Notes On Nerve Impulses

After the absolute refractory period, sodium channels begin to recover from inactivation and if strong enough stimuli are given to

The neuron membrane is responsible for the constraints on the free flow of ion across a neuron. This membrane is a lipid bilayer, which acts as a support that holds the inside of the cell together and limits or restrict the entry of substances through protein channels in different circumstances. In addition to its permeable nature, the membrane is characterized by being electrically polarized since its inner side contains negative charges, while its exterior is of positive charges. Hyperpolarization is when the membrane potential becomes more negative on the neuron membrane. Contrarily, depolarization is when the membrane potential becomes less negative and resting potential is an electrical potential across neurons .This takes place when

The plasma membrane of neurons, like all other cells, has an unequal distribution of ions and electrical charges between the two sides of the membrane. The outside of the membrane has a positive charge, inside has a negative charge. This charge difference is a resting potential and is measured in millivolts. Passage of ions across the cell membrane passes the electrical charge along the cell. The voltage potential is -65mV (millivolts) of a cell at rest (resting potential). Resting potential results from differences between sodium and potassium positively charged ions and negatively charged ions in the cytoplasm. Sodium ions are more concentrated outside the membrane, while potassium ions are more concentrated inside the membrane. This imbalance is maintained by the active transport of ions to reset the membrane known as the sodium potassium pump. The sodium-potassium pump maintains this unequal concentration by actively transporting ions against their concentration

The Cl- ions will move more easily from the outside into the cell through the permeable membrane, assuming it is the dominant ion in the cell and the concentration of Cl- is greater externally than internally. Since the equilibrium potential of Cl- is not equal to the membrane potential, Cl- will be able to pull the membrane potential towards its equilibrium potential (-70 mV to approximately -81mV) until the current equilibrates close to -81 mV. Chances are there are more ions involved that also go in and out of the membrane which is why the membrane potential will be close to the equilibrium potential and not equal to it.

Under resting conditions, all cells will have an electrical potential difference across the membrane so that the inside of the cell is negatively charged and the outside of the cell is positively charged. This RMP must be established before a neuron is able to conduct an electrical signal. The difference in charge across a membrane establishes a cell’s RMP. When the membrane is at rest, potassium ions collect inside the cell due to the net movement within the concentration gradient. The negative resting membrane potential is maintained by the increased concentration of cations outside the cell compared to the inside environment (cytoplasm) of the cell. The overall negative charge of the cell is due to the accumulation of more sodium ions outside

The neuron is then hyperpolarised when there are more K+ on the outside than Na+ in the inside of the cell, meaning the cell has a more negative charge than the outside of the cell. This causes the cell’s potential to be slightly lower than its’ initial resting potential. This is the last stage of an action potential, after which there is a refractory (resting) period until which the cell returns to its’ resting

2 K+ ions then bind to their high-affinity binding sites, and the enzyme is dephosphorylated. This reduces the ATPase's K+ affinity, causing the release of K+ into the cell (Lehninger et al. 2000). It is the above process that is responsible for approximately 25% of the bodies daily ATP breakdown and consequent energy usage (Lehninger et al. 2000). The sodium and potassium ions, and the large concentration gradients that exist, consist a vital physiological feature of the cell, and one that is implicated in myriad cellular processes.

Background: Neuronal excitability mediated by sodium-dependent action potentials (APs) is required for rapid and specific communication in our brains. This underlies our ability to sense and respond to stimuli and for higher order cognitive functions including learning and memory. Voltage gated sodium channels (NaVs) open in response to membrane depolarization and initiate the AP. The α subunit is the major functional unit of NaVs and is comprised of 4 homologous domains (DI-DIV), each containing 6 transmembrane segments (S1-6)4,5. S4, the voltage sensor that detects depolarization, contains 4-8 positively charged amino acids each separated by two hydrophobic residues4,6. The positive charges on S4 are pushed outward by the electric field during membrane depolarization leading to channel opening, allowing influx of positively charged sodium ions down their concentration gradient4. Fast inactivation helps return the membrane to rest by blocking the conductance of sodium ions through the channel pore 1,2.

(3) At the peak action potential, K+ channels open and K+ begins to leave the cell. At the same time, Na+ channels close.

An inactive or resting neuron actively pumps sodium out of the cell and potassium into the cell to maintain equilibrium. However, the plasma membrane is more permeable to potassium than to sodium, which results in some potassium to diffuse out of the neurons. Large, negatively charged proteins such as phosphate and sulfate cannot diffuse out of the neuron. This results in a net excess of positively charged ions outside the neuron membrane and net excess of negatively charged ions inside the neuron.

The K+ returns to the inside of the cell through a pump that exchanges it for Na+ so that there is little voltage change.

The first step of four is called the resting membrane potential, the resting membrane potential is also known as polarized. At this stage no ions move through the voltage-gated channels, both sodium and potassium gates are shut. A neuron (which is a specialized cell transmitting nerve impulses) is resting. At resting state, the membrane potential of a neuron is roughly -70mV (millivolts), so the cytoplasmic side (which is the inside) is negatively charged parallel to the outside. All gated Na+ and K+ channels are closed at this stage. A Na+ channel each has two gates, 1 being an activation gate which is closed at rest but swings open when depolarization occurs, the second being and inactivation gate that ceases the channel once swung open. Although for Na+ to enter both gates

Membrane permeability is very important as to maintain the cell in a stable condition as we can also describe as remain our cell a more homeostatic environment by control which substances could can go through cells. Membranes are essential for control the concentration of particular ion, and establish the concentration requires. We can observe those mechanisms of cell membrane from a considerable ATP synthesis and solute transport through the plasma membranes. Gradients which cause those ions to move cross the membranes are potential of cell .when a separation of charge occurred an electrical potential occurred results with voltages can be measured in the cell.

One of the key ways that membrane proteins are involved in neurone function is through the formation of the resting potential. The resting potential is the charge difference across a cell membrane when a neurone is at rest and not sending a signal, typically between -60 and -80 millivolts. Potassium and Sodium ions play a fundamental role in the formation of the resting potential (Professor Sandidge/Moyle, 2012) and these ions each have a concentration gradient across the membrane of a neuron. In the majority of neurones, the concentration of potassium is greater inside the cell,

The inhibition of calcium influx via the L-type calcium channels may be mediated by direct inactivation by the G-protein[6] and/or through induced hyperpolarization by activation of ATP-sensitive K+ channel[6]. Activation of the G-proteins results to activation of ATP-sensitive K+ channels. The active transport of K+ ion intracellularly results to hyperpolarization of the membrane. The hyperpolarization inactivates the voltage-sensitive L-type Ca2+ channels which only opens during membrane depolarization[8,6].