CoverModule 1.0. Homeostasis, Membranes, Electrophysiology and ANS (Essay Questions)1.1. 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 Contraction2.3.3. 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. Pneumothorax4.5. 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 Healings
2.7.5

Phototransduction

Now for the underlying question, how do the proteins that absorb photons of light produce the action potentials that travel to the brain to produce what we perceive as vision? This process is called phototransduction (see figure below). Since the process is essentially the same in both the rods and the cones we will look at the rods and then explain the subtle differences that occur in the cones. It all starts with the visual pigments that are embedded in the membranes of the disks found in the outer segment of the rods. This visual pigment is called rhodopsin and is composed of protein called opsin and a derivative of vitamin A called retinal. In the unexcited state, retinal has a bend in its hydrocarbon chain (11-cis retinal) and fits nicely in a binding site on the opsin. When light of the proper wavelength is absorbed by the visual pigment the energy of the light causes retinal to change shape and the hydrocarbon chain loses its bend (all-trans retinal) and no longer fits in the binding site. It should be noted that even though rods provide only non-color vision, light of the green wavelength is the most efficient in activating rhodopsin. When the retinal detaches from the opsin, the retinal essentially becomes inactive being unable to associate with opsin until it regains its original cis conformation. This process is known as bleaching. Although retinal becomes inactive, the left over Opsin protein becomes activated, stimulating the alpha subunit of its G-Protein coupled receptor (GPCR). Thus, by definition, since the GPCR opsin is activated by light we call it a photoreceptor. Once activated the GPCR activates the G-protein, separating the alpha subunit from the beta/gamma subunit. In the photoreceptors of the eye, the G-protein is called transducin. The alpha subunit then brings about a change in the cell. More on this later.

image075.jpg
Phototransduction
Created by BYU-Idaho student Hannah Crowder, 2013


Phototransduction. The top image of the cycle represents the photoreceptor in the dark. The green channel is the cGMP gated cation channel which is open and allowing cations (Na+ and Ca2+ ) to depolarize the cell. When light strikes and changes the retinal from 11-cis to all-trans retinal, it activates the G-protein transducin which results in the activation of PDE –“phosphodiesterase” ( which causes breakdown of cGMP) and the closing of the cation channel. The cell will then hyperpolarize. Finally, All-trans retinal is converted back to 11-cis retinal by the pigmented epithelium and it re-attaches to opsin (PDE no longer activated) allowing cGMP to open the cation channel and once again depolarize the cell.

Photoreceptors are different than any receptors we have discussed to date in that they release neurotransmitter when they are not being stimulated. Here is how this works.

There are three important ion channels in the membranes of the photoreceptor cells, K+ leak channelsvoltage-gated Ca2+ channels and cyclic GMP (cGMP) gated cation channels (Naand some Ca2+ move through this channel). When the photoreceptor is not being stimulated (in the dark), cGMP is bound to the cation channel and Naand Ca2+ diffuse into the cell maintaining it in a depolarized state. This depolarization causes the voltage gated Ca2+ channels to open, allowing more Ca2+ to diffuse into the cell. This Ca2+triggers the release of the neurotransmitter glutamate by the process of exocytosis. The binding of glutamate to receptors on the bipolar neurons may be excitatory or inhibitory; it depends on what receptors are expressed on the bipolar neuron. For now we will focus on just the bipolar neurons that express receptors that cause inhibition when glutamate is attached.

When light is absorbed by rhodopsin and the G-protein (called transducin) is activated, the alpha subunit of the G-protein activates the enzyme phosphodiesterase. This enzyme breaks down cGMP to GMP. Once the cGMP is removed the cGMP-gated cation channels close and the membrane hyperpolarizes. This results in the closing of the voltage-gated Ca2+ channels and glutamate release ceases. Removal of the inhibitory signal to the bipolar neurons allows them to fire and an action potential is sent to the brain. Eventually, the G-protein is inactivated and phosphodiesterase is turned off. However, the rhodopsin cannot respond to light again until the retinal is returned to its bent, 11-cis, state. To do this, it diffuses into the pigment epithelium where enzymes act to restore the 11-cis state. It can then diffuse back into the rod cell and bind to opsin. The rod cell is ready to be activated again. The original bleaching process is very fast, fractions of seconds, but restoring the rhodopsin to its intact state can take several minutes. During the day, when we are exposed to sufficient light, the rhodopsin remains in the bleached state and the rods are essentially unresponsive to light. The mechanism is similar in the cones. The main difference is in the proteins of the visual pigment. The visual pigments in cones are similar to rhodopsin but they respond to different wavelengths of light allowing us to perceive different colors. Another difference, as stated above, is that the cones are much less sensitive to light. This is why the cones do well in full daylight when everything is brightly illuminated. Finally, cones do not stay deactivated (bleached) as long as rods. Cones appear to be fairly resistant to large scale “bleaching” as they are able to recover 11-cis-retinal much more quickly so that at any given time there are at least some visual pigments ready for stimulation.

It is interesting that what we perceive isn’t always what our eyes see. For example, as you gaze around the room everything seems like it is in sharp focus. The reality is that our eye is only capable of producing sharp vision on a very small portion of our visual field. If you hold your thumb at arm’s length in front of you, the area covered by your thumbnail is about all the eye can focus sharply. Why then does everything seem clear? It is because our brain makes us think it is clear. Try focusing on something and then pay attention to the things on either side. They will not be in sharp focus but you didn’t notice that until you thought about it. In reality, much of what we see is a product of our brains and not necessarily what the eye is seeing.

For proof of this statement watch or listen to the TED talk below about, but beware they may blow your mind.

https://books.byui.edu/-Rxv 

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