CoverModule 1.0. Homeostasis, Membranes, Electrophysiology and ANS1.1. Homeostasis1.1.1. Homeostasis Defined1.1.2. Homeostatic Control Systems1.1.3. Feedback Response Loop1.2. Cell Transport; Water & Solutes1.2.1. Fluid Compartments1.2.2. Osmosis1.2.3. Diffusion of Solutes1.2.4. Active Transport1.2.5. Bulk Transport1.3. Electrophysiology1.3.1. Ions and Cell Membranes1.3.2. Membrane Potentials1.3.3. Graded Potential1.3.4. Action Potentials1.3.5. Refractory Periods1.3.6. Propagation of an Action Potential1.4. The Synapse1.5. The Autonomic Nervous System1.5.1. Organization of the Nervous System1.5.2. Structural Organization of the ANS1.5.3. The SNS and the PNS1.5.4. The Enteric Nervous System1.5.5. Physiology of the ANS1.5.6. Neurotransmitters of the ANS1.5.7. Receptors of the ANS1.5.8. Actions of the Autonomic Nervous System1.5.9. Table of Actions for the SNS and PNS and Some Common DrugsModule 2.0. Skeletal Muscle and Special Senses2.1. Structural Organization of Skeletal Muscle2.2.1. Neuromuscular Junction, Excitation-Contraction Coupling2.2.2. Muscle Contractures and Cramps2.3. Whole Muscle Contraction, Fiber Type, Fatigue and Muscle Pharmacology2.3.1. Motor Units2.3.2. Factors that Influence the Force of Contraction2.3.2. Factors that Influence the Force of Muscle Contraction2.3.3. Energy Source for Muscle Contraction2.3.4. Skeletal Muscle Fiber Types2.3.5. Fatigue2.3.6. Muscle Pharmacology2.4. Smooth Muscle2.4.1. Smooth Muscle Contraction2.5. Control of Body Movement2.5.1. Voluntary Control of Muscle2.5.2. Reflexes2.6. Taste and Smell2.6.1. Taste2.6.2. The Sense of Smell2.7. Vision2.7.1. Structure of the Eye2.7.2. Focusing Light on the Retina2.7.3. Converting Light to Action Potentials2.7.4. The Retina2.7.5. Phototransduction2.7.6. Receptive Fields2.8. Hearing and Equilibrium2.8.1. The Nature of Sound2.8.2. The Hearing Apparatus2.8.3. Sound Vibrations to Action Potentials2.8.4. The Sense of Balance and EquilibriumModule 3.0. Cardiovascular System3.1. Structure of the Heart3.1.1. Chambers and Circulation3.2. Cardiac Cell Action Potentials3.2.1. Action Potentials in Cardiac Muscle Cells3.2.2. Action Potentials in Cardiac Autorhythmic cells3.2.3. Cellular Mechanisms of Inotropy and Chronotropy3.3. Electrophysiology of Heart Muscle3.3.1. Heart Conduction System3.3.2. Electrocardiogram (ECG)3.3.3. Abnormal ECG - Current of Injury3.4. The Cardiac Cycle3.4.1. Cardiac cycle3.4.2. Cardiac Measurements and Pressure Volume Loops3.5. Blood vessels and Blood Pressure3.5.1. Arteries and Veins3.5.2. Capillaries3.5.3. Blood Pressure Regulation and Shock3.5.4. Capillary Exchange3.5.5. Myogenic and Paracrine Regulation of Vasoconstriction and Vasodilation3.6. Blood3.6.1. Composition of Blood3.6.2. Hematopoeisis3.6.3. Breaking Down Red Blood Cells3.6.4. HemostasisModule 4.0. Urinary and Respiratory Systems4.1. Function and Structure of the Kidney4.1.1. Urinary System Function4.1.2. Functional Anatomy of the Urinary System4.1.3. The Nephron: Functional Unit of the Kidney4.1.4. The Renal Corpuscle: Bowman's Capsule4.2. Physiology of Urine Production4.2.1. Filtration4.2.2. Renal Clearance4.2.3. Tubular Reabsorption4.2.4. Urine Concentration and Dilution4.2.5. Hormonal Regulation of Urine Production4.3. Acid/Base Balance4.3.1. Buffers4.3.2. Acid/Base Disturbances4.4. The Respiratory System4.4.1. Respiratory System Structure and Function4.4.2. Respiratory Membrane4.4.3. Respiratory pressures and Inspriation/Expiration4.4.4. Alveoli and Surfactant4.4.5. Pneumothorax4.4.6. Pressure-Volume Loops and the Work of Breathing4.5. Gas Exchange and Transport4.5.1. Gas Laws4.5.2. Partial Pressure Gradients in the Lung4.5.3. Alveolar Gas Equation4.5.4. Oxygen and Carbon Dioxide Transport in the Blood4.5.5. Alveolar Ventilation4.5.6. Ventilation/Perfusion Ratio4.6. Chronic Bronchitis and Emphysema4.6.1. Respiratory Control by the Medulla Oblongata4.6.2. Chemicals that Regulate VentilationModule 5.0. Digestive, Endocrine and Reproductive Systems5.1. Functional Anatomy of the Digestive System5.1.1. Layers of the Digestive Tract5.1.2. Enteric Nervous System5.1.3. Organs of the Digestive System5.2. Digestion5.2.1. Carbohydrates5.2.2. Proteins5.2.3. Lipids5.2.4. Lipoproteins5.3. Regulation of Digestive Secretions5.4. Endocrine System5.4.1. Overview of the Endocrine System5.4.2. Hormone Receptors5.4.3. Hormones of the Body5.4.4. Other Hormones: Melatonin and Pheromones5.5. The Hypothalamus and Pituitary Gland5.5.1. Structure and Function of the Hypothalamus and Pituitary Gland5.5.2. The Posterior Pituitary5.5.3. The Anterior Pituitary5.5.4. Growth Hormone5.5.5. Prolactin5.5.6. Thyroid Hormones5.5.7. Adrenal Hormones5.6. Pancreas5.6.1. Insulin and Glucagon5.6.2. Diabetes Mellitus5.7. Reproductive System Anatomy5.7.1. Female Reproductive Anatomy5.7.2. Male Reproductive Anatomy5.7.3. Sexual Development at Puberty5.7.4. Male Reproductive Endocrine Axis5.7.5. Spermatogenesis5.7.6. Female Reproductive System: Oogenesis5.7.7. Ovulation and Fertilization5.7.8. The Ovarian Cycle5.7.9. The Uterine Cycle5.7.10. PregnancyAppendix A. GenderAppendix B. The Placebo EffectB.2.1. The Placebo EffectB.2.2. Examples of the Placebo EffectB.2.3. How do Placebos Work?B.2.4. Are Placebos Ethical?B.2.5. How do we validate actual effectiveness of placebosB.2.6. Tips for evaluating scientific evidenceB.2.7. What about Faith Healingstest chapter
1.3.3

Graded Potential

Because we are dealing with charge differences and electrical currents, we use some unique terms to describe certain states of the membrane. At rest, the membrane is in a polarized state—polarized because of charge separation caused by the permeabilities and gradients of different ions. At steady state equilibrium, this polarized state is referred to as the resting membrane potential. As already emphasized, the inside of the cell membrane will be negative in relation to the outside of the membrane. We can show this graphically by using the units of mV on the y-axis and time on the x-axis (see figure below). Thus, any change in the membrane toward zero will be termed a depolarization. Note the prefix de-, which means “away from.” Any change in the membrane that moves back toward the resting potential would be a repolarization with the prefix re-, meaning “again.” A change resulting in the movement away from the resting potential, but in a more negative direction, away from zero, will be termed hyperpolarization with the prefix hyper, meaning “excessive.”

Graded_potentials.png
Graphical representation of graded potentials. On the left, it shows electrical movement away from rest or the "polarized state" and toward zero is called "depolarization". The graded potential returns to rest or polarized state again but never gets high enough to reach threshold. The representation on the right shows electrical movement away from rest. This movement is called hyperpolarization, and we see that hyperpolarization moves farther from the threshold rather than towards it.
Image by BYU-I student, 2013

Now for some application. Opening channels for Na+ or Ca2+  would cause a depolarization, while opening channels for K+ or Cl- (sometimes) would cause a repolarization or even a hyperpolarization. These changes in the resting potential come in two forms, graded potentials or action potentials. Graded potentials always precede action potentials, so we will address them first.

With graded potentials, the magnitude of the response is proportional to the strength of the stimulus. Hence, a strong stimulus might result in a 10 mV change in the membrane potentials, while a weaker stimulus may produce only a 5 mV change. Graded potentials result from the opening of mechanical or ligand-gated channels. Graded potentials can be summed (added) on top of each other to increase the change. Stated another way, if a stimulus is repeated over and over, it can result in an even larger deviation toward zero, from rest or away from rest to more negative values. This is the reason why the changes are called graded. The amplitude (change in the membrane potential) is determined by the number of channels activated, which, in turn, is determined by the number of stimuli, such as the concentration of chemicals or the number of channels opened. However, if a change in the depolarizing direction is really strong, the change may exceed the threshold for the cell and the graded potential changes into an action potential. Another characteristic of graded potentials is that they are conducted only short distances. As the signal spreads from the site of stimulation, it loses strength and eventually dies out completely; think of the ripples that spread in a pond when you throw a rock in.

For this reason, these signals are also sometimes referred to as local potentials, meaning that they happen locally but do not travel long distances. As stated, graded potentials can be induced intentionally by ligands or mechanical stimuli. In addition, graded potentials can occur because of changes in extracellular ion concentrations independent of ligands or mechanical stimuli. This is because protein voltage-gated channels are sensitive to the distribution of charge along the membrane. For example, the voltage-gated Na+ channel gating mechanism is sensitive to the extracellular concentration of Ca2+. If the extracellular Ca2+  ion concentration decreases below normal values (hypocalcemia) the gating mechanism will become hypersensitive, even opening spontaneously. In contrast, extracellular Ca2+  concentrations that increase above normal (hypercalcemia) will desensitize the gating mechanism, making the channel more difficult to open (effectively moving the threshold value further away from RMP). Thus, the Ca2+  ion has a direct effect on the Na+ channel gating mechanism.

An indirect effect (not directly binding to the gating mechanism of the Na+ channel) is observed with extracellular K+ ion concentrations. Since K+ is the main driver for membrane charge separation, any change in the extracellular concentration of K+ will affect the K+ concentration gradient such that the resting membrane potential will shift closer or further away from threshold. Hyperkalemia (extracellular K+ above normal) will cause the RMP to be closer to threshold because of the weakened gradient (less K+ leaves). Hypokalemia (extracellular K+ below normal) will cause the RMP to move further away from threshold because of the increased gradient (more K+ leaves). Changes in the membrane potential or the gating mechanisms of Na+ channels can make the graded potential much more likely to cause or prevent an action potential. Thus, monitoring extracellular ion concentrations is important clinically because if the concentrations move outside of normal it can induce hyper excitability or hypo excitability of both muscle and neuronal cells. 

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