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Openstax Biology Nervous System

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Openstax Biology Nervous System

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CHAPTER 35 The Nervous System Figure 35.1 An athlete's nervous system is hard at work during the planning and execution of a ‘movement as precise as a high jump. Parts of the nervous systam are involved in determining how hard to push off and when to turn, as well as controlling the muscles throughout the body that make this complicated movement possible without knocking the bar down-—all in ust a few seconds. (credit: Scott Ray) INTRODUCTION When you're reading this book, your nervous system is performing several functions simultaneously. The visual system is processing what is seen on the page; the motor system controls the ‘num ofthe pages (or click of the mouse); the prefrontal cortex maintains attention, Even fundamental fanctions, ke breathing and regulation of body temperature, are controlled bythe nervous system. A 0 OG nervous system isan organisms control center: it processes sensory information from outside and ony inside) he body and conceos all behaviors—feom eating to sleeping to finding a mate Eo Coons Prem Oy po Pee Poon rane oe cy Dene 35.1 Neurons and Glial Cells By the end of this section, you will be able to do the following: «List and describe the functions of the structural components of a neuron «List and describe the four main types of neurons + Compare the functions of afferent types of glial ces Nervous systems throughout the animal Kingdom vary in structure and complexity, as illustrated by the variety of animals shown in Figure 35.2, Some organisms, lke sea sponges, lack a true nervous system. ‘others, lke jellyfish lack a true brain and instead havea system of separate but connected nerve cells neurons) called a "nerve net.” Echinoderms such as sea stars have nerve cells that are bundled into fibers called nerves. Flatworms ofthe phylum Platynelminthes have both 2 central nervous system (CNS), made up ‘ofa small “brain’ and two nerve cords, and 2 peripheral nervous system (PNS) containing a system of nerves that extend throughout the body. The insect nervous system is more complex but also fairly decentralized. It ‘contains a brain, ventral nerve cord, and ganglia (clusters of connected neurons). These ganglia can control ‘movements and behaviors without input ftom the brain. Octopi may have the most complicated of invereebrate nervous systems-—they have neurons that are organized in specialized lobes and eyes that are structurally similar to vertebrate species. eget News conn (eran (cata (0) zpnate erteanan ‘say ‘sens ‘dae ‘Caines pin cence ‘og Segnent grate neve (orev coyonsk nyoraae ‘se (eons) ‘saan Figure 35.2 Nervous systems vary in structure and complexity. In (a cnidarians, nerve cells form a decentralized nerve net. In () echinoderms, nerve cells are bundled ino fides called nerves. In animals exhibiting bilateral symmetry suchas) lanarans, neurons cluster into a anterior brain that processes infrmation. In adtion toa brain (arthropods have clusters of nerve cell bodies, called peripheral ganglia, located along the ventral nerve cor olusks such as squid and ()octopl, which must hunt te survive, have complex rains containing mills of neurons. In( vertebrates, the bran an spinal cord comprise the central nervous system, wile neurons extenaing, into the rest ofthe body comprise the peripheral nervous system. (cede: meditation af work by Michael Vecchione, Clyde FE. Roper, ané Michael 2. Sweeney, NOAA; crest: modification of work by NIH) ‘Compared to invercebrates, vertebrate nervous systems are more complex, centralized, and specialized, ‘While there is great diversity among different vertebrate nervous systems, chy all share a basi scucrure:a ‘CNS that contains a brain and spinal cord and 2 PNS made up of peripheral sensory and motor nerves. One inceresting difference between the nervous systems of invertebrates and vertebrates is that the nerve cords ‘of many invertebrates are located ventrally whereas the vertebrate spinal cords are located dorsally. There is debate among evolutionary biologists as to whether these dferenc nervous system plans evolved separately ‘Access for free at openstaxor ‘or whether the invertebrate body plan arrangement somehow “Dipped! during the evolution of vertebrates, @ LINK TO LEARNING ‘Watch this video of biologist Mark Kirschner discussing the “flipping” phenomenon of vertebrate evo (Glick to view content (htsnsJhvwwopenstas orglvercebrate evel) ‘The nervous system is made up of neurons, specialized cells that can receive and transmit chemical or electrical signals, and alia, cells that provide support functions for the neurons by playing an information processing role that is complementary to ‘neurons. A neuron can be compared to an clectrcal wire—it transmits a signal from one place to another. Glia can be compared tothe workers atthe ele the vidence suggests that they also wsurp some of the signaling company who make sure wires go are broken. Akhough pia have been compared ro workers, rece functions of neurons. he places, maintain the wires, and take down wites that “there is great diversity in the types of neurons and gia that are present indifferent pars ofthe nervous system. There are four major types of neurons, and they share several important celllar compone! Neurons ‘The nervous system of the common laboratory ly, Drosophila melanogaster, contains around 100,000 neurons, the same ‘number asa lobster. This number compares to 75 milion inthe mouse and 200 milion inthe octopus. Ahumsan brain contains around a6billion neurons. Despite these very diferent numbers, the nervous systems ofthese animals control many ofthe same bbchaviors from basic reflexes to more complicated bebaviors like finding food and courting mates. The ability of neurons to ‘communicate with each other as well as with other types of ells underlies al ofthese behaviors Most neurons share the same cellular components. But neurons are also highly specialized-—different types of neurons have different sizes and shapes that relate to thet fanctional rales Parts of a Neuron Like other cells, each neuron has a cell body (or soma) that contains a nucleus, smooth and rough endoplasmic reticulum, Golgi apparatus, mitochondeia, and other cellular components. Neurons also contain unique structures, illustrated in Figure 3.3 for receiving and sending the electrical signals that make newronal communication possible. Dendites ae tee like structares that ‘extend avay from the eell body to receive messages from ather neurons at specialized junctions called synapses. Although some neurons do not have any dendtites, some sypes of neurons have multiple dendeites, Dendrites can have small protrusions called dendriti spines, which further increase surface area for possible synaptic connections. ‘Once. signal is received by the dendrite, itthen travels passively tothe cel body the eel body contains a specialized structure, the axon hillock that integrates signals from multiple synapses and serves as ajunction between the cell body and an axon. An axon sa tube-like structure that propagates the integrated signal to specialized endings called axon terminals. These terminals ‘insur synapse on other neurons, muscle, or target organs. Chemicals released at axon terminals allow signals to be ‘communicated to these other cell Neurons usually have one or twa axons, b some neurons, like amacrine cells inthe resin, donot contain any asons, Some axons are covered with myelin, which acts a8 an insulator to minimize dissipation ofthe lectcial signal ast travels down the axon, greatly increasing the speed of conduction. This insulation is important asthe axon froma human motor neuron can beas long as a meter—from the base ofthe spine tothe toes, The myelin sheath isnot actually part ofthe neuron. Myelin is produced by glial cells. Along the axon there are periodic gaps in the myelin sheath, These gaps are called nodes of Ranvier and are sites where the signal is “recharged” asi travels along the axon, Iris important o note that single neuron does not act alone—neuronal communic neurons make with one another (as well as with other cel, synaptic contact from many ather neurons, For example, dendrites from a Purkine cell inthe cerebellum ate thought to receive contact from as many a8 200,000 other neurons, n depends on the connections that ce muscle cells. Dendrites from single neuron may receive VISUAL CONNECTION ‘csgodendronye col membrane Synapse Figure 35.3 Neurons contain organelles commen to many other cells, such asa nuious and mitochondria. Thy also have more specialized sruetures, including dendrites and axons. ‘Which of the following statements is false? ‘The soma isthe cell body ofa nerve cel, -Myelin sheath provides an insulating layer co the dendrites. Axons carty the signal from the soma tothe target. Dendeitescarty the signal tothe soma, ‘Types of Neurons ‘There are different types of neurons, and the functional role ofa given neuronis intimately dependent on is structure. There is anamazing diversity of ncuron shapes and sizes found in different parts of the nervous system (and across species), 35, itlsteated by the neurons shown in Figure 3.4 for free at openstaxors. Y 7% ct (@) Pyramidal cell ofthe (6) Purkinje cell of the (6) Otfactory neurons. cerebral cortex carabelar conex Figure 35.4 There is great diversity inthe size and shape of neurons throughout the nervous system: Examples include (a) pyramidal col ‘tom th cerebral cortex, (a Purkinje cel from the cerebellar cortex and (c) ltactory cals rom the olfactory epithelium and olfactory ut ‘While there are many defined neuron cell subtypes, neurons are broadly divided into fous basic types unipolar, bipolar, multipolar, and pseudounipolar. Figure 35. illustrates these four basic neuron types. Unipolar neurons have only one structure ‘that extends away from the soma, These neurons are not found in vertebrates but ae found in inseets where they stimulate _muscles or glands. A bipolar neuron has one axon and one dendrite extending fom the soma. An example ofa bipolar neuron is retinal bipolar cel, which eceives signals from photoreceptor cells chat are sensitive to ight and transmit these signals to ganglion cells tha cary the signal to the brain. Multipolar neurons are the most common type of neuron. Each multipolar ‘neuron contains one axon and multiple dendrites. Multipolar neurons can be found in the central nervous system (brain and spinal cord), An example of a multipolar neuron i Purkinje cell in the cerebellum, which has many branching dendrites bat only one axon. Pseudounipola cells share characteristics with both unipolar and bipolar cells. pseudounipolar cellhas a single process that extends from the soma, like a unipolar cell, but this process later branches into two distnet structures, ikea bipolar cell. Most sensory neurons are pseudounipelar and have an axon that branches into two extensions: one connected to dendrites that receive sensory information and another that transmits this information co the spinal cord, ae 4 Unipolar neuron Muitipolar neuron Bipolar neuron Pseudounipolar neuron Figure 35.5 Neurons are broadly divided int four mala types based onthe number ané placement of axons: (2) vnipoay, (2) bpels (3) ‘mutiola, and () pseudounipolr. Everyday Connection Neurogenesis {tone rime, scientists belived cht people were born with ll the neurons they would ever have, Research performed during the last few decades indieates that neurogenesis, the birt of new neurons, continues ito adulthood. Neurogenesis was first discovered in songbirds that produce new neurons while learning songs. For mammals, new neurons also play 2n important ole in learning: about 1000 new neurons develop inthe hippocampus a brain structute involved in learning and ‘memory each day. While most of the new neurons wil de, researchers found that an increase inthe numberof surviving ‘new neurons in the hippocampus cortelated with how well ats earned 2 new tsk. Interestingly, both exercise and some antidepressant medications also promote neurogenesis in the hippocampus. Stress has the opposite effect. While neurogenesis is quite limited compared to regeneration in other tissues, research inthis area may ead to new treatments for disorders such as Alzheimer’, stoke, and epilepsy. How do scientists identify new neurons? A researcher can inject a compound called bromodecxyuridine (BrdU into the brain of an animal. While al cells wil be exposed to BrdU, BrdU will only be incorporated into the DNA of newly generated cells that are in S phase, Ateehnique called irsmunohistochemistry can be used to attach a fluorescent labelto the {incorporated BrdU, and a researcher can use luorescent microscopy to visualize the presence of BrdU, and thus new neurons in brain tissue. Figure 25.6 is micrograph which shows fluorescently labeled neurons in th hippocampus ofa rat ‘Access for free at openstax.ora U/Nestin ae Neut00 Figure 35.6 This mierograph shows fluorescently labeled new neuron ina rat hippocampus. Coll that are setively diving have protein (GFAP) are AP. Thus, calls that ate abeles oth red and green are actively cviing bromedexyuriine (BrdU) incorporated into their DNA and ae labsledin red. Coli that express glal ilar a labeled in green Astrocy astrocytes, whereas cals labeled red only are actively aviing neurons. ret: modifeation of work by Dr. Maryam Faz ta University of Barcelona; sale-bar data from Matt Russo) @ LINK TO LEARNING “this sie (hte /openstax. org neurogenesis) contains more information about neurogenesis, including an interactive laboratory simulation and a video that explains how BrdU labels new cells, Glia ‘While glia are often thought of as the supporting cast ofthe nervous system, the number Hal cellsin the brain actually sambers the number of neurons by a factor of en, Neurons would be unable to function without the vital roles that are alle by harm neurons, and provide myelin sheaths around axons. Scientists have recently discovered that they also play a role in responding to nerve activity and modulating communication berween nerve cells, When glia do not function propery, the result se glial cells. Gla guide developing neurons to their destinations, buffer ions and chemicals that would otherwise ‘canbe disastrous—most brain tumors are caused by mutations in glia Types of Glia ‘There are several different types of glia with different functions, tw of which ate shown in Figure 25.7, Astoeyte, shown in Figure 2s. ¢a make contact with both capillaries and neurons in the CNS. They provide nutrients and other substances to ‘neurons, regulate the concentrations of ions and chemicals in the extracellular fluid, and provide structural support for synapses. Aste ‘Astrocytes, in particular, have been shown through calcium imaging experiments to become active in response to nerve activi ‘ransmic calcium waves between astrocytes, and modulate the activity of surrounding synapses. Satelite glia provide nutrients and structural support for neuronsin the PNS, Microglia scavenge and degrade dead cells and protect the brain from invading xyes als form the blood-brain barrier—a structure that blocks entrance of toxic substances into the brain, microorganisms. Oligodendrocytes, shown in Figure s.8h form myelin sheaths around axons in the CNS. One axon can be ryelinated by several oligodendrocytes, and one oligodendrocyte can provide myelin for multiple neutons. This di from the PNS where a single Schwann cll provides myelin for only one axon as the entire Schwann cell surrounds the axon, Radial glia serve as scafolds for developing neurons as they migrate ro their end destinations. Ependymal cells line fluid-filled ventricles of the brain and the central canal ofthe spinal cord. They are involved in the production of cerebrospinal fluid, which 1 the choroid servesasa cushion forthe brain, moves the fuid between the spinal cord and the brain, and isa component plexus. Pseudouiplar Otgodereroaye (0) Central nervous sytem (0) Perera nerous system Figure 35.7 lal cells support neurons and maintain thei nvionment. Glial cols ofthe (a) central nervous system include oligodendrocytes astrocytes, epandymal calls, and microglial calls. Cligadendrocytes frm the myelin sheath around axons. Astrocytes provide nuronts to neurons, malntaln their extracellular environment, and provide structural suppor. lcrogla scavenge pathogens anc dead cols. Epandyma als produce corebrospinal id that eushions the neuron. lal cols ofthe (b) peripheral nervous sytem include Schwann call, which form the myelin sheath, and satelite cell, which provide nutrients and structural supporto neurons. aseecye (©) Omgocendroaye Figure 35.84) Astrocytes and (+) ligodonéracytes ae gal cols ofthe contra nervous systom. credit: modification of work by Uniformed Services Unversity ret b: modification of work by Jurjen Broek; scale-bar data from Matt Russel 35.2 How Neurons Communicate By the end of this section, you will be able to do the following: + Descrive the basis of the resting memibrane potential «+ Explain the stages of an action potential end how action potentials are propagated + Explain the similarities and differences between chemical and electrical synapses + Describe long-term potentiation and long-term depression All functions performed by the nervous system—from a simple motor reflex to more advanced functions like making a memory ora decision—require neurons to communicate with one another, While humans use words and body language to communicate, neurons use electrical and chemical signals, Just like a person in a commitee, one neuron usualy receives and synthesizes messages from multiple other neurons before “making the decision to send the meseage on to other neurons. Nerve Impulse Transmission within a Neuron For the nervous system to function, neurons must be able to send and receive signals, These signals ae possible because each neuron has a charged celular membrane (a voltage difference berween the inside and the outside), and che charge of this ‘membrane can change in response to neurotransmitter molecules released from other neurons and environmental tim, To ‘understand how neurons communicate, one must frst understand the bass ofthe baseline or resting membrane charge Neuronal Charged Membranes ‘The lipid bilayer membrane that surrounds a neuron is impermeable ro charged molecules or ions, To enter or ext the neuron, {ons must pass through special proteins called ion channels that span the membrane. fon channels have different configurations: open, closed, and inactive as illustrated in Figure 3s.9. Some ion channels need tobe activated in order to open and allow ions to pass into or out ofthe cell. These ion chanel ae sensitive tothe enviconmment and can change thet shape accordingly. on channels that change their structure in response to voltage changes are called voltage-gated ion channels Voleage-gated ion channels regulate the relative concentrations of different ions inside and outside the cell. The difference in total charge between the inside and outside of the cellis called the membrane potential ‘Gosed the resin potent ‘open n response toa pee mule, Imactvated Fo 2 bret prot fotowing ‘hanwel i coced ‘Mogale opens and ia" entre te ei _Sehaon, hecharnal es At open in esponée anew sonal Figure 35.8 Voltage-gated ion channels open in esponse to changes in membrane voltage. Ate activation, they become inactivated fora brie period and will no longer open in response toa signal @ LINK TO LEARNING “This vdeo discusses the basis ofthe resting membrane potential (lick o view content huunsvuwopenstax.orglresting neuron) Resting Membrane Potential ‘neuron at rest is negatively charged: the inside ofa cell is approximately 70 millivolts more negative than the outside (-70 mV, note that this number varies by neuron type and by species). This voltage is called the resting membrane potential itis caused by differences inthe concentrations of ions inside and outside the cell. the membrane were equally permeable oallions, each type afon would flow across the membrane and the system would reach equilibrium. Because ions eannot simply cross the ‘membrane at wil, there are different concentrations of several ions inside and outside the cel, as shown in Table 3.1. The difference inthe numberof positively charged potassium ions (K"inside and outside the cell dominates the resting membrane potential (Figure 5.10). When the membrane is at rest, K" fons accumulate inside the cell due toa net movement with the concentration gradient. the negative resting membrane potential is created and maintained by increasing the concentration of «ations outside the cell (inthe extracellular lui) relative co inside the cell inthe eytoplastn). The negative charge within the cell is created by the cell membrane being more permeable to potassium ion movement than sodium ion movement. In neurons, ‘potassium ions are maintained at high concentrations within the cell while sodium ions are maintained at high concentrations ‘outside ofthe cell. th cell possesses potassium and sodium leskage channels that allow the two cations to diffuse down their concentration gradient. However, the neurons have Far more potassium leakage channels than sodium leakage channels. ‘Therefore, pocassium diffuses out ofthe cell at a much faster rate than sodium leaks in, Because more cations ae leaving the cell than are entering, this causes the interior ofthe cello be negatively charged relative ro the outside ofthe call. The actions ofthe sodium potassium pump help to maintain the resting potential, once established. Recall that sodium potassium pumps brings two K" ions into the ell while removing three Na* ions per ATP conswumed. As more cations are expelled from the cellthan taken. in, the inside ofthe cell remains negatively charged relative ro the extracellular fluid. It should be noted that chloride ions (CI") ‘tend ro accumulate outside ofthe cell because they are repelled by negatively-charged proteins within the cyeoplasm. lon Concentration Inside and Outside Neurons ton Extracellular concentration Intracellular concentration Ratio outside (mM) (mM) inside Nat us 2 2 Ke 4 155 0.026 cr 220 4 x reeianons eo ‘Table 35:1 The resting membrane potential is a result of diferent concentrations inside and outside the cll. for free at openstaxors. 352.+How Neurons Communicate 987 ‘the resting pot, al votage ged Nat channels and most vag gated Khanna ate csed. The Nak“ wanepoter furs Kons he el and Ne ors ok (@)Depotarizaton Oe er @® @ © (GS Raie the mamiranc aang Wie necks octane eine ad ete chan pa (9 Myparpolaation @ Over ‘tthe peak action pont Nat chants close who K* charms open" leaes the cl. ang the moma event tecomes Myerpetied. Figure 35.10 The (a) resting membrane potential is @ result of diferent concentrations of Na" and k* Ions inside and outside thecal. A resultngin () depolarization. atthe peak ation potential K* channels open andthe call nerve impulse causes Na” fo enter th ‘becomes (©) hyperpolarized. Action Potential ‘neuron can receive input ftom other neurons an, if this input is strong enough, send the signal so downstream neurons. ‘Transmission ofa signal between neurons is generally carried by a chemical called a neurotransmitter. Transmission ofa signal within a neuron from dencite ro axon terminal) is carried by a brief reversal ofthe resting membrane potential called an action potential. When neurotransmitter molecules bind to receptors located on a neuroris dendrites, jon channels open, At excitatory ‘synapses, this opening allows positive ions to enter the neuron and resutsin depolarization ofthe membrane—a decrease in the difference in voltage between the inside and outside ofthe neuron. A stimulus from a sensory cello another neuron, depolarizes the target neuron tots threshold potential (-55 mV). Na" channels inthe axon hillock open, allowing positive fons to ‘enter the cll (Figure 35.10 and Figure 35.1). Once the sodium channels open, the neuron completely depolaizes toa membrane potential of about +40 mV, Action potentials are considered an 'all-or nothing’ event, in that, once the threshold potential is reached, the neuron always completely depolarizes. Once depolarization is complete, the cell must now ‘reset’ its membrane voltage back othe resting potential. To accomplish this, the Na* channels close and cannot be opened. This begins the neurons refractory period, in which it cannot produce another action potential because its sodium channels will nt open. At the same ‘time, voltage-gated K° channels open, allowing K” co leave the cel. As K" ions leave the cell, the membrane potential once again becomes negative. The diffusion of K" out of the cell actually hyperpolarizes the ell n thatthe membrane potential becomes ‘more negative than the cells normal resting potential. At this point, the sodium channels will return to theit resting state, meaning they aze ready to open again ifthe membrane potential again exceeds the threshold potential Eventwally the extra K ions diffuse ou of the cll through the potassium leakage channels, bringing te cel fom is hyperpolarized state, back its resting membrane potential VISUAL CONNECTION GB Peak action potential é Repolarization ‘Threshold of Membrane potential (mV) Time Figure 35.12 The formation of an action potential can be divided into five steps: (2) Astimulus from a sensory clr another neuron ‘causes the target cal to depolarize toward the chreshold potential (2) the threshold of excitation i reached, all Nat channels open and the membrane depolarizes (3) A the peak action potential, K"ehannels open and K” begins oleae the ell. tthe same tie, Na? ‘channel los. (4) The membrane becomes hyperpolarized ask fons continue to leave the eel, The hyperpolariaed| membranoisina refractory period and cannet fre (5) The K* channel lose and the Na“/k* transporter restores the resting potenti Potassium channel blockers, such a8 amiodarone and procainamide, which are used to treat abnormal electrical activity in the heart, called cardiac dyschythmia, impede the movement of K° through voltage-gated K° channels. Which par of the action Potential would you expect potassium channels o affect? 25 for foe at openstox.rg 2. In esponse to a signal the soma end ofthe axon Becomes depolarized, '. The depolarization spreads down the axon. Meanwhile, the frst pat of the membrane repolarzes. Because [Na* channels are activated and ‘dtionalK" channels have opened, {he membrane cannot depolarize agai, The action potential continues to travel down the axon, Figure 35.12 The action potential is conducted down the axon asthe axon membrane depolarizes, then repolarizes, @ LINK TO LEARNING “This video (herpsopenstax.org/l/aevionpotential) presents an overview of action potential Myelin and the Propagation of the Action Potential Foran action potential to communicate information to another neuron, it must travel along the axon and reach the axon terminals where itcan initiate neurotransmitter release. The speed of conduction ofan action potential along an axon is influenced by both the diameter ofthe axon and the axons resistance to current leak. Myelin acts as an insulator that prevents current from leaving the axon; this inereases the speed of action potential conduction. In demyelinating diseases like multiple sclerosis, action potential conduction slows because current leaks from previously insulated axon areas. The nodes of Ranvier, illsteated in Figure 3.1 ae gaps i the myelin sheath along the axon, These unmyelinated spaces ae aboxt one micrometer Jong and contain voltage-gated Na and K’ channels. Flow of ions chrough these channels, particularly the Na" channels, ‘egenerates the action potential over and over aguin along the axon. This jumping of the action potential from one node tothe next called saltatory conduction. [Fnodes of Ranvier were not present along an axon, the action potential would propagate very slowly since Nat and K* channels would have to continously regenerate action potentials a every point along the axon instead of at specific points. Nodes of Ranvier also save energy for the neuron since the channel only need tbe present at the nodes and notalong the entire x00, axon Nodes of Ranvier Myelin sheath Depolarized ‘Membrane at ‘membeane resting potential Figure 35.13 Notes of Ranvier aro gaps in myelin coverage along axons. Nodes contain voltage-gated K" and Na" channels. Action potentials travel down the axon by jumping rom one nod othe next. Synaptic Transmission ‘The snaps orgy isthe place where informations tansmited from oe neuron to another, Smapses wal frm berwen axon terminals and dendriispine, bu thi i nor niversly true. here ate slo axon-o-anon, dendrite-to-dendrite, and ‘ono cel body synapses. The neuron ransmtsng the signals eld the presyapic neuron, ad the neuron recevng te Signals ead she postsynaptic nearon Note tha these designations ae relive to particular syrapiemow neuron are beh resrayicand postsynaptic. Tere atetworypes of synapses chemia and ele. Chemical Synapse ‘When an action potential reaches the axon terminal it depolarizes the membrane and opens voltage-gated No" channels, Na ions enter th cll, farther depolarizing the presynaptic membrane. This depolarization causes voltage-gated Ca channels to ‘open. Calum ions entering the cll initiate a signaling cascade that causes small membrane-bound vesicles, called synaptic vesicles, containing neerotransmier molecules to se with the presynaptic membrane, Synaptic vesicles are shown in Fizure 235.4, which isan image from a scanning electron microscope. Figure 35.14 This pseudocolored image taken with a scanning electron microscope shows an axon terminal that was broken open to reveal _saptic vesicles (ue and orang) inside the neuron. (rei mocifiaton of werk by Tina Carvalho, NIH-NIGMS; scale-bar data from Matt Russel) Fusion of vesicle with the presynaptic membrane causes neurotransmitter tobe released into the synaptic cleft, the ‘extracellular space between the presynaptic and postsynaptic membranes, as illustrated in Figure 5.15. The neurotransmitter digfuses across the synaptic cleft and binds to receptor proteins on the postsynaptic membrane 25 for foe at openstox.rg a ® earoganeminconaing ree ass ,® votage gated cat” ‘hannete open and Ca enters the Neurtransmiter oifuses across the synapue cet ae ads 0 ligand gated lon chanson the postsynape membrane. ‘Binding of eurorarsmiter opens bpand gated © Fewptae ty the presyrapic neuron, enzymatic degradation tom enarnos, resulting grated potent, [and sien reduce neuroransniter eves trmctng he ‘inal Figure 35.15 Communication at chemical synansee requires release of neuratransmiters, When the presynaptic membrane is depolarized, vottage-gated Cat channels open and allow Cato enter the cell The calcium entry causes synaptic ves and release neurotransmitter molecules into the synaptic cet. The neurotransmitter difuses across the synaptic lett and binds to igand 0 fuse with the membrane ‘gate ionchannolsin the postsynaptic membrane, resulting ina localized depolarization or hyperpoarization of the postsynaptic neuron, ‘The Binding ofa specifc neurotransmitter causes particular ion channels, in this case ligand-gated channels, on the postsynaptic membrane to open. Neurotransmitters can cither have excitatory or inhibitory effects on the postsynaptic ‘membrane, as detailed in Table 35.1, For example, when acetylcholine is released atthe synapse between a nerve and muscle (called the neuromuscular junction) by a presynaptic neuron, it eauses postsynaptic Na° channels to open. Na" enters the postsynaptic cell and causes the postsynaptic membrane ro depolarize, This depolarization is called an excitatory postsynaptic potential (EPSP) and makes the postsynaptic neuron more likely to fire an action potential. Release of neurotransmitter at inhibitory synapses causes inhibitory postsynaptic potentials ([PSPa), a hyperpolarization of the presynaptic membrane. For ‘example, when the neurotransmitter GABA (gamma-aminobutyric acid) is released from a presynaptic neuron, it binds toand ‘opens CI’ channels. CI ions enter the cll and hyperpolarizes the membrane, making the neuron les likely to fire an action potential ‘Once neurotransmission has accurted, the neurotransmicer must be removed from the synaptic cleft so the postsynaptic ‘membrane can "reset and be ready to receive another signal. This can be accomplished in three ways: the neurotransmitter can diffuse away from the synaptic clef, it can be degraded by enzymes inthe synaptic cleft, ort can be recycled (sometimes called reuptake) by the presynaptic neuron. Several drugs act at this step of neurotransmission. For example, some drugs that are given to Alzheimer’s patients work by inhibiting acetycholinesterase, the enzyme that degrades acetycholine. This inhibition of ‘the enzyme essentially increases neurotransmission at synapses tha release acetylcholine. Once released, the acetylcholine staysin the cleft and can continually bind and unbind to postsynaptic receptors Neurotransmitter Punetion and Location Neurotransmitter Example Locati Acetylcholine - CNS andlor PNS Biogenicamine | Dopamine, serotonin, norepinephrine ‘CNS andlor PNS ‘Amino acid Glycine, glutamate, aspartare, gamma aminobueyric acid CNS Neuropeptide Substance , endorphins NS andjor PNS Tableas.2 Electrical Synapse ‘While electrical synapses are fewer in number than chemical synapses they are found inall nervous systems and play important and unique roles. The mode of neurocransmission in electrical synapses is quite different fom that in chemical synapses. Inan lectricl synapse, the presynaptic and postsynaptic membranes are very close together and are actually physically connected by ‘channel proteins forming gap junctions. Gap junctions allow curent to pass directly from one cell to the next. In addition tothe ions that carry this cuzrent, other molecules, such as ATP, can diffuse through the large gap junction pores. ‘There are key differences between chemical and electrical synapses. Because chemical synapses depend onthe release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there i an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally this signaling is unidirectional. Signaling in electrical synapses, in contrast, is virtually instantaneous (which is important for synapses involved in key reflexes), and some electrical synapses ate bidirectional Electrical synapses are alsa mote reliable as they are less likely tobe blocked, and they are important for synchronizing the electrical activity ofa group of neurons. For example, electrical synapses in the thalamus are thought to regulate slow-wave sleep, and disruption of these synapses ean cause seizures, Signal Summation Sometimes a single EPSP is strong enough a induce an action potential in the postsynaptic neuron, but often multiple presynaptic inputs must create EPSPs around the se time for the postsynaptic newron to be sufficiently depolarized to fie an action potential. This process scaled summation and occurs atthe axon hillock, as illustrated in Figure 25.26, Additionally, one neuron often has inpucs from many presynaptic neurons—some excitatory and some inhibitory—so IPSPs can cancel out EPSPS and vice versa, It sche net change in postsynaptic membrane voltage that determines whether the postsynaptic cll bas reached its threshold of excitation needed to fire an action potential, Together, synaptic summation and the threshold for excitation act 2 filter so that random “noise” in the system isnot transmitted as important information. 25 for foe at openstox.rg ‘Axon hillock ‘Summation of membrane potentials at the axon hillock EPSPs Threshold of activation —IPsPs & 6 Membrane potential (mV) 4 3 oo Time Figure 35.16 A single neuron can ceive bath exeitaory and inhibitory inputs rom multile neurons, resulting is leeal membrane opoarization (EPSP input) and hyp ‘rong enough te overcome the IPSPs and reach the threshold of axcitation, the neuron wl Fir. olrization (IPSP in) Al hese inputs are added together atthe axon hillock. Ifthe EPSPs are Everyday Connection Brain-computer interface Amyotrophic lateral sclerosis (ALS, also called Low Gebiigs Disease) isa neurological disease characterized by the degeneration ofthe motor neurons that control voluntary movements. Te disease begins with muscle weakening and Ick of coordination and eventually destroys the neurons that control speech, breathing, and swallowing; in the end, the disease can lead to paralysis. At that point, patients require assistance from machines to be able to breathe and to communicate ‘Several special technologies have been developed to allow “locked-in patients to communicate with the rest ofthe world. One technology for example, allows patients to ype out sentences by twitching their check. These sentences can then be read aloud by a computer. ‘Arelatively new line of research for helping paralyzed patients, including those with ALS, to communicate and retain a degree of self-sufficiency is called brain-computer interface (BCD technology and is illustrated in Figure 35.17. This technology sounds like something out of science fiction: it allows paralyzed patients to control a computer using only their thoughts. There are everal forms of BC. Some forms use FEG recordings from electrodes taped onta the skull. These recordings contain information from large populations of neurons that can be decoded by a computer. Other forms of BCL require the implantation ofan aray of electrodes smaller than a postage stamp in the arm and hand azea of the motor cortex. This form of BCI, while more invasive, is very powerful a each electrode can record actual action potentials from one ‘or more neurons. These signals are then sent toa computer, which has been trained to decode the signal an feed it toa tool-such as a cursor on a computer sereen, this means that a patient with ALS can use e-mail, read the Internet, and communicate with others by thinking of moving his or her hand or arm (eventhough the paralyzed patient cannot make that bodily movement) Recent advances have allowed a paralyzed locked-in patient who suffered a stroke 15 years ago to control robotic arm and even to feed herself coffee using BCI technology. Despite the amazing advancements in BC! technology, italso has limitations. The technology can require many hours of «raining and long periods of intense concentration for the patient it an aso require brain surgery to implant the devices. Neural signals ave to computer Figure 35.17 with brin-computer interface technology nera signals from a paralyzed patent ae collected, decoded, and then fed toa tool, such as a computer a wheelchair, or 8 robotic arm. @ LINK TO LEARNING ‘Watch this vdeo (hep, openstax.org/l/paralyzation) in which a paralyzed woman uses a brain-controlled robotic arm to bring a drink to her mouth, among other images of brain-computer interface technology inaction. Click to view content (https: /ynvwopenstsx.0r aralyzation) Synaptic Plasticity Synapses are not state structures. Tey can be weakened or scrngthened They cn be broken, and new synapses canbe made Symapic plasty aliowe for hese changes, which areal neded for functioning nervous sytem. n fc, synaptic plastic is the basi oflerning and memory. Two processes in particular, lng-term potentiation (LTP) and long-term depression (TD) are important forms of synaptic plasticity that occur in synapses in the hippocampus, 2 brain region that is involved in storing Long-term Potentiation (LTP) long-term potentiation (LTP) is persistent strengthening ofa synaptic connection. LTP is based on the Hebbian principle: cells that fire together wire together. there are various mechanisms, none fly understood, bind the synaptic strengthening seen with LTP. One known mechanise involves a typeof postsynaptic glutamate receptor called NMDA (N-Methyl-D-aspartate) receptors, shown in Figure 3.8, These receptors are normally blocked by magnesium ions; however, when the postsynaptic neuron is depolarized by muliple presynaptic inputs in quick succession (either ftom one neuron or multiple neuron), the magnesium ions are forced out allowing Ca ions to pass into the postsynaptic cell. Next, Ca" ions entering the cll ntiatea signaling cascade that causes a diferent type of glutamate receptor, called AMPA (a- amino-s-hydroxg-s-methl-s-isoxazolepropionic acid) receptors tobe inserted into the postsynaptic membrane, since activated AMPA receptors allow positive ions to enter the cll So, the next time glutamate is released from the presynaptic ‘membrane it wil have larger excitatory effect (EPSP) onthe postsynaptic cell eeause the binding of glutamate to these AMPA receptors wil allow more positive fons int the cell. The insertion of additional AMPA receptors strengthens the synapse and sean that the postsynaptic neuron is mor likely to fire in response to presynaptic neurotransmitter release. Some drugs of abuse co-opt the IP pathway, and this synaptic strengthening can lead to addition. ‘Access for free at openstax.ora, Long-term Depression (LTD) ‘Long-term depression (LID) is essentially the reverse of UTP: itis long-term weakening ofa synaptic connection. One ‘mechanism known to cause LTD also involves AMPA receptors. In tis situation, calcium that enters through NMDA receptors initiates a different signaling cascade, which resus in the removal of AMPA receptors fom the postsynaptic membrane, 38 illustrated in Figure 35.18. the deeease in AMPA receptors in the membrane makes the postsynaptic neuron less responsive 10 glutamate released from the presynaptic neuron, While it may seem counterintuitive, LED may be ust as important for learning and memory a LTP The weakening and praning of unused synapses allows for unimportant connections tobe lost and makes ‘the synapses that have undergone LP that much stronger by compar \, Presnap on requeny simulation resutsin adteert Ca 'Sejming cascade, AMA ‘ecoptor ls emoved om ‘ne monbrane, sod as becomos te responsive ‘oguamate Sore AVPA recep ae ipesentin he membrane inreate tact’ C22 “Te NMDA receptors actvated oy gutarate ‘anna but ony ater serait ores Ineoy Mig Once Nig removed Ca can berth cet ‘Figure 35.18 Calcium entry though postsynaptic NMDA receptors can inate two diferent forms of synaptic plastic: on potentiation (UTP an long-term depression (LT), LTP arises whan a single synapse is repeatedly stimatod. Ths stimula

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