthetic agents, cooling measures such as ice packs or cold compresses, and medications to help regulate body temperature and reduce muscle rigidity. In severe cases, mechanical ventilation may be necessary to support breathing.
Overall, malignant hyperthermia is a rare but potentially life-threatening condition that requires prompt recognition and treatment to prevent serious complications and improve outcomes.
The condition is characterized by the excessive growth of gum tissue, which can lead to:
1. Redness and swelling of the gums
2. Bleeding while brushing or flossing
3. Bad breath (halitosis)
4. Pocket formation between the teeth and gums
5. Gum recession
6. Tooth loss
Gingival hyperplasia can be treated by addressing the underlying cause, improving oral hygiene, and undergoing scaling and root planing procedures to remove plaque and tartar. In severe cases, surgical intervention may be necessary to remove excess gum tissue and restore the natural contours of the mouth.
It is important for individuals to practice good oral hygiene, including brushing at least twice a day with fluoride toothpaste, flossing daily, and receiving regular dental cleanings to prevent gingival hyperplasia and other gum diseases. Early detection and treatment can help prevent the progression of the condition and restore the health of the teeth and gums.
Myocardial ischemia can be caused by a variety of factors, including coronary artery disease, high blood pressure, diabetes, and smoking. It can also be triggered by physical exertion or stress.
There are several types of myocardial ischemia, including:
1. Stable angina: This is the most common type of myocardial ischemia, and it is characterized by a predictable pattern of chest pain that occurs during physical activity or emotional stress.
2. Unstable angina: This is a more severe type of myocardial ischemia that can occur without any identifiable trigger, and can be accompanied by other symptoms such as shortness of breath or vomiting.
3. Acute coronary syndrome (ACS): This is a condition that includes both stable angina and unstable angina, and it is characterized by a sudden reduction in blood flow to the heart muscle.
4. Heart attack (myocardial infarction): This is a type of myocardial ischemia that occurs when the blood flow to the heart muscle is completely blocked, resulting in damage or death of the cardiac tissue.
Myocardial ischemia can be diagnosed through a variety of tests, including electrocardiograms (ECGs), stress tests, and imaging studies such as echocardiography or cardiac magnetic resonance imaging (MRI). Treatment options for myocardial ischemia include medications such as nitrates, beta blockers, and calcium channel blockers, as well as lifestyle changes such as quitting smoking, losing weight, and exercising regularly. In severe cases, surgical procedures such as coronary artery bypass grafting or angioplasty may be necessary.
There are several types of acidosis, including:
1. Respiratory acidosis: This occurs when the lung's ability to remove carbon dioxide from the blood is impaired, leading to an increase in blood acidity.
2. Metabolic acidosis: This type of acidosis occurs when there is an excessive production of acid in the body due to factors such as diabetes, starvation, or kidney disease.
3. Mixed acidosis: This type of acidosis is a combination of respiratory and metabolic acidosis.
4. Severe acute respiratory acidosis (SARA): This is a life-threatening condition that occurs suddenly, usually due to a severe lung injury or aspiration of a corrosive substance.
The symptoms of acidosis can vary depending on the type and severity of the condition. Common symptoms include:
5. Nausea and vomiting
6. Abdominal pain
7. Difficulty breathing
8. Rapid heart rate
9. Muscle twitching
If left untreated, acidosis can lead to complications such as:
1. Kidney damage
4. Heart arrhythmias
5. Respiratory failure
Treatment of acidosis depends on the underlying cause and the severity of the condition. Some common treatments include:
1. Oxygen therapy
2. Medications to help regulate breathing and heart rate
3. Fluid and electrolyte replacement
4. Dietary changes
5. Surgery, in severe cases.
In conclusion, acidosis is a serious medical condition that can have severe consequences if left untreated. It is important to seek medical attention immediately if you suspect that you or someone else may have acidosis. With prompt and appropriate treatment, it is possible to effectively manage the condition and prevent complications.
There are many different types of epilepsy, each with its own unique set of symptoms and characteristics. Some common forms of epilepsy include:
1. Generalized Epilepsy: This type of epilepsy affects both sides of the brain and can cause a range of seizure types, including absence seizures, tonic-clonic seizures, and atypical absence seizures.
2. Focal Epilepsy: This type of epilepsy affects only one part of the brain and can cause seizures that are localized to that area. There are several subtypes of focal epilepsy, including partial seizures with complex symptoms and simple partial seizures.
3. Tonic-Clonic Epilepsy: This type of epilepsy is also known as grand mal seizures and can cause a loss of consciousness, convulsions, and muscle stiffness.
4. Lennox-Gastaut Syndrome: This is a rare and severe form of epilepsy that typically develops in early childhood and can cause multiple types of seizures, including tonic, atonic, and myoclonic seizures.
5. Dravet Syndrome: This is a rare genetic form of epilepsy that typically develops in infancy and can cause severe, frequent seizures.
6. Rubinstein-Taybi Syndrome: This is a rare genetic disorder that can cause intellectual disability, developmental delays, and various types of seizures.
7. Other forms of epilepsy include Absence Epilepsy, Myoclonic Epilepsy, and Atonic Epilepsy.
The symptoms of epilepsy can vary widely depending on the type of seizure disorder and the individual affected. Some common symptoms of epilepsy include:
1. Seizures: This is the most obvious symptom of epilepsy and can range from mild to severe.
2. Loss of consciousness: Some people with epilepsy may experience a loss of consciousness during a seizure, while others may remain aware of their surroundings.
3. Confusion and disorientation: After a seizure, some people with epilepsy may feel confused and disoriented.
4. Memory loss: Seizures can cause short-term or long-term memory loss.
5. Fatigue: Epilepsy can cause extreme fatigue, both during and after a seizure.
6. Emotional changes: Some people with epilepsy may experience emotional changes, such as anxiety, depression, or mood swings.
7. Cognitive changes: Epilepsy can affect cognitive function, including attention, memory, and learning.
8. Sleep disturbances: Some people with epilepsy may experience sleep disturbances, such as insomnia or sleepiness.
9. Physical symptoms: Depending on the type of seizure, people with epilepsy may experience physical symptoms such as muscle weakness, numbness or tingling, and sensory changes.
10. Social isolation: Epilepsy can cause social isolation due to fear of having a seizure in public or stigma associated with the condition.
It's important to note that not everyone with epilepsy will experience all of these symptoms, and some people may have different symptoms depending on the type of seizure they experience. Additionally, some people with epilepsy may experience additional symptoms not listed here.
Symptoms of pheochromocytoma can include:
* Rapid heartbeat
* High blood pressure
* Weight loss
* Nausea and vomiting
If left untreated, pheochromocytoma can lead to complications such as heart failure, stroke, and even death. Therefore, it is important that individuals who experience any of the above symptoms seek medical attention as soon as possible.
Treatment options for pheochromocytoma may include surgery to remove the tumor, medication to manage symptoms, and in some cases, radiation therapy. In rare cases, the tumor may recur after treatment, so regular monitoring is necessary to ensure that any new symptoms are detected early on.
Overall, while pheochromocytoma is a rare and potentially life-threatening condition, prompt medical attention and appropriate treatment can help manage symptoms and prevent complications.
Calcium channel blocker
Calcium channel opener
R-type calcium channel
Calcium-dependent chloride channel
T-type calcium channel
N-type calcium channel
Calcium channel blocker toxicity
Calcium-activated potassium channel
Dihydropyridine calcium channel blockers
L-type calcium channel
Voltage-gated calcium channel
Calcium release activated channel
Q-type calcium channel
P-type calcium channel
Calcium channel associated transcriptional regulator
Ryanodine-Inositol 1,4,5-triphosphate receptor calcium channels
Transient receptor potential calcium channel family
Calcium-activated potassium channel beta subunit
Calcium-activated potassium channel subunit alpha-1
Calcium channel, voltage-dependent, T type, alpha 1H subunit
Ionic Coulomb blockade
Quantitative models of the action potential
List of pastoral visits of Pope Francis
Voltage-gated ion channel
List of cardiology mnemonics
Peel River (Canada)
Environmental effects of shipping
Hyperosmolar hyperglycemic state
Basal electrical rhythm
Olfactory receptor neuron
Lists of Canadians
Extended periodic table
Histamine H3 receptor
List of retired numbers in association football
Novel Therapeutic Targets for Antiarrhythmic Drugs
Mark A Gillman
Atmosphere of Mercury
Blood Pressure Medicines | MedlinePlus
Plasticity of calcium channels in dendritic spines | Nature Neuroscience
Antagonists of neuronal calcium channels: structure, function, and therapeutic implications
DailyMed - Search Results for Calcium Channel Antagonists
Calcium channel blockers and Edema - ProgressiveHealth.com
Caffeine Toxicity Medication: Benzodiazepines, Vasopressors, Beta-blockers, Calcium channel blockers, Antidysrhythmics, GI...
Voltage-dependent calcium channel gamma-2 subunit (dog) | Protein Target - PubChem
Store-operated calcium channels - PubMed
IP3 Receptors | Calcium Channels | Tocris Bioscience
calcium channel regulator activity Antibodies | Invitrogen ...
Sympathomimetic Toxicity Medication: Benzodiazepines and other sedatives, Cardiovascular agents, Calcium Channel Blockers
NIH VideoCast - Voltage and Calcium Activated Potassium Channels
Browsing by Subject "Calcium Channel Blockers"
Calcium Channel Blockers - PubMed
NIH Guide: PILOT STUDY OF A CALCIUM CHANNEL BLOCKER IN FEMALES WITH BIPOLARDISORDER
Presynaptic GABAB Autoreceptor Modulation of P/Q-Type Calcium Channels and GABA Release in Rat Suprachiasmatic Nucleus Neurons ...
Calcium-channel blockade can mask the diagnosis of Conn's syndrome | Postgraduate Medical Journal
A native prokaryotic voltage-dependent calcium channel with a novel selectivity filter sequence | eLife
Extracellular pH modulates block of both sodium and calcium channels by nicardipine. | Scholars@Duke
Medical Science Monitor | Calcium-Activated Chloride Channel A4 (CLCA4) Plays Inhibitory Roles in Invasion and Migration...
View of Antidiarrheal and antispasmodic activities of Vincetoxicum stocksii are mediated through calcium channel blockade
Altmetric - Maintenance therapy with calcium channel blockers for preventing preterm birth after threatened preterm labour
Maitotoxin: effects on calcium channels, phosphoinositide breakdown, and arachidonate release in pheochromocytoma PC12 cells. |...
Molecular determinants of drug binding ad action on L-type calcium channels<...
Calcium Channels (definition)
BrainPharm: Publication facts - Low threshold calcium spikes were antagonized by T-channel blockers in rat
JCI Insight - SNAP23 depletion enables more SNAP25/calcium channel excitosome formation to increase insulin exocytosis in type...
Reactome | Calcium Influx through Voltage-gated Calcium Channels
Role of Voltage-Gated Calcium Channels in Hearing - the UWA Profiles and Research Repository
Association of Ca<sub>v</sub>1.3 L-type calcium channels with...
- Ingestion of excessive calcium channel blockers (CCBs) is one of the most potentially lethal prescription drug overdoses. (medscape.com)
- Calcium Channel Blockers are often considered as a potential cause of developing edema. (progressivehealth.com)
- Healthcare experts around the world prescribe calcium channel blockers to treat several health conditions, including migraine headaches, high blood pressure , circulatory issues, and complications of brain aneurysms. (progressivehealth.com)
- Calcium channel blockers, come in many forms, including short-acting medications and long-acting medications. (progressivehealth.com)
- Verapamil, diltiazem, and nifedipine are among the calcium channel blockers listed by MedlinePlus. (progressivehealth.com)
- The common side effects of calcium channel blockers include peripheral edema or swelling of the legs , feet, and ankles from the accumulation of fluid. (progressivehealth.com)
- According to Mayo Clinic, calcium channel blockers are medications that prevent calcium from entering into the muscle cells in the heart and around the blood vessels. (progressivehealth.com)
- Muscle cells require calcium to contract, so the main purpose of calcium channel blockers is to make it difficult for the muscle cells in the heart and blood vessels to contract. (progressivehealth.com)
- According to a study published in the 'Journal of Clinical Hypertension' in 2003, calcium channel blockers may cause edema due to their effects on the blood pressure in different blood vessels. (progressivehealth.com)
- The most effective way of treating edema associated with calcium channel blockers is to change the medication being used. (progressivehealth.com)
- As per the Journal of Clinical Hypertension, some calcium channel blockers are less likely to cause peripheral edema . (progressivehealth.com)
- Tachydysrhythmias may be treated with calcium channel blockers or beta-blockers (preferred) for rate control or with antidysrhythmics, depending on the rhythm disturbance. (medscape.com)
- Calcium-channel blockers are a type of medicine used to treat high blood pressure and heart rhythm disturbances. (medlineplus.gov)
- Other medicines may also contain calcium-channel blockers. (medlineplus.gov)
- Calcium channel blockers : a need for reassessment? (who.int)
- The calcium channel blockers act by blocking the influx of calcium ions into vascular smooth muscle and cardiac muscle cells during membrane depolarization. (nih.gov)
- Thus, the major effects of the calcium channel blockers are relaxation of vascular and arterial smooth muscle cells resulting in arterial vasodilation. (nih.gov)
- The major use of the calcium channel blockers is for hypertension and angina pectoris (variant, exertional, and unstable). (nih.gov)
- Some calcium channel blockers are also used for supraventricular arrhythmias and heart failure. (nih.gov)
- These agents are also commonly referred to as being first generation (verapamil, diltiazem, nifedipine) or second generation (amlopine, felodipine, isradipine, nicardipine, nimodipine and others) calcium channel blockers. (nih.gov)
- Among the different classes of antihypertensive drugs, calcium channel blockers (CCBs) are widely used for the management of hypertension. (psychreg.org)
- Calcium-channel blockers or calcium antagonist have several possible modes of action in hypertension. (nursinganswers.net)
- Because calcium-channel blockers inhibit renin release, the renin-angiotensin system may also be suppressed. (nursinganswers.net)
- Calcium-channel blockers prove to be useful in hypertensive patients who also have stable angina and spastic angina (Brunton, Chabner, & Knollman, 2011). (nursinganswers.net)
- The vasodilation properties of calcium-channel blockers lead to a reduction in after-load, and their regional smooth muscle relaxant properties are useful in relieving coronary spasms. (nursinganswers.net)
- Calcium-channel blockers are also useful in treating patients who cannot take beta-blocking agents (Katzung, Mastes, & Trevor, 2012). (nursinganswers.net)
- Calcium channel blockers are medicines that relax the muscles that make up the walls of your arteries. (www.nhs.uk)
- Grapefruit juice interacts with some calcium channel blockers and increases the level of the medicine in your blood. (www.nhs.uk)
- Effect of dihydropyridine calcium channel blockers on blood pressure variability in the SPRINT trial: a treatment effects approach. (nih.gov)
- Prior research has suggested that dihydropyridine calcium channel blockers (CCB) may reduce vvBPV, which we attempted to verify in a high-quality dataset with robust statistical methodology. (nih.gov)
- The image below illustrates the chemical structure of the calcium channel blocker diltiazem. (medscape.com)
- Before administration, control ventricular rate with another agent (eg, calcium channel blocker). (medscape.com)
- Calcium-channel blocker overdose occurs when someone takes more than the normal or recommended amount of this medicine. (medlineplus.gov)
- The specific ingredients in each type of calcium-channel blocker vary. (medlineplus.gov)
- Taking too much of a calcium-channel blocker can be very dangerous. (medlineplus.gov)
- Verapamil (a type of calcium channel blocker) overdose is associated with the highest mortality risk. (medlineplus.gov)
- This learning resource is a 5-minute animation about calcium channel blocker in YouTube. (merlot.org)
- In fact, there is no need for too much investigation can aspirin help to lower blood pressure As early as the beginning of the earthquake, the US troops stationed in the cities along the Sea of Japan calcium channel blocker blood pressure pills. (leduel.com)
- At the end of the game, the Real Madrid players hugged each other, looking very excited This feeling is not much how much will Ativan lower blood pressure different from that at the end of the calcium channel blocker blood pressure pills Champions League final. (leduel.com)
- But I didn't want Zhang Xiaolong to say calcium channel blocker blood pressure pills lightly We are here only to save people, not to fight fiercely. (leduel.com)
- However, the main ingredient is called a calcium-channel antagonist. (medlineplus.gov)
Blocking calcium influx1
- Decreases conduction velocity in AV node and increases refractory period by blocking calcium influx, converting SVT or slowing rate in atrial fibrillation. (medscape.com)
Influx of calcium2
- Because muscle contraction is largely dependent upon influx of calcium, its inhibition causes relaxation, particularly in arterial beds. (nih.gov)
- However, we have recently found that under hyperpolarized conditions, the T-type calcium channel can trigger a large after-depolarization and a corresponding influx of calcium into dopamine neuron dendrites. (nih.gov)
- Lercanidipine is a third-generation dihydropyridine CCB that selectively blocks L-type calcium channels in vascular smooth muscle cells. (psychreg.org)
- Calcium-activated chloride channel A4 (CLCA4) is known as a tumor suppressor which contributes to the progression of a number of types of malignant tumors. (medscimonit.com)
- Calcium-activated chloride channel ANO1 promotes breast cancer progression by activating EGFR and CAMK signaling. (nih.gov)
- The calcium-activated chloride channel anoctamin 1 (ANO1) is located within the 11q13 amplicon, one of the most frequently amplified chromosomal regions in human cancer, but its functional role in tumorigenesis has remained unclear. (nih.gov)
- Moreover, ANO1 chloride channel activity was important for cell viability. (nih.gov)
- Mechanistically, ANO1 knockdown or pharmacological inhibition of its chloride-channel activity reduced EGF receptor (EGFR) and calmodulin-dependent protein kinase II (CAMKII) signaling, which subsequently attenuated AKT, v-src sarcoma viral oncogene homolog (SRC), and extracellular signal-regulated kinase (ERK) activation in vitro and in vivo. (nih.gov)
- Our results highlight the involvement of the ANO1 chloride channel in tumor progression and provide insights into oncogenic signaling in human cancers with 11q13 amplification, thereby establishing ANO1 as a promising target for therapy in these highly prevalent tumor types. (nih.gov)
- Overall, we have indentified an unrecognized regulation pathway of T-type calcium channels by SNARE proteins, and proposed the first molecular mechanism by which T-type channels could mediate low-threshold exocytosis. (inserm.fr)
- The CRAC channels are composed of three plasma membrane based proteins, known as Orai1, Orai2 and Orai3 and two Ca2+ sensor proteins STIM1 and STIM2 in the endoplasmic reticulum. (cmos.org.tr)
- Another system regulated by intracellular calcium is the release of renin by the cells of the kidney. (nursinganswers.net)
- Synergistic activation by membrane voltage and intracellular Ca2+ is a unique property of large conductance Ca2+ activated K+ (BK) channels, which are found in many cell types including smooth muscles, neurons and endocrine cells. (wustl.edu)
Voltage gated c1
- While all affect the L type voltage gated calcium channel, the structure and site of interaction within the channel varies among the agents. (nih.gov)
- There are four types of β subunits (β1- β4) that can associate with the pore forming Slo1 subunit to uniquely modulate the Ca2+ and voltage sensitive properties in BK channels. (wustl.edu)
- In the first study, using a mutation that alters Ca2+ dependent activation, I show that in the presence of the β subunits, with the exception of β3b subunit, the mutation generally increased Ca2+ sensitivity to the same extent as in Slo1-only channels. (wustl.edu)
- Violin plots show distribution of expression levels for Calcium activated potassium channel subunit (SMED30030583) in cells (dots) of each of the 12 neoblast clusters. (stowers.org)
- Expression of Calcium activated potassium channel subunit (SMED30030583) in the t-SNE clustered sub-lethally irradiated X1 and X2 cells. (stowers.org)
- We found that the A-type potassium channel subunit Kv4.2 is highly expressed in the dendritic regions of CA1 neurons in the hippocampus and, as one of the primary regulators of dendritic excitability, plays a pivotal role in information processing. (nih.gov)
- Our lab used a combination of molecular, electrophysiological, and imaging techniques to show that Kv4.2, an A-type voltage-gated potassium channel subunit, controls action potential (AP) half-width, frequency-dependent AP broadening, and dendritic AP propagation. (nih.gov)
- There are previous reports suggesting a role for calcium ions in the secretory response of adrenocortical cells to ACTH. (nih.gov)
- Specifically we have used computational modeling, electrophysiology, and two-photon calcium imaging in mouse midbrain slices to show that this hyperpolarization-induced afterdepolarization (HI-ADP) depends on T-type, but not L-type calcium channels. (nih.gov)
- Low-voltage-activated t-type calcium channels : proceedings from the International Electrophysiology meeting, Montpellier, 21-22 October 1996 / guest editors: Richard W. Tsien, Jean-Paul Clozel, Joël Nargeot. (who.int)
- Most work on this calcium toxicity hypothesis implicates the L-type calcium channel. (nih.gov)
- Because these channels can cause large calcium transients they may contribute to the vulnerability of specific SNc dopamine neurons in Parkinson's Disease. (nih.gov)
- In general, these agents block the slow channel in the cell membrane and prevent calcium entry into the cell. (nursinganswers.net)
- Current flowing through single Ca- and voltage-activated K channels has been recorded from cell-attached and inside-out excised membrane patches of cultured Y-1 adrenocortical cells. (nih.gov)
- In intact cells, single-channel current amplitude and the time a channel stays in the open state increase with membrane depolarization. (nih.gov)
- Therefore, it is possible that, as in other endocrine cells, these K channels modulate Ca influx across the plasma membrane and thus contribute to regulate steroid biosynthesis and release. (nih.gov)
- Ion channels are the elementary excitable elements in the cell membranes of nerve, muscle, and many other cells where they produce and transduce electrical signals. (nih.gov)
- This interaction that relies on specific Ca(v)3.2 molecular determinants, not only modulates T-type channel activity, but was also found essential to support low-threshold exocytosis upon Ca(v)3.2 channel expression in MPC 9/3L-AH chromaffin cells. (inserm.fr)
- Signal of nerve impulses are transmitted to excitatory cells to induce action of organs via activation of Ca 2+ entry through voltage-gated Ca 2+ channels, which are classified based on their activation threshold into high- and low-voltage activated channels, expressed specifically for each organ. (mdpi.com)
- Several reports have uncovered an unrecognized feature of T-type channels in the control of vesicular neurotransmitter and hormone release, a process so far thought to be mediated exclusively by high-voltage-activated calcium channels. (inserm.fr)
- These channels are uniformly distributed in the plasma membrane, since one to four channels were seen in more than 99% of the patches isolated in this study. (nih.gov)
- In spite of intense research, the signal that relays the store Ca(2+) content to CRAC channels in the plasma membrane, as well as the molecular identity of the Ca(2+) sensor within the stores, remains elusive. (ox.ac.uk)
- Resolution of these issues would be greatly helped by the identification of the CRAC channel gene. (ox.ac.uk)
- Store-operated Ca2+ entry (SOCE) through the Ca2+ release activated Ca2+ (CRAC) channels and mitochondrial Ca2+ uptake via the mitochondrial Ca2+ uniporter (MCU) complex are collective signaling mechanisms responsible for a variety of cellular functions. (cmos.org.tr)
- In excised patches bathed in symmetrical 130 mM K solutions, single-channel conductance is 170 pS. (nih.gov)
- More recently, we examined the role of A-type K+ channels in regulating synaptic plasticity, neuronal development and disease (1). (nih.gov)
- If calcium influx is decreased, then norepinephrine vasoconstriction is reduced. (nursinganswers.net)
- Low-voltage-activated T-type calcium channels act as a major pathway for calcium entry near the resting membrane potential in a wide range of neuronal cell types. (inserm.fr)
- In a recent study, we have reported that Ca(v)3.2 T-type channel forms a signaling complex with the neuronal Q-SNARE syntaxin-1A and SNAP-25. (inserm.fr)
- However, the dendrites contain an abundance of ion channels that are involved in receiving, transforming, and relaying information in the dendrites, adding an additional layer of complexity to neuronal information processing. (nih.gov)
- Although recent molecular cloning studies found that several families of voltage-gated K+ channel genes are expressed in the mammalian brain, information about the relationship between the protein products of these genes and their various neuronal functions is still lacking. (nih.gov)
- In addition, we are investigating the role of dendritic voltage-gated channels in CNS disorders, including autism-spectrum disorder and Alzheimer's disease. (nih.gov)
- With larger Ca concentrations, channel open probability increases and its voltage dependence is greater. (nih.gov)
- This protein allows calcium to move into a nerve cell, and activates, deactivates, or stabilizes the electrical activity of the nerve. (sleep-disorders.net)
- Collectively, these results provide a basis for future studies identifying the molecular basis for modulation by the β3 and β4 subunits in BK channels. (wustl.edu)
- Functional variation of BK channels in different tissues is largely accounted by the association with accessory subunits, which have tissue-specific distributions. (wustl.edu)
- Alpha-2-delta calcium channel ligands are a class of drugs used for chronic, persistent restless legs syndrome (RLS) when iron supplements do not work. (sleep-disorders.net)
- Do not take alpha-2-delta calcium channel ligands with other drugs that depress the central nervous system. (sleep-disorders.net)
- In the second study, taking advantage of differential effect of 2 modulation on two BK channel orthologs, different chimeras were designed and coexpressed with β2 subunits. (wustl.edu)
- This may occur because alpha sympathetic vasoconstriction is produced by enhanced calcium influx into the cell. (nursinganswers.net)
- The present study was undertaken to explore the relative contributions of Cav3.2 T-type channels to mediating the antihyperalgesic activity of joint manipulation (JM) therapy . (bvsalud.org)