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The nervous system

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  • 1. The Nervous System The nervous system collects and processes information, analyzes it, and generates coordinated output to control complex behaviors. The nervous system also is partly responsible for homeostasis. It works in conjunction with the endocrine system by employing nerve impulses and by responding rapidly to stimuli to adjust body processes. The general organization of the Nervous System The nervous system is broken down into two major systems the Central Nervous System and the Peripheral Nervous System. These two systems are in control of sensory input, integration, and motor output. The Central Nervous system is made up of mainly the brain and spinal cord. The CNS is in control of the input from sensory receptors from the chemical and electrical signals sent from the PNS. The CNS takes the information and integrates it, then sends out the necessary motor output to the effector cells of the body. The PNS is divided into two systems as well, the Somatic Nervous System, and the Autonomic Nervous System. The SNS consists of sensory neurons that send information from cutaneous and special sensor receptors in the head, body wall, and extremities to the CNS where the information is integrated and sent back out via motor neurons to skeletal muscles. The sensory neurons convey input from receptors from senses like vision, hearing, taste, smell and others. They also convey input from proprioceptors and general somatic receptors (pain, temperature, and tactile sensations). Motor neurons innervate skeletal muscle and produce voluntary movement. The ANS sends information from sensory neurons to viscera of the CNS. In the ANS the CNS sends information through motor neurons to smooth muscles, cardiac muscles and glands. The ANS is controlled by the hypothalamus and medulla oblongata of the brain, which regulate the smooth muscle, cardiac muscle, and specific glands. The output portion of the autonomic nervous system further breaks down into two divisions, the sympathetic and parasympathetic. The parasympathetic division is the energy control center; it regulates energy through conservation and restoration. The sympathetic division is in charge of the flight of fight responses of the body. It is in charge of the excitatory processes of the body. This division is in charge of the usage of energy. In summary, the nervous system has three overlapping functions. These functions are sensory input, integration, and motor output. Input is the conduction of signals from sensory receptors to integration centers of the nervous system. Integrating the information requires that the sensations triggered by environmental stimulation of receptors be interpreted and associated with appropriate responses of the body. Motor output is the conduction of signals from the brain or other processing center of the nervous system to effector cells. Effector cells are the muscle cells or gland cells that actually perform the body’s responses to stimuli. Neurons Neurons come in a variety of sizes and shapes, but they all have basically the same functional regions. Signals from other neurons or sensory cells are received on the dendrites and cell body (soma) and cause localized changes in membrane polarization. The electrical changes spread across the cell body and are combined at the axon hillock, located at the base of the axon. This is the region responsible for generating action potentials, which then travel quickly along the axon and its branches to the terminal knobs - small swollen areas at the end of the axon branches. Here the neuron interfaces with other cells at junctions called synapses through which signals are transmitted. Neurons that bring signals to the central nervous system (the brain and spinal cord) are referred to as sensory neurons, whereas those that carry signals from the central nervous system to the rest of the body are called motor neurons. Within the central nervous system there are also small, highly branched interneurons that help neurons communicate with one another. The axons of some vertebrate neurons have a fatty myelin sheath formed by supporting Schwann cells. This sheath helps
  • 2. support the fine axon and also increases the conduction velocity of nerve impulses (action potentials). The supporting cells and their functions The supporting cells outnumber neurons tenfold to fiftyfold in the nervous system. They are essential for the structural integrity of the nervous system and for the normal functioning of neurons. They provide intimate structure and perhaps metabolic support for neurons. There are different types in the body. Oligodendrocytes, are located in the CNS. Schwann cells of the peripheral nervous system wrap each axon in an insulating myelin sheath, which contributes to assuring reliable and rapid transmission of action potentials. Although some glial cells have voltage-gated ion channels in their membranes, glial cells generally do not produce action potentials and their role in the nervous system has long been a puzzle. One suggestion has been that glial cells help to regulate the concentration of K+ and the pH in the extracellular fluid of the nervous system. Glial cell membranes are highly permeable to K+ and adjacent glial cells are often electrically coupled by junctions that allow K+ to flow between them. This flux permits glial cells to take up and redistribute extracellular K+, which otherwise could build up to high concentrations in narrow extracellular spaces following activity in neurons. Glial cells also may take up neurotransmitter molecules from the extracellular space, thereby limiting the amount of time a neurotransmitter could be active at synapses. Electrochemical equilibrium? All living cells maintain some differences between the concentration of ions and other solutes inside and outside the cell. This is the purpose of a cell membrane in the first place - to help maintain differences between the inside and the outside. The combination of differences in the chemical concentrations of solutes and the distribution of the charges of the ions establishes an electrochemical gradient between the inside and outside of the cell membrane. If the chemical concentration gradients are offset by a difference in the distribution of electrical charges so that no net movement of ions takes place, we have a condition known as electrochemical equilibrium. In this equilibrium condition any tendency of solutes to diffuse down their respective concentration gradients (from high to low concentration) is regulated by not only the difference in chemical concentration and by their electrical attraction to or repulsion by other charged molecules, but also their ability to pass through the cell membrane. Lipid soluble molecules can pass through the cell membrane. Molecules that are not lipid soluble must pass through channels in the membrane, and are therefore limited by the size and number of these channels. When in electrochemical equilibrium, living cells have a net negative charge along the inside of the cell membrane. This is due primarily to the surplus of large negatively charged molecules, such as proteins, in the cytoplasm. These large molecules cannot diffuse down their concentration gradient and move to the outside of the cell because they are too big to pass through small channels in the cell membrane. The surplus of these large negatively charged ions inside the cell tends to repel other negatively charged ions, such as chloride, resulting in a higher concentration of these smaller negatively charged ions on the outside of the cell. Meanwhile, an ion pump actively transports positively charged sodium ions from the inside to the outside of the cell, creating a surplus of sodium ions outside the cell membrane. The ion pump does exchange some potassium (also positively charged) for the sodium, but it is an uneven exchange, with the amount of sodium leaving the cell exceeding the amount of potassium being brought in. Sodium and potassium ions are small enough to slowly diffuse down their chemical concentration gradients by passing through small channels in the cell
  • 3. membrane, but the ion pump keeps up with this slow leakage and maintains the electrochemical equilibrium. The result of all of this is that the ion pump maintains an equilibrium condition in which there is more sodium outside the cell, more potassium inside the cell, and the inside of the cell has a net negative charge with respect to the outside. This balance between electrical and chemical gradients and the regulation of the passage of these ions back and forth is what distinguishes a living cell from an inert bag of ions. It also permits certain cells to respond to stimuli. Membrane potential and his related to an action potential The difference in electrical charge between the two sides of a cell membrane is known as the membrane potential. When a cell is not being stimulated, and is therefore "at rest", we refer to the membrane potential as the resting potential. If a cell becomes stimulated, perhaps by some mechanical or chemical disturbance, the permeability of the cell membrane can be momentarily affected resulting in a temporary change in the electrochemical balance. Most cells in an animal's body don't show much of a response to such a stimulus, other than to reestablish electrochemical equilibrium. Some cells, however, show a dramatic, active response at the level of the cell membrane that results in a momentary but striking reversal of charge distribution known as an action potential. This ability to generate action potentials is what makes certain cells excitable, and it is these excitable cells that are responsible for sensory, nerve, and muscle function. Stimuli alter the permeability of the cell membrane by causing ion channels to open. For example, a slight stimulus may cause some sodium channels to open. With this route now available, sodium ions flow rapidly into the cell, driven by their own concentration gradient and the attraction of the excess negative ions. The sodium-potassium pump still is transporting some sodium out of the cell, but it is overwhelmed by this rapid influx of sodium ions. This results in a decrease in the electrical potential difference between the inside and the outside of the cell, so the membrane potential decreases (depolarization). If the sodium channels now close, the ion pump will reestablish electrochemical equilibrium. In excitable cells, the sodium gates may not close right away, however. If the membrane potential becomes altered to a critical level, known as the "threshold potential", more sodium gates will open, thereby allowing even more sodium to flow into the cell even more rapidly. These sodium channels open in response to voltage change across the membrane. Therefore, they are referred to as voltage-regulated channels. As more sodium flows in, more sodium gates open, and so on. This example of positive feedback to rapidly allow more sodium into the cell is called the Hodgkin cycle. The net result of this rapid influx of sodium ions is that the inside of the cell has now become positive with respect to the outside. In this extremely depolarized condition the cell membrane cannot respond to another stimulus until its original polarity is reestablished. This extreme depolarization event is very brief, however, because the sodium gates close when the membrane potential reaches a certain point, preventing any further sodium influx. The cell membrane then "repolarizes" by opening potassium gates (also voltage-regulated) and allowing potassium ions to flow out, driven by their concentration gradient and the repulsion of the positively charged sodium ions that are now abundant inside the cell . The sodium-potassium pump could repolarize the membrane, but it would take too long to be biologically useful. This rapid repolarization of the cell membrane reestablishes the resting potential of the cell, and puts the cell in a condition where it now can respond to another stimulus. Gradually, the sodium-potassium exchange pump will move sodiums out and potassiums in, thereby reestablishing the original ion distribution. This brief exchange of sodium and potassium ions only affects those ions immediately adjacent to the cell membrane. It does not have a significant impact on the overall intracellular and extracellular concentration of sodium or potassium. The rapid depolarization and repolarization of the membrane of an excitable cell is called an "action potential", and it is important to understand this series of events in order to understand the events involved in the functioning of the nervous system.
  • 4. How do neurons receive and integrate signals? The reception of signals from other neurons or sensory cells causes a small change in the membrane potential at the site of the synapse. These changes in membrane potential are proportional to the intensity of the stimulus (graded potentials) and are referred to as postsynaptic potentials (PSPs) because they occur on the postsynaptic (receiving) membrane. These PSPs spread outward from the synapse and across the membrane of the dendrites and cell body. As they spread they may encounter and combine with PSPs from other synaptic junctions that also are being stimulated. (At any given moment a neuron may be receiving stimuli from many different sources.) The PSPs are continually being combined in the axon hillock, and if at any given moment the sum of all of the PSPs is sufficient to bring the membrane potential of the axon hillock to its threshold, an action potential is generated. If the summation of the PSPs fails to reach threshold, an action potential will not be generated. Are all postsynaptic potentials excitatory? No - postsynaptic potentials can be either excitatory (EPSPs) or inhibitory (IPSPs). EPSPs depolarize the postynaptic membrane, often by increasing the inward flow of sodium, thereby increasing the number of positive charged ions on the inside of the cell membrane. This results in a decrease in the voltage difference across the membrane, bringing the membrane potential of the axon hillock closer to threshold. This increases the likelihood that an action potential will be generated, which is why these depolarizing PSPs are called excitatory. IPSPs, however, hyperpolarize the postsynaptic membrane, often by increasing the leakage of potassium ions out of the cell or increasing the flow of chloride ions into the cell. This increases the voltage difference across the membrane, and pushes the membrane potential further from the threshold voltage. This decreases the likelihood that an action potential will be generated, which is why these hyperpolarizing PSPs are called inhibitory. How is an action potential generated and propagated along an axon? The generation of an action potential involves the rapid depolarization and repolarization of the cell membrane. If an action potential is generated, the Hodgkin cycle assures that it is of maximal force, regardless of whether the sum of all PSPs greatly exceeded threshold or was just barely strong enough to reach threshold. This gives action potentials and "all-or-none" property. In other words, if threshold is reached or exceeded, the action potential will be maximal; if threshold is not reached an action potential will not be generated. There is no in- between at the level of the individual neuron. (Nerves are bundles of neurons and can show different levels of response because the individual neurons may exhibit different thresholds.) If an action potential is generated at the axon hillock it now will spread quickly along the axon as a "wave" of depolarization. An important property of action potentials is that they do not lose intensity as they travel because they are regenerated as they move along the axon. This regeneration of the action potential occurs because the depolarization of one region of the axon depolarizes the adjacent region and brings it to its threshold, thereby generating another action potential. In axons that lack a fatty, insulating myelin sheath, this propagation of the action potential occurs continuously along the length of the axon. The opening and closing of the appropriate ion gates slows the signal down somewhat, but the signal's intensity does not diminish as it travels. Role of a myelin sheath in action potential propagation Most vertebrate axons do have a myelin sheath, however, which helps the signal move more quickly by limiting action potential regeneration to the nodes of Ranvier. Action potentials can occur only where the axon cell membrane is in close contact with extracellular fluid. Therefore areas of the axon covered with a myelin sheath cannot regenerate action potentials. They can, however, rapidly conduct an electrical field to the next exposed section of axon membrane - the next node of Ranvier. Here the action potential is regenerated and
  • 5. transmitted further along the axon. Because fewer regeneration events take place, the signal moves more quickly than if the myelin were not present. The myelin sheath, then, increases the conduction velocity of an axon. Axon diameter affect the velocity of an action potential Another way to increase conduction velocity is to increase the diameter of an axon. As in electrical wires, there is some resistance to current flow along the periphery. Increasing the diameter of a wire increases the proportional cross-sectional area of the wire that is not in direct contact with the periphery, thereby decreasing the effect of peripheral resistance. In other words, more charge can flow quickly because proportionally less is slowed by peripheral resistance. Large diameter axons, therefore, can transmit action potentials faster than those with small diameters. Some invertebrates have very large diameter non-myelinated axons responsible for rapid reflexes. For example, the "giant axon" associated with the stellate ganglion of squid is responsible for the rapid contraction of the mantle which provides jet propulsion for squid escaping a predator. Large diameter axons with myelin sheaths can transmit action potentials extremely fast. The Mauthner cells in fishes have among the highest conduction velocity known among the vertebrates (50 to 100 m/s). These large-diameter, myelinated neurons are responsible for the startle response that helps a fish rapidly curl its body and flick its tail, resulting in rapid movement away from a stimulus (think of this the next time that you tap on the side of an aquarium). Nerve impulses carried across synapses When an action potential reaches the end of a neuron, the signal is transmitted to another cell, such as a muscle cell or another neuron. The area of signal transmission is called a synapse, and these come in two general varieties - electrical and chemical. In electrical synapses the presynaptic (transmitting) and postsynaptic (receiving) membranes are in direct contact with one another and small channels permit ions to flow through almost as if there was no barrier at all. Electrical synapses, therefore, transmit signals very rapidly. Chemical synapses, which are more common, require the release of a chemical transmitter substance by the presynaptic membrane in order to stimulate the postsynaptic membrane. There are two types of chemical syapses - fast (direct) and slow (indirect). In both types, the arrival of the action potential at the presynaptic knob results in an opening of calcium channels on the presynaptic membrane. The resulting influx of calcium ions causes vesicles of transmitter substance to bind to the presynaptic membrane and release their contents. In a fast chemical synapse, molecules of transmitter substance diffuse from the presynaptic membrane across the synaptic cleft and bind to receptor molecules on the postsynaptic membrane. These receptor proteins also form the ion channel, and the binding of the neurotransmitter directly alters the configuration of the proteins and opens the ion channels of the postsynaptic membrane. (This is why these channels are referred to ligand-gated channels.) This allows molecules such as sodium to move across the membrane and alter its membrane potential, creating postsynaptic potentials. In a slow chemical synapse, the binding of the neurotransmitter to a receptor on the cell membrane activates nearby G-proteins. This catalyzes a series of reactions that results in the release of another molecule (a second messenger) which binds to the proteins that form an ion channel. This alters the configuration of the channel, thereby opening it and allowing ions to flow through. This is an indirect, and therefore slower, mechanism because it requires a series of biochemical reactions. Transmission at slow chemical synapses is slower, longer lasting, and may be more widespread spatially than the rapid, localized and immediate response seen at fast chemical synapses. Both types of synapses may be found on the dendrites or soma of a receiving neuron, and the effects of slow synapses may play a role in
  • 6. modulating the effects of a fast synapse by altering the membrane potential of the postsynaptic membrane. Molecules of transmitter substances in the synaptic cleft and those bound to receptor molecules on the postsynaptic membrane are quickly broken down by enzymes. This is important for two reasons. First, the resulting components are taken up by the presynaptic membrane and recycled to produce more transmitter substance. Second, the postsynaptic membrane must be relieved of the stimulation by the transmitter substance molecules so that it can reestablish its resting potential. If transmitter substance molecules remained bound to their receptor sites, the associated ion channels would remain open and the receiving cell could not function properly. Neurotoxins affect nerve function Understanding the cellular mechanisms of the nerve function helps us understand ways in which certain neurotoxins have their effects. Inhibition of proper nerve function can lead to death, often due to respiratory paralysis. Tetrodotoxin, the toxin from the viscera of puffer fish (Tetraodontiformes) binds to the extracellular surface of the proteins that make up sodium channels. This blocks the sodium channel, thereby inhibiting the proper function of neurons or other excitable cells. Saxitoxin, a paralytic shellfish toxin produced by some dinoflagellates responsible for "red tides", has the same specific effect as tetrodotoxin. The venom of the krait, one of the highly poisonous cobra snakes, contains alpha-bungarotoxin, which binds irreversibly to a particular group of neurotransmitter receptors, thereby inactivating them. The toxin responsible for botulism, which is produced by the bacterium Clostridium botulinum, prevents the release of an important group of neurotransmitters from their vesicles, thereby preventing neurotransmission.
  • 7. modulating the effects of a fast synapse by altering the membrane potential of the postsynaptic membrane. Molecules of transmitter substances in the synaptic cleft and those bound to receptor molecules on the postsynaptic membrane are quickly broken down by enzymes. This is important for two reasons. First, the resulting components are taken up by the presynaptic membrane and recycled to produce more transmitter substance. Second, the postsynaptic membrane must be relieved of the stimulation by the transmitter substance molecules so that it can reestablish its resting potential. If transmitter substance molecules remained bound to their receptor sites, the associated ion channels would remain open and the receiving cell could not function properly. Neurotoxins affect nerve function Understanding the cellular mechanisms of the nerve function helps us understand ways in which certain neurotoxins have their effects. Inhibition of proper nerve function can lead to death, often due to respiratory paralysis. Tetrodotoxin, the toxin from the viscera of puffer fish (Tetraodontiformes) binds to the extracellular surface of the proteins that make up sodium channels. This blocks the sodium channel, thereby inhibiting the proper function of neurons or other excitable cells. Saxitoxin, a paralytic shellfish toxin produced by some dinoflagellates responsible for "red tides", has the same specific effect as tetrodotoxin. The venom of the krait, one of the highly poisonous cobra snakes, contains alpha-bungarotoxin, which binds irreversibly to a particular group of neurotransmitter receptors, thereby inactivating them. The toxin responsible for botulism, which is produced by the bacterium Clostridium botulinum, prevents the release of an important group of neurotransmitters from their vesicles, thereby preventing neurotransmission.