Learning Objectives<\/h2>\n<\/header>\n\n\nBy the end of this section, you will be able to:\n\n \t- Appreciate some of the history associated with studying the brain<\/li>\n \t
- Be aware of the basic parts of a neuron and familiarise yourself with the vocabulary of the nervous system<\/li>\n \t
- Consider how neurons communicate with each other<\/li>\n \t
- Recognise how drugs act as agonists or antagonists for a given neurotransmitter system<\/li>\n<\/ul>\n<\/div>\n<\/div>\n
The History of Studying Brains is Old!<\/h1>\nPresent day psychologists and neuroscientists interested in the workings of the brain have access to advanced technology (covered in-depth later in this chapter) to attempt to answer questions about the brain\u2019s workings. But, their efforts did not reach this modern state without guidance from scientists before them. Less credit is given to some of the earlier neuroanatomists (those who study the anatomy of the nervous system) like Hasan Ibn al-Haytham, also known as Alhazen (born 965). A Persian scientist, al-Haytham is credited with what is possibly the world\u2019s first known illustration of the nervous system.\n\n \n\n[caption id=\"attachment_92\" align=\"aligncenter\" width=\"350\"]![\"An](\"https:\/\/opentextbc.ca\/psychologymtdi\/wp-content\/uploads\/sites\/470\/2024\/02\/Alhazen1652.png\")
Figure BB.1. <\/strong>Illustration of the early visual system by Hasan Ibn al-Haytham\u2019s \u201cKitab al-Manazir\u201d<\/strong>.<\/em>\u00a0This image comes from an 11th century copy of al-Haytham\u2019s manuscript held in the S\u00fcleymaniye Library in Istanbul, Turkey (MS Fatih 3212, vol. 1, fol. 81b, S\u00fcleymaniye Mosque Library, Istanbul). The structure of the human eye according to al-Haytham. Eyeballs are depicted connecting via presumed optic nerves to another system (presumably the brain as part of the nervous system).[\/caption]\n\nInterested in vision, al-Haytham argued against hundreds of years of theories by Euclid and Ptolemy, renowned Greek and Alexandrian scholars respectively, that suggested vision was due to our eyes emitting light (Lindberg, 1967). By theorising that vision requires light to actually enter our eyes, al-Haytham got closer to what modern scientists have confirmed.\n\nThe illustration of the beginnings of the visual system credited to al-Haytham depicts broadly the components of the eye (which you will become familiar with later in this chapter) but also the eye\u2019s physical connection with something behind it\u2026 the processing of the brain! In fact, you will learn that the light-sensitive tissue at the back of the eye, the retina, is just an outgrowth from our brain that extends during early development. This image and the writing of al-Haytham are the only historical evidence, an indication that curiosity about the brain is much older than the invention of the microscope.\nModern Understanding of the Human Brain<\/h1>\nPsychologists striving to understand the human mind may study the nervous system. Learning how the body\u2019s cells and organs function can help us understand the biological basis of human psychology. The nervous system is composed of two basic cell types: [pb_glossary id=\"643\"]glia[\/pb_glossary] and neurons. Glia (a single one is a glial cell) are traditionally thought to play a supportive role to neurons, both physically and metabolically (i.e., supplying nutrients and maintaining their function). Glia provide scaffolding on which the nervous system is built, help neurons line up closely with each other to allow neuronal communication, provide insulation to neurons, transport nutrients and waste products, and mediate immune responses.\n\nFor years, researchers believed that there were many more glia than neurons; however, more recent work from Suzanna Herculano-Houzel\u2019s laboratory has called this long-standing assumption into question and has provided important evidence that there may be a nearly 1:1 ratio of glia to neurons. This is important because it suggests that human brains are more similar to other primate brains than previously thought (Azevedo et al, 2009; Hercaulano-Houzel, 2012; Herculano-Houzel, 2009). [pb_glossary id=\"645\"]Neurons[\/pb_glossary], on the other hand, serve as interconnected information processors that are essential for all of the tasks of the nervous system. This means that these cells can act as different parts of a machine (the entire nervous system) to carry out a function (like moving your leg, or retrieving a memory). This section briefly describes the structure and function of neurons.\nNeuron Structure<\/h1>\nNeurons are the central building blocks of the nervous system, 100 billion strong at birth. Like all cells, neurons consist of several different parts, each serving a specialised function (Figure BB.2). A neuron\u2019s outer surface is made up of a [pb_glossary id=\"647\"]semipermeable membrane[\/pb_glossary]. The semipermeable nature of the membrane allows smaller molecules and molecules without an electrical charge to pass through it, while stopping larger or highly charged molecules.\n\n[caption id=\"attachment_92\" align=\"aligncenter\" width=\"2560\"]![\"A](\"https:\/\/opentextbc.ca\/psychologymtdi\/wp-content\/uploads\/sites\/470\/2024\/08\/neuron-structure-image-scaled-1.jpg\" "\\"A")
Figure BB.2. Prototypical neuron.<\/strong> This illustration shows a prototypical neuron, which is being myelinated by glia. (credit: Molly Wells Art<\/a>)[\/caption]\n\nThe nucleus of the neuron is located in the [pb_glossary id=\"649\"]soma[\/pb_glossary], or cell body. The soma has branching extensions known as [pb_glossary id=\"651\"]dendrites[\/pb_glossary]. The neuron is a small information processor, and dendrites serve as input sites where signals are received from other neurons. These signals are transmitted electrically across the soma and down a major extension from the soma known as the [pb_glossary id=\"653\"]axon[\/pb_glossary], which ends at multiple [pb_glossary id=\"655\"]terminal buttons[\/pb_glossary] (also commonly referred to as boutons\u2013the French word for buttons). The terminal buttons contain [pb_glossary id=\"657\"]synaptic vesicles[\/pb_glossary] that house [pb_glossary id=\"659\"]neurotransmitters[\/pb_glossary], the chemical messengers of the nervous system.\n\nAxons range in length from a fraction of an inch to several feet. In some axons, glia form a fatty substance known as the [pb_glossary id=\"661\"]myelin sheath[\/pb_glossary], which coats the axon and acts as an insulator, increasing the speed at which the signal travels. The myelin sheath is not continuous and there are small gaps that occur down the length of the axon. These gaps in the myelin sheath are known as the [pb_glossary id=\"663\"]Nodes of Ranvier[\/pb_glossary]. The myelin sheath is crucial for the normal operation of the neurons within the nervous system; the loss of the insulation it provides can be detrimental to normal function.\n\nTo understand how this works, let\u2019s consider an example. Phenylketonuria (fen-ul-key-toe-NU-ree-uh), also called PKU, causes a reduction in myelin and abnormalities in white matter cortical and subcortical structures (regions of the brain below the surface). This disorder is associated with a variety of issues including severe cognitive deficits (i.e., difficulties with everyday functioning or learning), exaggerated reflexes, and seizures (Anderson & Leuzzi, 2010; Huttenlocher, 2000). Another disorder, multiple sclerosis (MS), an autoimmune disorder, involves a large-scale loss of the myelin sheath on axons throughout the nervous system. The resulting interference in the electrical signal prevents the quick transmission of information by neurons and can lead to a number of symptoms, such as dizziness, fatigue, loss of motor control, and sexual dysfunction. While some treatments may help to modify the course of the disease and manage certain symptoms, there is currently no known cure for multiple sclerosis.\n\nWatch this video: Tricky Topics: Neuronal Structure (17.5 minutes)<\/a>\n\nhttps:\/\/youtu.be\/zpWZ5PgZFF0\n\n\u201cTricky Topics: Neuronal Structure\u201d video by FirstYearPsych Dalhousie is licensed under the Standard YouTube licence.\n\nHere is the Tricky Topics: Neuronal Structure transcript<\/a>.\n\nIn typically functioning nervous systems, the neuronal signal moves rapidly down the axon to the terminal buttons, where synaptic vesicles release neurotransmitters into the [pb_glossary id=\"665\"]synaptic cleft[\/pb_glossary] (Figure BB.3). The synaptic cleft is a very small space between two neurons and is an important site where communication between neurons occurs. Once neurotransmitters are released into the synaptic cleft, they travel across it and bind with corresponding receptors on the dendrite of an adjacent neuron. [pb_glossary id=\"667\"]Receptors[\/pb_glossary], proteins on the cell surface where neurotransmitters attach, vary in shape, with different shapes matching different neurotransmitters.\n\nHow does a neurotransmitter know which receptor to bind to? The neurotransmitter and the receptor have what is referred to as a lock-and-key relationship \u2014 specific neurotransmitters fit specific receptors similar to how a key fits a lock. The neurotransmitter binds to any receptor that it fits.\n\n![\"Image](\"https:\/\/opentextbc.ca\/psychologymtdi\/wp-content\/uploads\/sites\/470\/2024\/08\/Figure-BB.3-Synaptic-Space-Between-Two-Neurons-Micrograph-of-Spherical-Terminal-Button.jpeg\")
\n\nFigure BB.3. Neurotransmitter.<\/strong> The synaptic cleft is the space between the terminal button of one neuron and the dendrite of another neuron. (b) In this pseudo-coloured image from a scanning electron microscope, a terminal button (green) has been opened to reveal the synaptic vesicles (orange and blue) inside. Each vesicle contains about 10,000 neurotransmitter molecules.Watch this video: Tricky Topics: Synaptic Transmission (9 minutes)<\/a>\n\nhttps:\/\/youtu.be\/M7OMTco-qV4\n\n\u201cTricky Topics: Synaptic Transmission\u201d video by FirstYearPsych Dalhousie is licensed under the Standard YouTube licence.\n\nHere is the Tricky Topics: Synaptic Transmission transcript<\/a>.\nNeuronal Communication<\/h1>\nNow that we have learned about the basic structures of the neuron and the role that these structures play in neuronal communication, let\u2019s take a closer look at the signal itself \u2014 how it moves through the neuron and then jumps to the next neuron, where the process is repeated.\n\nWe start our journey at the neuronal membrane. The neuron exists in a fluid environment; it is surrounded by fluid outside the cell, called extracellular fluid, and contains fluid inside the cell, known as intracellular fluid or cytoplasm. The neuronal membrane acts as a barrier, keeping these two fluids separate. This role is crucial because the electrical signal passing through the neuron relies on the electrical difference between the intra- and extracellular fluids. This charge difference, called the [pb_glossary id=\"669\"]membrane potential[\/pb_glossary], supplies the energy for the signal.\n\nThe electrical charge of the fluids is caused by charged molecules (ions) dissolved in the fluid. The semipermeable nature of the neuronal membrane somewhat restricts the movement of these charged molecules, and, as a result, some of the charged particles tend to become more concentrated either inside or outside the cell.\n\nBetween signals, the neuron membrane\u2019s potential is held in a state of readiness, called the [pb_glossary id=\"671\"]resting potential[\/pb_glossary]. The typical resting potential of a neuron is -70 millivolts (mV). Like a rubber band stretched out and waiting to spring into action, ions line up on either side of the cell membrane, ready to rush across the membrane when the neuron goes active and the membrane opens its gates (i.e., a sodium-potassium pump that allows movement of ions across the membrane). Ions in high-concentration areas are ready to move to low-concentration areas in a process called osmosis (you may have come across the term before), and positive ions are ready to move to areas with a negative charge. This is a fundamental process, where negatively charged particles are attracted to positive charges, just like the interaction of two magnets.\n\nIn the resting state, sodium (Na+) is at higher concentrations outside the cell, so it will tend to move into the cell. Potassium (K+), on the other hand, is more concentrated inside the cell, and will tend to move out of the cell (Figure BB.4). In addition, the inside of the cell is slightly negatively charged compared to the outside. This difference in charge, known as the electrochemical gradient, acts on sodium, causing it to move into the cell.\n\n \n\n[caption id=\"attachment_92\" align=\"aligncenter\" width=\"975\"]![\"A](\"https:\/\/opentextbc.ca\/psychologymtdi\/wp-content\/uploads\/sites\/470\/2024\/08\/Figure-BB.4-Difference-in-CHarges-across-the-Cell-Membrane-NA-K-CI-.jpeg\" "\\"A")
Figure BB.4. Electrochemical gradient.<\/strong> At resting potential, Na+ (blue pentagons) is more highly concentrated outside the cell in the extracellular fluid (shown in blue), whereas K+ (purple squares) is more highly concentrated near the membrane in the cytoplasm or intracellular fluid. Other molecules, such as chloride ions (yellow circles) and negatively charged proteins (brown squares), help contribute to a positive net charge in the extracellular fluid and a negative net charge in the intracellular fluid.[\/caption]\n\nFrom this resting potential state, the neuron receives a signal and its state changes abruptly (Figure BB.5). When a neuron receives signals at the dendrites \u2014 due to neurotransmitters from an adjacent neuron binding to its receptors \u2014 small pores, or gates, open on the neuronal membrane, allowing Na+ ions, propelled by both charge and concentration differences, to move into the cell. With this influx of positive ions, the internal charge of the cell becomes more positive. If that charge reaches a certain level, called the [pb_glossary id=\"673\"]threshold of excitation[\/pb_glossary], the neuron becomes active and the [pb_glossary id=\"637\"]action potential[\/pb_glossary] begins.\n\nSeveral additional pores open, leading to a massive influx of positively charged sodium ions creating a significant spike in the membrane potential, the peak of the action potential. At this peak, the sodium gates close, and the potassium gates open. Positively charged potassium ions start to exit the cell rapidly, initiating the process of repolarization. Initially, the cell becomes more negative than its resting potential, known as hyperpolarization, and then it stabilises, returning to its resting potential.\n\n\u00a0<\/em>\n\n[caption id=\"attachment_92\" align=\"aligncenter\" width=\"487\"]![\"A](\"https:\/\/opentextbc.ca\/psychologymtdi\/wp-content\/uploads\/sites\/470\/2024\/08\/Figure-BB.5-Membrane-Potential-Graph.jpeg\" "\\"A")
Figure BB.5. Membrane potential graph.<\/strong> During the action potential, the electrical charge across the membrane changes dramatically.[\/caption]\n\nThis positive spike represents the action potential: the electrical signal that typically moves from the cell body down the axon to the axon terminals. The electrical signal moves down the axon with the impulses jumping in a leapfrog fashion between the Nodes of Ranvier. The Nodes of Ranvier are natural gaps in the myelin sheath. At each point, some of the sodium ions that enter the cell diffuse to the next section of the axon, raising the charge past the threshold of excitation and triggering a new influx of sodium ions. The action potential moves all the way down the axon in this way until reaching the terminal buttons.\n\nThe action potential is an [pb_glossary id=\"675\"]all-or-none[\/pb_glossary] phenomenon. In simple terms, this means that an incoming signal from another neuron is either sufficient or insufficient to reach the threshold of excitation. There is no in-between, and there is no turning off an action potential once it starts. Think of it like sending an email or a text message. You can think about sending it all you want, but the message is not sent until you hit the send button. Furthermore, once you send the message, there is no stopping it.\n\nSince it's an all-or-none response, the action potential is reproduced, or propagated, at its full strength along every point of the axon. Imagine it like a lit fuse on a firecracker \u2014 it doesn't lose intensity as it travels down the axon. This all-or-none property explains why your brain perceives an injury to a distant body part, such as your toe, as equally painful as one to your nose (which is closer to your brain).\n\nAs noted earlier, when the action potential arrives at the terminal button, the synaptic vesicles release their neurotransmitters into the synaptic cleft. The neurotransmitters travel across the synapse and bind to receptors on the dendrites of the adjacent neuron, and the process repeats itself in the new neuron (assuming the signal is sufficiently strong to trigger an action potential). Once the signal is delivered, excess neurotransmitters in the synaptic cleft drift away, break down into inactive fragments (degradation), or are reabsorbed in a process known as reuptake.\n\n[pb_glossary id=\"677\"]Reuptake[\/pb_glossary] involves the neurotransmitter being pumped back into the neuron that released it, in order to clear the synapse (Figure BB.6). Clearing the synapse serves both to provide a clear \u201con\u201d and \u201coff\u201d state between signals and to regulate the production of neurotransmitter (full synaptic vesicles signal that no additional neurotransmitters need to be produced). The synapse can also be cleared via [pb_glossary id=\"679\"]degradation[\/pb_glossary] of the neurotransmitter, which typically involves an enzyme breaking the neurotransmitter down into its components, so that it can no longer interact with the receptors on the postsynaptic neuron.\n\n[caption id=\"attachment_92\" align=\"aligncenter\" width=\"649\"]![\"The](\"https:\/\/opentextbc.ca\/psychologymtdi\/wp-content\/uploads\/sites\/470\/2024\/08\/Figure-BB.6-Reuptake-Graph.jpeg\" "\\"The")
Figure BB.6. Reuptake.<\/strong> Reuptake involves moving a neurotransmitter from the synapse back into the axon terminal from which it was released.[\/caption]\n\nNeuronal communication is often referred to as an electrochemical event. The movement of the action potential down the length of the axon is an electrical event, and movement of the neurotransmitter across the synaptic space represents the chemical portion of the process. However, there are some specialised connections between neurons that are entirely electrical. In such cases, the neurons are said to communicate via an electrical synapse. In these cases, two neurons physically connect to one another via gap junctions that allow the current from one cell to pass into the next. There are far fewer electrical synapses in the brain, but those that do exist are much faster than the chemical synapses that have been described above (Connors & Long, 2004).\n\nWatch this video: Tricky Topics: Action Potentials (18 minutes)<\/a>\n\nhttps:\/\/youtu.be\/vWSmSIQbO0Q\n\n\u201cTricky Topics: Action Potentials\u201d video by FirstYearPsych Dalhousie is licensed under the Standard YouTube licence.\n\nHere is the Tricky Topics: Action Potentials transcript<\/a>.\nNeurotransmitters and Drugs<\/h1>\nThere are several different types of neurotransmitters released by different neurons, and we can speak in broad terms about the kinds of functions associated with different neurotransmitters (Table BB.1). Much of what psychologists know about the functions of neurotransmitters comes from research on the effects of drugs in psychological disorders. Psychologists who take a [pb_glossary id=\"681\"]biological perspective[\/pb_glossary] and focus on the physiological causes of behaviour assert that psychological disorders like depression and schizophrenia are associated with imbalances in one or more neurotransmitter systems. From this perspective, psychotropic medications can help improve the symptoms associated with these disorders. [pb_glossary id=\"683\"]Psychotropic medications[\/pb_glossary] are drugs that treat psychiatric symptoms by restoring neurotransmitter balance.\n
- \n \t
- Appreciate some of the history associated with studying the brain<\/li>\n \t
- Be aware of the basic parts of a neuron and familiarise yourself with the vocabulary of the nervous system<\/li>\n \t
- Consider how neurons communicate with each other<\/li>\n \t
- Recognise how drugs act as agonists or antagonists for a given neurotransmitter system<\/li>\n<\/ul>\n<\/div>\n<\/div>\n
The History of Studying Brains is Old!<\/h1>\nPresent day psychologists and neuroscientists interested in the workings of the brain have access to advanced technology (covered in-depth later in this chapter) to attempt to answer questions about the brain\u2019s workings. But, their efforts did not reach this modern state without guidance from scientists before them. Less credit is given to some of the earlier neuroanatomists (those who study the anatomy of the nervous system) like Hasan Ibn al-Haytham, also known as Alhazen (born 965). A Persian scientist, al-Haytham is credited with what is possibly the world\u2019s first known illustration of the nervous system.\n\n \n\n[caption id=\"attachment_92\" align=\"aligncenter\" width=\"350\"]
Figure BB.1. <\/strong>Illustration of the early visual system by Hasan Ibn al-Haytham\u2019s \u201cKitab al-Manazir\u201d<\/strong>.<\/em>\u00a0This image comes from an 11th century copy of al-Haytham\u2019s manuscript held in the S\u00fcleymaniye Library in Istanbul, Turkey (MS Fatih 3212, vol. 1, fol. 81b, S\u00fcleymaniye Mosque Library, Istanbul). The structure of the human eye according to al-Haytham. Eyeballs are depicted connecting via presumed optic nerves to another system (presumably the brain as part of the nervous system).[\/caption]\n\nInterested in vision, al-Haytham argued against hundreds of years of theories by Euclid and Ptolemy, renowned Greek and Alexandrian scholars respectively, that suggested vision was due to our eyes emitting light (Lindberg, 1967). By theorising that vision requires light to actually enter our eyes, al-Haytham got closer to what modern scientists have confirmed.\n\nThe illustration of the beginnings of the visual system credited to al-Haytham depicts broadly the components of the eye (which you will become familiar with later in this chapter) but also the eye\u2019s physical connection with something behind it\u2026 the processing of the brain! In fact, you will learn that the light-sensitive tissue at the back of the eye, the retina, is just an outgrowth from our brain that extends during early development. This image and the writing of al-Haytham are the only historical evidence, an indication that curiosity about the brain is much older than the invention of the microscope.\nModern Understanding of the Human Brain<\/h1>\nPsychologists striving to understand the human mind may study the nervous system. Learning how the body\u2019s cells and organs function can help us understand the biological basis of human psychology. The nervous system is composed of two basic cell types: [pb_glossary id=\"643\"]glia[\/pb_glossary] and neurons. Glia (a single one is a glial cell) are traditionally thought to play a supportive role to neurons, both physically and metabolically (i.e., supplying nutrients and maintaining their function). Glia provide scaffolding on which the nervous system is built, help neurons line up closely with each other to allow neuronal communication, provide insulation to neurons, transport nutrients and waste products, and mediate immune responses.\n\nFor years, researchers believed that there were many more glia than neurons; however, more recent work from Suzanna Herculano-Houzel\u2019s laboratory has called this long-standing assumption into question and has provided important evidence that there may be a nearly 1:1 ratio of glia to neurons. This is important because it suggests that human brains are more similar to other primate brains than previously thought (Azevedo et al, 2009; Hercaulano-Houzel, 2012; Herculano-Houzel, 2009). [pb_glossary id=\"645\"]Neurons[\/pb_glossary], on the other hand, serve as interconnected information processors that are essential for all of the tasks of the nervous system. This means that these cells can act as different parts of a machine (the entire nervous system) to carry out a function (like moving your leg, or retrieving a memory). This section briefly describes the structure and function of neurons.\n
Neuron Structure<\/h1>\nNeurons are the central building blocks of the nervous system, 100 billion strong at birth. Like all cells, neurons consist of several different parts, each serving a specialised function (Figure BB.2). A neuron\u2019s outer surface is made up of a [pb_glossary id=\"647\"]semipermeable membrane[\/pb_glossary]. The semipermeable nature of the membrane allows smaller molecules and molecules without an electrical charge to pass through it, while stopping larger or highly charged molecules.\n\n[caption id=\"attachment_92\" align=\"aligncenter\" width=\"2560\"]
Figure BB.2. Prototypical neuron.<\/strong> This illustration shows a prototypical neuron, which is being myelinated by glia. (credit: Molly Wells Art<\/a>)[\/caption]\n\nThe nucleus of the neuron is located in the [pb_glossary id=\"649\"]soma[\/pb_glossary], or cell body. The soma has branching extensions known as [pb_glossary id=\"651\"]dendrites[\/pb_glossary]. The neuron is a small information processor, and dendrites serve as input sites where signals are received from other neurons. These signals are transmitted electrically across the soma and down a major extension from the soma known as the [pb_glossary id=\"653\"]axon[\/pb_glossary], which ends at multiple [pb_glossary id=\"655\"]terminal buttons[\/pb_glossary] (also commonly referred to as boutons\u2013the French word for buttons). The terminal buttons contain [pb_glossary id=\"657\"]synaptic vesicles[\/pb_glossary] that house [pb_glossary id=\"659\"]neurotransmitters[\/pb_glossary], the chemical messengers of the nervous system.\n\nAxons range in length from a fraction of an inch to several feet. In some axons, glia form a fatty substance known as the [pb_glossary id=\"661\"]myelin sheath[\/pb_glossary], which coats the axon and acts as an insulator, increasing the speed at which the signal travels. The myelin sheath is not continuous and there are small gaps that occur down the length of the axon. These gaps in the myelin sheath are known as the [pb_glossary id=\"663\"]Nodes of Ranvier[\/pb_glossary]. The myelin sheath is crucial for the normal operation of the neurons within the nervous system; the loss of the insulation it provides can be detrimental to normal function.\n\nTo understand how this works, let\u2019s consider an example. Phenylketonuria (fen-ul-key-toe-NU-ree-uh), also called PKU, causes a reduction in myelin and abnormalities in white matter cortical and subcortical structures (regions of the brain below the surface). This disorder is associated with a variety of issues including severe cognitive deficits (i.e., difficulties with everyday functioning or learning), exaggerated reflexes, and seizures (Anderson & Leuzzi, 2010; Huttenlocher, 2000). Another disorder, multiple sclerosis (MS), an autoimmune disorder, involves a large-scale loss of the myelin sheath on axons throughout the nervous system. The resulting interference in the electrical signal prevents the quick transmission of information by neurons and can lead to a number of symptoms, such as dizziness, fatigue, loss of motor control, and sexual dysfunction. While some treatments may help to modify the course of the disease and manage certain symptoms, there is currently no known cure for multiple sclerosis.\n\nWatch this video: Tricky Topics: Neuronal Structure (17.5 minutes)<\/a>\n\nhttps:\/\/youtu.be\/zpWZ5PgZFF0\n\n\u201cTricky Topics: Neuronal Structure\u201d video by FirstYearPsych Dalhousie is licensed under the Standard YouTube licence.\n\nHere is the Tricky Topics: Neuronal Structure transcript<\/a>.\n\nIn typically functioning nervous systems, the neuronal signal moves rapidly down the axon to the terminal buttons, where synaptic vesicles release neurotransmitters into the [pb_glossary id=\"665\"]synaptic cleft[\/pb_glossary] (Figure BB.3). The synaptic cleft is a very small space between two neurons and is an important site where communication between neurons occurs. Once neurotransmitters are released into the synaptic cleft, they travel across it and bind with corresponding receptors on the dendrite of an adjacent neuron. [pb_glossary id=\"667\"]Receptors[\/pb_glossary], proteins on the cell surface where neurotransmitters attach, vary in shape, with different shapes matching different neurotransmitters.\n\nHow does a neurotransmitter know which receptor to bind to? The neurotransmitter and the receptor have what is referred to as a lock-and-key relationship \u2014 specific neurotransmitters fit specific receptors similar to how a key fits a lock. The neurotransmitter binds to any receptor that it fits.\n\n\n\nFigure BB.3. Neurotransmitter.<\/strong> The synaptic cleft is the space between the terminal button of one neuron and the dendrite of another neuron. (b) In this pseudo-coloured image from a scanning electron microscope, a terminal button (green) has been opened to reveal the synaptic vesicles (orange and blue) inside. Each vesicle contains about 10,000 neurotransmitter molecules.Watch this video: Tricky Topics: Synaptic Transmission (9 minutes)<\/a>\n\nhttps:\/\/youtu.be\/M7OMTco-qV4\n\n\u201cTricky Topics: Synaptic Transmission\u201d video by FirstYearPsych Dalhousie is licensed under the Standard YouTube licence.\n\nHere is the Tricky Topics: Synaptic Transmission transcript<\/a>.\nNeuronal Communication<\/h1>\nNow that we have learned about the basic structures of the neuron and the role that these structures play in neuronal communication, let\u2019s take a closer look at the signal itself \u2014 how it moves through the neuron and then jumps to the next neuron, where the process is repeated.\n\nWe start our journey at the neuronal membrane. The neuron exists in a fluid environment; it is surrounded by fluid outside the cell, called extracellular fluid, and contains fluid inside the cell, known as intracellular fluid or cytoplasm. The neuronal membrane acts as a barrier, keeping these two fluids separate. This role is crucial because the electrical signal passing through the neuron relies on the electrical difference between the intra- and extracellular fluids. This charge difference, called the [pb_glossary id=\"669\"]membrane potential[\/pb_glossary], supplies the energy for the signal.\n\nThe electrical charge of the fluids is caused by charged molecules (ions) dissolved in the fluid. The semipermeable nature of the neuronal membrane somewhat restricts the movement of these charged molecules, and, as a result, some of the charged particles tend to become more concentrated either inside or outside the cell.\n\nBetween signals, the neuron membrane\u2019s potential is held in a state of readiness, called the [pb_glossary id=\"671\"]resting potential[\/pb_glossary]. The typical resting potential of a neuron is -70 millivolts (mV). Like a rubber band stretched out and waiting to spring into action, ions line up on either side of the cell membrane, ready to rush across the membrane when the neuron goes active and the membrane opens its gates (i.e., a sodium-potassium pump that allows movement of ions across the membrane). Ions in high-concentration areas are ready to move to low-concentration areas in a process called osmosis (you may have come across the term before), and positive ions are ready to move to areas with a negative charge. This is a fundamental process, where negatively charged particles are attracted to positive charges, just like the interaction of two magnets.\n\nIn the resting state, sodium (Na+) is at higher concentrations outside the cell, so it will tend to move into the cell. Potassium (K+), on the other hand, is more concentrated inside the cell, and will tend to move out of the cell (Figure BB.4). In addition, the inside of the cell is slightly negatively charged compared to the outside. This difference in charge, known as the electrochemical gradient, acts on sodium, causing it to move into the cell.\n\n \n\n[caption id=\"attachment_92\" align=\"aligncenter\" width=\"975\"]
Figure BB.4. Electrochemical gradient.<\/strong> At resting potential, Na+ (blue pentagons) is more highly concentrated outside the cell in the extracellular fluid (shown in blue), whereas K+ (purple squares) is more highly concentrated near the membrane in the cytoplasm or intracellular fluid. Other molecules, such as chloride ions (yellow circles) and negatively charged proteins (brown squares), help contribute to a positive net charge in the extracellular fluid and a negative net charge in the intracellular fluid.[\/caption]\n\nFrom this resting potential state, the neuron receives a signal and its state changes abruptly (Figure BB.5). When a neuron receives signals at the dendrites \u2014 due to neurotransmitters from an adjacent neuron binding to its receptors \u2014 small pores, or gates, open on the neuronal membrane, allowing Na+ ions, propelled by both charge and concentration differences, to move into the cell. With this influx of positive ions, the internal charge of the cell becomes more positive. If that charge reaches a certain level, called the [pb_glossary id=\"673\"]threshold of excitation[\/pb_glossary], the neuron becomes active and the [pb_glossary id=\"637\"]action potential[\/pb_glossary] begins.\n\nSeveral additional pores open, leading to a massive influx of positively charged sodium ions creating a significant spike in the membrane potential, the peak of the action potential. At this peak, the sodium gates close, and the potassium gates open. Positively charged potassium ions start to exit the cell rapidly, initiating the process of repolarization. Initially, the cell becomes more negative than its resting potential, known as hyperpolarization, and then it stabilises, returning to its resting potential.\n\n\u00a0<\/em>\n\n[caption id=\"attachment_92\" align=\"aligncenter\" width=\"487\"] Figure BB.5. Membrane potential graph.<\/strong> During the action potential, the electrical charge across the membrane changes dramatically.[\/caption]\n\nThis positive spike represents the action potential: the electrical signal that typically moves from the cell body down the axon to the axon terminals. The electrical signal moves down the axon with the impulses jumping in a leapfrog fashion between the Nodes of Ranvier. The Nodes of Ranvier are natural gaps in the myelin sheath. At each point, some of the sodium ions that enter the cell diffuse to the next section of the axon, raising the charge past the threshold of excitation and triggering a new influx of sodium ions. The action potential moves all the way down the axon in this way until reaching the terminal buttons.\n\nThe action potential is an [pb_glossary id=\"675\"]all-or-none[\/pb_glossary] phenomenon. In simple terms, this means that an incoming signal from another neuron is either sufficient or insufficient to reach the threshold of excitation. There is no in-between, and there is no turning off an action potential once it starts. Think of it like sending an email or a text message. You can think about sending it all you want, but the message is not sent until you hit the send button. Furthermore, once you send the message, there is no stopping it.\n\nSince it's an all-or-none response, the action potential is reproduced, or propagated, at its full strength along every point of the axon. Imagine it like a lit fuse on a firecracker \u2014 it doesn't lose intensity as it travels down the axon. This all-or-none property explains why your brain perceives an injury to a distant body part, such as your toe, as equally painful as one to your nose (which is closer to your brain).\n\nAs noted earlier, when the action potential arrives at the terminal button, the synaptic vesicles release their neurotransmitters into the synaptic cleft. The neurotransmitters travel across the synapse and bind to receptors on the dendrites of the adjacent neuron, and the process repeats itself in the new neuron (assuming the signal is sufficiently strong to trigger an action potential). Once the signal is delivered, excess neurotransmitters in the synaptic cleft drift away, break down into inactive fragments (degradation), or are reabsorbed in a process known as reuptake.\n\n[pb_glossary id=\"677\"]Reuptake[\/pb_glossary] involves the neurotransmitter being pumped back into the neuron that released it, in order to clear the synapse (Figure BB.6). Clearing the synapse serves both to provide a clear \u201con\u201d and \u201coff\u201d state between signals and to regulate the production of neurotransmitter (full synaptic vesicles signal that no additional neurotransmitters need to be produced). The synapse can also be cleared via [pb_glossary id=\"679\"]degradation[\/pb_glossary] of the neurotransmitter, which typically involves an enzyme breaking the neurotransmitter down into its components, so that it can no longer interact with the receptors on the postsynaptic neuron.\n\n[caption id=\"attachment_92\" align=\"aligncenter\" width=\"649\"] Figure BB.6. Reuptake.<\/strong> Reuptake involves moving a neurotransmitter from the synapse back into the axon terminal from which it was released.[\/caption]\n\nNeuronal communication is often referred to as an electrochemical event. The movement of the action potential down the length of the axon is an electrical event, and movement of the neurotransmitter across the synaptic space represents the chemical portion of the process. However, there are some specialised connections between neurons that are entirely electrical. In such cases, the neurons are said to communicate via an electrical synapse. In these cases, two neurons physically connect to one another via gap junctions that allow the current from one cell to pass into the next. There are far fewer electrical synapses in the brain, but those that do exist are much faster than the chemical synapses that have been described above (Connors & Long, 2004).\n\nWatch this video: Tricky Topics: Action Potentials (18 minutes)<\/a>\n\nhttps:\/\/youtu.be\/vWSmSIQbO0Q\n\n\u201cTricky Topics: Action Potentials\u201d video by FirstYearPsych Dalhousie is licensed under the Standard YouTube licence.\n\nHere is the Tricky Topics: Action Potentials transcript<\/a>.\nNeurotransmitters and Drugs<\/h1>\nThere are several different types of neurotransmitters released by different neurons, and we can speak in broad terms about the kinds of functions associated with different neurotransmitters (Table BB.1). Much of what psychologists know about the functions of neurotransmitters comes from research on the effects of drugs in psychological disorders. Psychologists who take a [pb_glossary id=\"681\"]biological perspective[\/pb_glossary] and focus on the physiological causes of behaviour assert that psychological disorders like depression and schizophrenia are associated with imbalances in one or more neurotransmitter systems. From this perspective, psychotropic medications can help improve the symptoms associated with these disorders. [pb_glossary id=\"683\"]Psychotropic medications[\/pb_glossary] are drugs that treat psychiatric symptoms by restoring neurotransmitter balance.\n