Blood-brain Barrier and the Sodium-potassium Pump

Blood-brain Barrier and the Sodium-potassium PumpJocelyn Brown-EatonThe blood-brain restriction and the atomic number 11-potassium pump have some similarities and differences. Similarities include the fact that they both function to maintain a equaliser and that they both be selectively porous. Differences includes the way the mechanisms carry out those functions and what kind of isotropy they maintain. The blood-brain barrier is a mechanism that isolates the central nervous system neurons from chemicals coming from the rest of the body. It is made up of the w every(prenominal)s of brain capillaries that ar tightly joined together, opposite capillaries in the rest of the body do non align themselves so close together and they do allow chemicals to pass from the blood into the aras of the body they are flowing through. In contrast, the sodium-potassium pump is a protein in the membrane of cells that helps maintains the difference of electrical charges inside and out of the cell, keeping the cell polarized along with the difference in permeability of sodium and potassium within the rest of the membrane ( khan Academy 2010). The resting likely is maintained before an action potential arrives and then is restored when the action potential is over. Comparatively they are both maintaining balances. The blood-brain barrier is balancing chemicals and protecting the brain neurons from harmful substances since these neurons do not regenerate, merely the sodium-potassium pump is keeping an ionic balance. discriminating permeability is also a similarity of the two mechanisms. The blood-brain barrier is only a barrier for water soluble molecules and selectively allows lipid soluble molecules to pass, term the sodium-potassium pump only deals with sodium and potassium. The sodium-potassium pump set outs in two potassium ions for every three sodium ions it pushes out. Transporter proteins control the movement of these substances. The difference is that with t he blood-brain barrier there is a separate protein that actively transport the selected chemicals, while the sodium-potassium pump is a protein in itself. There are areas of the blood-brain barrier that are more permeable than the rest in order to allow the function of those specific parts of the brain. One such area is the area postrema. The area postrema detects toxins in the body and initiates vomiting.Khan Academy. (2010). Correction to Sodium and Potassium Pump Video. Online Video. 11 July 2010. Available from https//www.youtube.com/watch?v=ye3rTjLCvAU. Accessed 25 February 2017Before an action potential arrives, there is a balance between the extracellular fluid (on the outside of the cell) and the intracellular fluid (on the inside of the cell). This difference in the electrical charge is called the membrane potential. The membrane potential is created by diffusion of ions and electrostatic pressure. Diffusion refers to the process of molecules evenly distributing themselves. Molecules push away from areas that they are more concentrated in. Electrostatic pressure is the force that comes from the attraction or repulsion of ions. Positive charges repel other positive charges, negative charges repel other negative charges, and positive charges attract negative charges. The ions involved in these forces are organic anions, potassium ions, chloride ions, and sodium ions. Organic anions (A-) are negatively charged and found in intracellular fluid. These ions remain in the intracellular fluid because the membrane is impermeable to them. Potassium ions (K+) are positively charged. They try to get out of the membrane because of diffusion, there is a higher concentration of them inside than out. Electrostatic pressure, however, pushes grit against them because extracellular fluid is more positively charged inevitably keeping the ions where they were. Chloride ions (Cl-) are negatively charged. They try to get into the membrane due to diffusion but electrostatic pressure keeps them where they are as well. Sodium ions (Na+) are positively charged and get pushed into the membrane due to diffusion. Unlike the other ions sodium is not pushed back by electrostatic pressure. Instead, they are attracted in because the intracellular charge is more negative. The sodium-potassium pump helps maintain the resting potential, which is on average -70 mV. The sodium-potassium pump trades three sodium ions to the outside of the cell for two potassium ions to bring into the cell. During an action potential, a signal is sent to the membrane the membrane to become more permeable to sodium ions increasing the intracellular charge. The membrane potential reaches its threshold and a depolarization spike occurs. Depolarization is when the internal polarization of the cell increases when it gets closer to zero. Voltage capable sodium channels, triggered by the depolarization, open allowing sodium to enter at a faster rate. At a higher level of depolarization volt age capable potassium channels open and potassium flows away from the more positively charged interior. Voltage dependent potassium channels are less splendid than the sodium channels are. Next sodium channels close and go into a refractory state, preventing them from porta again until the resting potential is restored. The cell goes through hyperpolarization, where the intracellular charge drops in order to get back to normal. When hyperpolarization goes lower than the resting potential it is called the undershoot. When the undershoot is reached it signals the potassium channels to close and resting potential is closer to normal. After that all passes the sodium potassium pumps slowly help the resting potential return and everything is back to its original state.Neurotransmitters open ion channels in two ways, directly and indirectly. Directly opening the ion channels occur when there are ionotropic receptors. When a neurotransmitter binds to an ionotropic receptor the ion chann el immediately opens and let ions flow freely through. With metabotropic receptors, when a neurotransmitter binds to its binding site it starts a chain of chemical events (Carlson and Birkett, 2017). These chemical events involve the G protein being activated, which in turn activates the second messenger system. The second messenger travels to the nearby ion channel and signals it to open. Metabotropic receptors got their lift because they require extra steps that uses up some of the cells metabolic energy. The important differences between ionotropic receptors and metabotropic receptors are the speed of effect and the duration of effect after their activation. Ionotropic receptors are faster because when a neurotransmitter binds to it the ion channel is opened immediately and triggers a postsynaptic potential. The whole process happens very quickly. Metabotropic receptors are slower because the signal to the ion channel is transferred between a sequence of different molecules to g et to the ion channel and activate it. This process causes a delay in effect, they take longer to begin but they also choke longer. Serotonin has both ionotropic and metabotropic receptors. All but one receptor, the 5-HT3 receptor, are metabotropic. The 5-HT3 receptor is ionotropic and it controls a chloride ion channel, therefore producing inhibitory postsynaptic potentials. This receptor plays a role in illness and vomiting. Because ionotropic receptors act quickly, if the receptor is bound to by an agonist, which would open the ion channel, it would induce vomiting or nausea right away. An example of this would be when a person smells something stinky and immediately feels nausea. Antagonists of this receptor are used to treat the side effect of chemotherapy and radiation treatments. Serotonin is used for mood regulation, and that happens in the metabotropic receptors. This means that the effects take longer but will last longer. If this happened rapidly then there would be n o transitions between our moods. It allows the drugs for mood regulation (like SSRIs) to have compound effects and build up in our system by inhibiting the reuptake of serotonin.Carlson, N. R., Birkett, M. A., (2017). Physiology of Behavior, 12th Edition. BryteWave. Retrieved from https//shelf.brytewave.com//books/9780134517858/