Membrane Potential Lab Report

Next, to determine if contraction via the EMC pathway requires extracellular or intracellular calcium, the second type of stimulus was used and the tissue was stimulated using calcium free K+-depolarising solution. The bathing solution in this experiment was calcium free solution to make sure all extracellular calcium was eliminated, as without calcium, the EMC pathway is expected to produce no response.

This experiment seeks to analyze how the resting membrane potential of Orconectes rusticus muscle cells changes in response to increasing [K+]o solution concentrations. By recording the intracellular voltage of the DEM, DEL1, and DEL2 crayfish muscle cells at six concentrations of [K+]o solution, we determined whether the observed resting membrane potentials (Vrest) were significantly different from the predicted Nernst equilibrium potential values. We hypothesized that the Vrest of the crayfish muscles at each concentration would not significantly differ from the Nernst potential, which solely considers the permeability of potassium ions to the cell membrane. However, our findings suggested differently, and results indicated that the Nernst equation did not accurately predict the obtained values of the resting membrane potential. The differences in muscle cell Vrest reveal instead that the membrane is differentially permeable to other ions.

c. Why is Na+ movement important with regard to movement across the membrane? The movement of sodium ions via active transport is to generate an electrochemical gradient between the filtrate and the interstitial fluid.

Discuss how a change in Na+ or K+ conductance would affect the resting membrane potential. ___

When a membrane is excited depolarization begins. When the membrane depolarizes the resting membrane potential of -70 mV becomes less negative. When the membrane potential reaches 0 mV, indicating there is no charge difference across the membrane. the sodium ion channels start to close and potassium ion channels open. By the time the sodium ion channels finally close. The membrane potential has reached +35 mV. The opening of the potassium channels allows K+ to flow out of the cell down its electrochemical gradient ( ion of like charge are repelled from each other). The flow of K+ out of the cell causes the membrane potential to move in a negative direction. This is referred to as repolarization. ( Marieb & Mitchell, 2009). As the transmembrane potential comes back down towards its resting potential level and the potassium channels begins to close, the trasmembrane potential level goes just below -90mV, causing a brief period of hyperpolarization (Martini, Nath & Bartholomew, 2012). Finally, as the potassium channels close, the membrane turns back to its resting potential until it is excited or inhibited again.

The following figures 1 and 2 display what exactly happens at the postsynaptic membrane when affected by [MG].

The voltage gated potassium-complex are made of single ion pore with subunits. Located in the postsynaptic fold. The voltage gated potassium complex has a significant amount of roles such

Do you think urea will diffuse through the 20 MWCO membrane? Your answer : c. No, not at all.

It is responsible for carrying Na+ to activate action potentials. The sodium channel is affected and causes membrane depolarization and weakness. The voltage of the sodium channels slows down significantly and results in low serum K+ levels. With low serum K+

The Hodgkin and Katz study (1949) showed that the rising phase was due to voltage-dependent Na+ channels, and the falling phase was caused by voltage-dependent K+ channels. With this in mind, they observed that the potassium channel gating is more temperature sensitive than the sodium channels.

Although both studies used the presence of markers such as horseradish peroxide to identify the membrane during the stimulation of a frog neuromuscular junction; the first of the papers by Heuser and Reese found that portions of cellular membrane at the frog neuromuscular junction were taken up by the cell and converted back into synaptic vesicles whereas ceccarelli observed no vesicle depletion but an increase in the number of labelled vesicles over time. He and his co workers propsed that vesicle fusion involves the opening of a small pore, termed ‘fusion pore’ followed by its rapid closure without full dilation and collapse at the same site of fusion. (reese, n.d.) (cecerlli, n.d.) This composes the Kiss and Run Argument but the electron microscope evidence is neither compelling or persuasive as the images are unclear where the omega membrane profile in the fixed tissue is on the way to collapsing into the plasma membrane or to closing its

Na+ , K+ and Cl- cotransporter is envolved in electroneutral transport at apical surface, which is driven by low concentration of these ions. This low concentration of ions is achieved by basolateral Na+ and K+ contertransporter (sodium-potassium adenosine triphosphatase) and basolateral chloride ion channel by facilitated diffusion (CLC-kb). Potassium ion is capable of diffusing back to lumen through apical potassium channel (ROMK) and returns net positive charge to lumen, this is important for reabsorption of calcium and magnesium

Whenever the balance is altered, the process of transmitting electrical signals, which is called action potential initiates by carrying information across a neuron’s axon; which is called resting membrane potential. This process occurs as uneven ions distribution flow across cell membrane, creating electrical potential. As a result, the duration of active potential can be as fast as 1 ms. Similarly, the average resting membrane is between -40 mV and -80 mV. Since the membrane from inside is more negatively charged than the outside, it reflected on the negative average voltage readings of the resting membrane.

What will happen to the resting membrane potential if the extracellular K+ concentration is increase? Less negative

1. What is a membrane potential? Why is it so important in nerves and muscles?