Connect and share knowledge within a single location that is structured and easy to search. Is this correct? Also, how does intracellular injection of KCl affect neuron membrane potential as compared to extracellular KCl application?
In patch clamp experiments, often the pipette is loaded with KCl and injected into neurons that leads to depolarization. How can this be explained?
Membrane potential measured electrophysiologically, or calculated using the Goldman equation depends on two things: concentrations and permeabilities. In the Goldman equation you see this directly: concentrations multiplied by permeability, in both the numerator and denominator. In a typical resting neuron, in the absence of any synaptic activity, Chloride conductance is near zero compared to ions like potassium. I'm not as clear what you are asking about patch clamp experiments, I will try to just describe the process and hopefully that helps.
In a whole-cell patch clamp, the inside of the cell is continuous with the patch pipette solution, which usually contains high concentrations of potassium, like the normal intracellular environment. This is done on purpose, to try to record from cells in the most natural condition that can be replicated simply. During the process of making a whole-cell recording, however, the experimenter has to first place a patch pipette down near the cell. While doing this, some solution is leaking out of the pipette and increasing extracellular potassium concentrations, which can depolarize surrounding cells.
So, patch quickly my friends, you are making it uncomfortable for everybody before you make a good seal. Sign up to join this community. The best answers are voted up and rise to the top. Abstract Membrane depolarization is an important and common manipulation used to study the result of enhanced neuronal activity on adaptive changes, including alterations in gene expression.
Publication types Research Support, Non-U. Gov't Research Support, U. Hypoaldosteronism: Low levels of aldosterone will result in increased sodium excretion and potassium retention.
Distal renal tubular acidosis: In type I RTA, impaired reabsorption of sodium will lead to decreased potassium excretion. Other drugs: Spironolactone and ACE inhibitors both can decrease the renal excretion of potassium. Metabolic Acidosis: With the decrease in serum pH, extracellular hydrogen ions will pass into the intracellular fluid in order to minimize the extracellular decrease in pH.
To maintain electroneutrality, potassium ions will leave the intracellular space to replace the entering hydrogen ions. Beta-adrenergic Blockade: Nonselective beta-blockers can decrease the transport of potassium into cells. Insulin: In diabetes, decreased insulin will lead to reduced transport of potassium into cells.
Increased Tissue Breakdown: Injuries and conditions that lead to cellular breakdown can increase serum potassium levels. Such conditions include crush injuries, rhabdomyolysis, and tumor lysis syndrome. Pseudohyperkalemia occurs when intracellular potassium is released into the serum at the site of the blood sampling.
This will lead to a falsely elevated potassium level. The chances of this occurring are raised with increased trauma during venipuncture, hemolysis of the sample, use of a tourniquet, and drawing blood over a high resistance catheter or needle. Other diagnostic studies that may help identify the underlying cause or guide management include:. Basic metabolic panel: Helpful for identifying impaired renal function, aldosterone or cortisol derangements, and acid-base abnormalities.
Urinalysis: Can be helpful in identifying renal tubular acidosis, myoglobinuria or systemic hemolysis. If the patient has symptomatic paralysis or there are EKG changes consistent with hypokalemia, treatment should be initiated immediately.
Intravenous potassium replacement should also be considered for serum potassium levels less than 2. Intravenous potassium chloride replacement should be started at 0. Caution must be taken when replacing potassium in renal disease. If replacement is needed, consideration should be given to administering a smaller replacement 0. Intravenous replacement should be given through a central venous catheter or multiple peripheral intravenous catheters since potassium infusions greater than 0.
Repeat serum potassium levels should be evaluated after each replacement initially every 2 to 4hrs. If there is not a significant response to the initial replacements, a magnesium level should be evaluated as hypomagnesemia may be contributing to an intractable hypokalemic state.
If the patient is not critically ill, does not have symptoms of hypokalemia, and has no reason for ongoing potassium losses, mild hypokalemia is likely to self-resolve simply by ensuring adequate potassium intake in diet. Enteral replacement is less likely to lead to overtreatment and resultant hyperkalemia, and should always be considered if there is no urgency for treating mild hypokalemia. It is generally not necessary to exceed these concentrations under normal circumstances for mild hypokalemia.
If there are ongoing losses, scheduled enteral KCl replacement may need to be continued at a dose that is based on calculated losses estimated. Some circumstances may need consideration for ongoing potassium losses. These situations include: treatment of diabetic ketoacidosis, polyuric states such as diabetes insipidus, or severe diarrhea. Diabetic Ketoacidosis: In diabetic ketoacidosis, total body potassium levels are depleted due to extracellular movement of serum potassium levels, and resultant increased renal excretion of potassium.
Initially, serum potassium levels will be elevated on presentation. But once treatment with an insulin infusion is initiated, serum potassium levels will fall, and potassium replacement will often be necessary. Serum potassium levels should be monitored every 2 to 4 hours at the onset of treatment. Once serum potassium levels fall below 4. Potassium levels are continued to be monitored every 4 to 6 hrs depending on the response. Once the insulin infusion is complete, and the patient is stabilized out of diabetic ketoacidosis, further potassium replacement is not necessary provided the serum potassium level is normalized.
This may lead to clinically significant potassium loss with high levels of urine output. Most of the time, close monitoring with potassium replacements as needed is sufficient. Including potassium in IVF replacement should be considered if above IV replacement strategies are unable to keep up with potassium losses. If there are no EKG changes, eliminate all potassium from diet and intravenous fluid replacement.
If there are no risk factors for potassium levels to continue increasing e. The patient should be followed on cardiorespiratory monitoring to watch for rhythm changes or changes in T waves. Repeat potassium levels should be performed at least every 12 to 24 hours to ensure resolution of hyperkalemia. If there are risk factors for potassium levels to continue increasing, such as in renal failure, additional measures should be taken to eliminate potassium.
Recheck serum potassium levels every 6 hrs or sooner if there signs of EKG changes on cardiorespiratory monitoring. If the serum potassium level is greater than 6.
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