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How does low calcium increase motor nerve excitability?
I know calcium is necessary for acetyl choline secretion, so I would think that too little calcium would decrease neuron activity.
8 Answers
- RMLv 61 decade agoFavorite Answer
Calcium is needed both for neurotransmitter release (ACh) neuromuscular junction (as you noted) and its release from the sarcoplasmic reticulum is needed for activation of muscle fiber contraction. HOWEVER, these calcium functions are NOT the primary source of the excitability.
The main reason hypocalcemia causes neural excitability and tetany is due to its effect on the threshold potential of nerve axons. Low calcium reduces the amount that the threshold must change to initiate a full depolarization of the axon while leaving the resting potential unchanged. To put it another way, the resting potential stays the same but as calcium levels drop the amount of partial depolarization needed to allow sodium influx to be self-perpetuating is reduced.
Hyperkalemia (high potassium) has much the same effect as low calcium on the axonal excitability. In fact, the emergent treatment for hyperkalemia is...you guessed it...calcium!
Clinical signs you may want to google: carpopedal spasm, Trousseau's sign, and Chvostek's sign.
- Anonymous5 years ago
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It's been a few hours and no one answered yet... So I figured I'd give it a shot just internet research. XD Hyperkalemia will do two things - it will depolarize the cell somewhat, but also, since the conductance of potassium channels is also dependent on extracellular potassium concentration, hyperkalemia increases potassium channel conductance. So, in the hyperkalemic state, the delayed outward potassium current will be greater, decreasing repolarization time, so in a way, it increases excitability by allowing the cell to fire again sooner (which is why it leads to a susceptibility for arrhythmias in the heart). Because the cell is also slightly depolarized, at first, the excitability may also be increased because of this - however, being in a depolarized state also means that more sodium channels will be in the refractory state, which will eventually prevent excitability (which is why potassium is used to stop the heart). Hypokalemia will decrease potassium channel conductance and lengthen repolarization time and the refractory period (when the cell can't fire again), decreasing excitability in that sense. SOooo I think that is how an elevation in potassium K+/hyperkalemia could decrease heart excitability at the same time. lol If that doesn't help then good luck.
- 6 years ago
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How does low calcium increase motor nerve excitability?
I know calcium is necessary for acetyl choline secretion, so I would think that too little calcium would decrease neuron activity.
Source(s): calcium increase motor nerve excitability: https://tinyurl.im/bqS1C - How do you think about the answers? You can sign in to vote the answer.
- Anonymous5 years ago
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- 5 years ago
low ca concentration will altar ca/Na co transporter on cell membrane so when ca is in low concentration low ca/Na co transportation took place and most of Na remain tapped inside the cell leading its depolarization potential always near to threshold so increase cell excitibility
from dr zeb
- gangadharan nairLv 71 decade ago
Hypocalcemia is total plasma Ca concentration < 8.8 mg/dL (< 2.20 mmol/L) in the presence of normal plasma protein concentrations or a plasma ionized Ca concentration < 4.7 mg/dL (< 1.17 mmol/L). Causes include hypoparathyroidism, vitamin D deficiency, and renal disease. Manifestations include paresthesias, tetany, and, when severe, seizures, encephalopathy, and heart failure. Diagnosis involves measurement of plasma Ca with adjustment for plasma albumin concentration. Treatment is administration of Ca, sometimes with vitamin D.
Long-term hypocalcemia results in poor bone formation, which may lead to very brittle bones that are prone to breaking.
Source(s): http://www.nlm.nih.gov/medlineplus/ency/article/00... http://en.wikipedia.org/wiki/Hypocalcemia http://www.merck.com/mmpe/sec12/ch156/ch156g.html#...