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Anatomy & Physiology 2e: 12.4 Communication Between Neurons

Anatomy & Physiology 2e
12.4 Communication Between Neurons
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table of contents
  1. Cover
  2. Title Page
  3. Copyright
  4. Table Of Contents
  5. Chapter 1. An Introduction to the Human Body
    1. 1.0 Introduction
    2. 1.1 How Structure Determines Function
    3. 1.2 Structural Organization of the Human Body
    4. 1.3 Homeostasis
    5. 1.4 Anatomical Terminology
    6. 1.5 Medical Imaging
  6. Chapter 2. The Chemical Level of Organization
    1. 2.0 Introduction
    2. 2.1 Elements and Atoms: The Building Blocks of Matter
    3. 2.2 Chemical Bonds
    4. 2.3 Chemical Reactions
    5. 2.4 Inorganic Compounds Essential to Human Functioning
    6. 2.5 Organic Compounds Essential to Human Functioning
  7. Chapter 3. The Cellular Level of Organization
    1. 3.0 Introduction
    2. 3.1 The Cell Membrane
    3. 3.2 The Cytoplasm and Cellular Organelles
    4. 3.3 The Nucleus and DNA Replication
    5. 3.4 Protein Synthesis
    6. 3.5 Cell Growth and Division
    7. 3.6 Cellular Differentiation
  8. Chapter 4. The Tissue Level of Organization
    1. 4.0 Introduction
    2. 4.1 Types of Tissues
    3. 4.2 Epithelial Tissue
    4. 4.3 Connective Tissue Supports and Protects
    5. 4.4 Muscle Tissue
    6. 4.5 Nervous Tissue
    7. 4.6 Tissue Injury and Aging
  9. Chapter 5. The Integumentary System
    1. 5.0 Introduction
    2. 5.1 Layers of the Skin
    3. 5.2 Accessory Structures of the Skin
    4. 5.3 Functions of the Integumentary System
    5. 5.4 Diseases, Disorders, and Injuries of the Integumentary System
  10. Chapter 6. Bone Tissue and the Skeletal System
    1. 6.0 Introduction
    2. 6.1 The Functions of the Skeletal System
    3. 6.2 Bone Classification
    4. 6.3 Bone Structure
    5. 6.4 Bone Formation and Development
    6. 6.5 Fractures: Bone Repair
    7. 6.6 Exercise, Nutrition, Hormones, and Bone Tissue
    8. 6.7 Calcium Homeostasis: Interactions of the Skeletal System and Other Organ Systems
  11. Chapter 7. Axial Skeleton
    1. 7.0 Introduction
    2. 7.1 Divisions of the Skeletal System
    3. 7.2 Bone Markings
    4. 7.3 The Skull
    5. 7.4 The Vertebral Column
    6. 7.5 The Thoracic Cage
    7. 7.6 Embryonic Development of the Axial Skeleton
  12. Chapter 8. The Appendicular Skeleton
    1. 8.0 Introduction
    2. 8.1 The Pectoral Girdle
    3. 8.2 Bones of the Upper Limb
    4. 8.3 The Pelvic Girdle and Pelvis
    5. 8.4 Bones of the Lower Limb
    6. 8.5 Development of the Appendicular Skeleton
  13. Chapter 9. Joints
    1. 9.0 Introduction
    2. 9.1 Classification of Joints
    3. 9.2 Fibrous Joints
    4. 9.3 Cartilaginous Joints
    5. 9.4 Synovial Joints
    6. 9.5 Types of Body Movements
    7. 9.6 Anatomy of Selected Synovial Joints
    8. 9.7 Development of Joints
  14. Chapter 10. Muscle Tissue
    1. 10.0 Introduction
    2. 10.1 Overview of Muscle Tissues
    3. 10.2 Skeletal Muscle
    4. 10.3 Muscle Fiber Excitation, Contraction, and Relaxation
    5. 10.4 Nervous System Control of Muscle Tension
    6. 10.5 Types of Muscle Fibers
    7. 10.6 Exercise and Muscle Performance
    8. 10.7 Smooth Muscle Tissue
    9. 10.8 Development and Regeneration of Muscle Tissue
  15. Chapter 11. The Muscular System
    1. 11.0 Introduction
    2. 11.1 Describe the roles of agonists, antagonists and synergists
    3. 11.2 Explain the organization of muscle fascicles and their role in generating force
    4. 11.3 Explain the criteria used to name skeletal muscles
    5. 11.4 Axial Muscles of the Head Neck and Back
    6. 11.5 Axial muscles of the abdominal wall and thorax
    7. 11.6 Muscles of the Pectoral Girdle and Upper Limbs
    8. 11.7 Appendicular Muscles of the Pelvic Girdle and Lower Limbs
  16. Chapter 12. The Nervous System and Nervous Tissue
    1. 12.0 Introduction
    2. 12.1 Structure and Function of the Nervous System
    3. 12.2 Nervous Tissue
    4. 12.3 The Function of Nervous Tissue
    5. 12.4 Communication Between Neurons
    6. 12.5 The Action Potential
  17. Chapter 13. The Peripheral Nervous System
    1. 13.0 Introduction
    2. 13.1 Sensory Receptors
    3. 13.2 Ganglia and Nerves
    4. 13.3 Spinal and Cranial Nerves
    5. 13.4 Relationship of the PNS to the Spinal Cord of the CNS
    6. 13.5 Ventral Horn Output and Reflexes
    7. 13.6 Testing the Spinal Nerves (Sensory and Motor Exams)
    8. 13.7 The Cranial Nerve Exam
  18. Chapter 14. The Central Nervous System
    1. 14.0 Introduction
    2. 14.1 Embryonic Development
    3. 14.2 Blood Flow the meninges and Cerebrospinal Fluid Production and Circulation
    4. 14.3 The Brain and Spinal Cord
    5. 14.4 The Spinal Cord
    6. 14.5 Sensory and Motor Pathways
  19. Chapter 15. The Special Senses
    1. 15.0 Introduction
    2. 15.1 Taste
    3. 15.2 Smell
    4. 15.3 Hearing
    5. 15.4 Equilibrium
    6. 15.5 Vision
  20. Chapter 16. The Autonomic Nervous System
    1. 16.0 Introduction
    2. 16.1 Divisions of the Autonomic Nervous System
    3. 16.2 Autonomic Reflexes and Homeostasis
    4. 16.3 Central Control
    5. 16.4 Drugs that Affect the Autonomic System
  21. Chapter 17. The Endocrine System
    1. 17.0 Introduction
    2. 17.1 An Overview of the Endocrine System
    3. 17.2 Hormones
    4. 17.3 The Pituitary Gland and Hypothalamus
    5. 17.4 The Thyroid Gland
    6. 17.5 The Parathyroid Glands
    7. 17.6 The Adrenal Glands
    8. 17.7 The Pineal Gland
    9. 17.8 Gonadal and Placental Hormones
    10. 17.9 The Pancreas
    11. 17.10 Organs with Secondary Endocrine Functions
    12. 17.11 Development and Aging of the Endocrine System
  22. Chapter 18. The Cardiovascular System: Blood
    1. 18.0 Introduction
    2. 18.1 Functions of Blood
    3. 18.2 Production of the Formed Elements
    4. 18.3 Erythrocytes
    5. 18.4 Leukocytes and Platelets
    6. 18.5 Hemostasis
    7. 18.6 Blood Typing
  23. Chapter 19. The Cardiovascular System: The Heart
    1. 19.0 Introduction
    2. 19.1 Heart Anatomy
    3. 19.2 Cardiac Muscle and Electrical Activity
    4. 19.3 Cardiac Cycle
    5. 19.4 Cardiac Physiology
    6. 19.5 Development of the Heart
  24. Chapter 20. The Cardiovascular System: Blood Vessels and Circulation
    1. 20.0 Introduction
    2. 20.1 Structure and Function of Blood Vessels
    3. 20.2 Blood Flow, Blood Pressure, and Resistance
    4. 20.3 Capillary Exchange
    5. 20.4 Homeostatic Regulation of the Vascular System
    6. 20.5 Circulatory Pathways
    7. 20.6 Development of Blood Vessels and Fetal Circulation
  25. Chapter 21. The Lymphatic and Immune System
    1. 21.0 Introduction
    2. 21.1 Anatomy of the Lymphatic and Immune Systems
    3. 21.2 Barrier Defenses and the Innate Immune Response
    4. 21.3 The Adaptive Immune Response: T lymphocytes and Their Functional Types
    5. 21.4 The Adaptive Immune Response: B-lymphocytes and Antibodies
    6. 21.5 The Immune Response against Pathogens
    7. 21.6 Diseases Associated with Depressed or Overactive Immune Responses
    8. 21.7 Transplantation and Cancer Immunology
  26. Chapter 22. The Respiratory System
    1. 22.0 Introduction
    2. 22.1 Organs and Structures of the Respiratory System
    3. 22.2 The Lungs
    4. 22.3 The Process of Breathing
    5. 22.4 Gas Exchange
    6. 22.5 Transport of Gases
    7. 22.6 Modifications in Respiratory Functions
    8. 22.7 Embryonic Development of the Respiratory System
  27. Chapter 23. The Digestive System
    1. 23.0 Introduction
    2. 23.1 Overview of the Digestive System
    3. 23.2 Digestive System Processes and Regulation
    4. 23.3 The Mouth, Pharynx, and Esophagus
    5. 23.4 The Stomach
    6. 23.5 Accessory Organs in Digestion: The Liver, Pancreas, and Gallbladder
    7. 23.6 The Small and Large Intestines
    8. 23.7 Chemical Digestion and Absorption: A Closer Look
  28. Chapter 24. Metabolism and Nutrition
    1. 24.0 Introduction
    2. 24.1 Overview of Metabolic Reactions
    3. 24.2 Carbohydrate Metabolism
    4. 24.3 Lipid Metabolism
    5. 24.4 Protein Metabolism
    6. 24.5 Metabolic States of the Body
    7. 24.6 Energy and Heat Balance
    8. 24.7 Nutrition and Diet
  29. Chapter 25. The Urinary System
    1. 25.0 Introduction
    2. 25.1 Internal and External Anatomy of the Kidney
    3. 25.2 Microscopic Anatomy of the Kidney: Anatomy of the Nephron
    4. 25.3 Physiology of Urine Formation: Overview
    5. 25.4 Physiology of Urine Formation: Glomerular Filtration
    6. 25.5 Physiology of Urine Formation: Tubular Reabsorption and Secretion
    7. 25.6 Physiology of Urine Formation: Medullary Concentration Gradient
    8. 25.7 Physiology of Urine Formation: Regulation of Fluid Volume and Composition
    9. 25.8 Urine Transport and Elimination
    10. 25.9 The Urinary System and Homeostasis
  30. Chapter 26. Fluid, Electrolyte, and Acid-Base Balance
    1. 26.0 Introduction
    2. 26.1 Body Fluids and Fluid Compartments
    3. 26.2 Water Balance
    4. 26.3 Electrolyte Balance
    5. 26.4 Acid-Base Balance
    6. 26.5 Disorders of Acid-Base Balance
  31. Chapter 27. The Sexual Systems
    1. 27.0 Introduction
    2. 27.1 Anatomy of Sexual Systems
    3. 27.2 Development of Sexual Anatomy
    4. 27.3 Physiology of the Female Sexual System
    5. 27.4 Physiology of the Male Sexual System
    6. 27.5 Physiology of Arousal and Orgasm
  32. Chapter 28. Development and Inheritance
    1. 28.0 Introduction
    2. 28.1 Fertilization
    3. 28.2 Embryonic Development
    4. 28.3 Fetal Development
    5. 28.4 Maternal Changes During Pregnancy, Labor, and Birth
    6. 28.5 Adjustments of the Infant at Birth and Postnatal Stages
    7. 28.6 Lactation
    8. 28.7 Patterns of Inheritance
  33. Creative Commons License
  34. Recommended Citations
  35. Versioning

12.4 Communication Between Neurons

Learning Objectives

By the end of this section, you will be able to:

Describe signal conduction at chemical synapses. 

  • Describe the steps of the chemical synapse
  • Explain the differences between the types of graded potentials, including ions involved
  • Categorize the major neurotransmitters by chemical type and effect
The electrical changes taking place within a neuron, as described in the previous section, are similar to a light switch being turned on. A stimulus starts the depolarization (hand on switch), but the action potential runs on its own once a threshold has been reached (electricity moving through the wires to the light). The question is now, “What flips the light switch on?” Temporary changes to a neuron’s cell membrane voltage can result from stimuli in the environment, or from the action of one neuron on another. These temporary changes in membrane potential influence a neuron and determine whether an action potential will occur or not.

Synapses

A synapse is the site of communication between a neuron and another cell. There are two types of synapses: chemical synapses and electrical synapses. In a chemical synapse, a chemical signal— a neurotransmitter—is released from the neuron and it binds to a receptor on the other cell. In an electrical synapse, the membranes of two cells directly connect through a gap junction so that ions can pass directly from one cell to the next, transmitting a signal. Both types of synapses occur in the nervous system, though chemical synapses are more common.

An example of a chemical synapse is the neuromuscular junction (NMJ) described in the chapter on muscle tissue. In the nervous system, there are many additional synapses that utilize the same mechanisms as the NMJ. All chemical synapses have common characteristics, which can be summarized in Table 12.2:

Example Chemical Synapse (Table 12.2)
Common Chemical Synapse ElementSpecific element in a Skeletal Muscle Neuromuscular Junction
presynaptic elementsomatic motor neuron axon terminal
neurotransmitter (packaged in vesicles)acetylcholine
synaptic cleftspace between somatic motor neuron and muscle cell membrane
receptor proteinsnicotinic acetylcholine (cholinergic) receptor
postsynaptic elementpostsynaptic element is the motor end plate of the sarcolemma
neurotransmitter elimination or re-uptakedegrading enzyme: acetylcholinesterase

Neurotransmitter Release

When an action potential reaches the axon terminals, voltage-gated Ca2+ channels in the membrane of the synaptic end bulb open. Ca2+ diffuses down its concentration gradient and enters into the presynaptic neuron axon terminal (end bulb). Once Ca2+ is inside the presynaptic end bulb, it associates with proteins to trigger the exocytosis of neurotransmitter vesicles. The released neurotransmitter moves into the small gap between the cells, the synaptic cleft.

Once in the synaptic cleft, the neurotransmitter diffuses the short distance to the postsynaptic membrane and can bind to neurotransmitter receptors. Receptors are specific for the neurotransmitter, and the two fit together like a lock and key, and so a neurotransmitter will not bind to receptors for other neurotransmitters (Figure 12.4.1).

This diagram shows a postsynaptic neuron. An axon from a presynaptic neuron is synapsing with the dendrites on the post synaptic neuron. The axon of the presynaptic neuron branches into several club shaped axon terminals. A magnified view of one of the synapses reveals that the axon terminal does not contact the dendrite of the postsynaptic neuron. Instead, there is a small space between the two structures, called the synaptic cleft. The axon terminal of the presynaptic neuron contains several synaptic vesicles, each holding about a dozen neurotransmitter particles. The synaptic vesicles travel to the edge of the axon terminal and release their neurotransmitters into the synaptic clefts The neurotransmitters travel through the synaptic cleft and bind to carrier proteins on the postsynaptic neuron that contain receptors foe neurotransmitters.
Figure 12.4.1 – The Synapse: The synapse is a connection between a neuron and its target cell (which is not necessarily a neuron). The presynaptic element is the synaptic end bulb of the axon where Ca2+ enters the bulb to cause vesicle fusion and neurotransmitter release. The neurotransmitter diffuses across the synaptic cleft to bind to its receptor. The neurotransmitter is cleared from the synapse either by enzymatic degradation, neuronal reuptake, or glial reuptake.

Neurotransmitter and Receptor Systems

Neurotransmitters vary greatly throughout the body, but one principle applies to all: neurotransmitters must bind to their own specific receptor, of which there can be subtypes. We will use acetylcholine (neurotransmitter) and its receptor (cholinergic) as an example. There are two subtypes of cholinergic receptors both of which bind acetylecholine: nicotinic receptors and muscarinic receptors (their names are based on the other chemicals that can also bind to the receptor). Nicotine will bind to the nicotinic receptor and activate it, just like acetylcholine. Muscarine, a product of certain mushrooms, will bind to the muscarinic receptor, just like acetylcholine. However, nicotine will not bind to the muscarinic receptor and muscarine will not bind to the nicotinic receptor. Skeletal muscle NMJs always involve nicotinic cholinergic receptors and when acteylcholine binds to nicotinic receptors, a Na+ ligand gated channel opens. Muscarinic receptors are found sometimes with with K+ ligand gated channels and other times with Na+ ligand gated channels, differing throughout the body. For example, when acetylcholine binds to a muscarinic receptor on the pace-maker cells of the heart, K+ ligand gated channels open and heart rate slows down. When acetylcholine binds to a muscarinic receptor on the small intestine muscle, a Na+ ligand gated channel opens and the muscle activates (contracts). This variability in receptor/channel combinations is common throughout the body and occurs for many other neurotransmitters like epinephrine (adrenaline), serotonin and dopamine.

Neurotransmitters are classified in many ways based on their structural chemical make up or their functional common effects. Chemically, neurotransmitters can be small, amino acid based molecules, released from neurons as amino acids themselves (ie: glutamate, glycine) or as enzymatically modified relatively simple molecules (acetylecholine, ATP or biogenic amines such as dopamine). Larger molecule neurotransmitters are more complex proteins (3-36 amino acids long) called neuropeptides. There are more than 100 different peptides and include those such as enkephalins or endorphins, each with their own receptor types and subtypes that bind them.

Types of Neurotransmitters

Small Molecule Neurotransmitters: Amino Acids, Acetylcholine, and Purine Neurotransmitters

Amino Acids: Glutamate (Glu), GABA (gamma-aminobutyric acid, a derivative of glutamate), and glycine (Gly) are common amino acid neurotransmitters. These amino acids have an amino group and a carboxyl group in their chemical structures. Glutamate is one of the 20 amino acids that are used to make proteins. Each amino acid neurotransmitter would be part of its own system, namely the glutamatergic, GABAergic, and glycinergic systems. They each have their own receptors and do not interact with each other. Amino acid neurotransmitters are eliminated from the synapse by reuptake in the neuron that released them. A pump in the presynaptic cell membrane, or sometimes a neighboring glial cell, removes the amino acid from the synaptic cleft so that it can be recycled, repackaged in vesicles, and released again.

The amino acid neurotransmitters, glutamate, glycine, and GABA, are almost exclusively associated with just one effect. Glutamate is often considered an excitatory amino acid, but only because glutamate receptors in the adult cause depolarization of the postsynaptic cell (by changing membrane permeability to Na+ or Ca2+). Glycine and GABA are considered inhibitory amino acids, because their receptors typically cause hyperpolarization (by chaniging membrane permability to Cl– or K+).

Acetylcholine and ATP: Acetylcholine was described above, including its excitatory or inhibitor effects when binding to various cholinergic receptors. ATP, the energy molecule and a purine chemically, has been found to act as a neurotransmitter in both the peripheral and central nervous system, often associated with excitatory effects.

Small Molecule Neurotransmitters: Biogenic Amines

Biogenic amines are a group of neurotransmitters that are enzymatically made from amino acids. They have amino groups in them, but no longer have carboxyl groups and are therefore no longer classified as amino acids. Members of this group include serotonin, histamine and the catecholamines (dopamine, norepinephrine/noradrenaline and epinephrine/adrenaline). Serotonin (which is the basis of the serotonergic system) is made from tryptophan and has its own specific receptors. Dopamine is part of its own system, the dopaminergic system, which has dopamine receptors. Norepinephrine and epinephrine belong to the adrenergic neurotransmitter system. The two molecules are very similar and bind to the same receptors, which are referred to as alpha and beta receptors. The chemical epinephrine (epi- = “on”; “-nephrine” = kidney) is also known as adrenaline (renal = “kidney”), and norepinephrine is sometimes referred to as noradrenaline. The adrenal gland produces epinephrine and norepinephrine to be released into the blood stream as hormones. Once released into the synatpic cleft, all of these neurotransmitters are transported back into their respective presynaptic end bulb for repackaging and re-release.

The biogenic amines have mixed effects. For example, the dopamine receptors that are classified as D1 receptors are excitatory whereas D2-type receptors are inhibitory. Biogenic amine receptors can have even more complex effects because some may not directly affect the membrane potential, but rather have an effect on gene transcription or other metabolic processes in the neuron. The characteristics of the various neurotransmitter systems presented in this section are organized in Table 12.3.

Large Molecule Neurotransmitters: Neuropeptides

A neuropeptide is a neurotransmitter molecule made up of chains of amino acids connected by peptide bonds; essentially a mini-protein. Neuropeptides are often released at synapses in combination with another neurotransmitter, and they often act as hormones in other systems of the body, such as oxytocin, vasoactive intestinal peptide (VIP) or substance P. In addition, sometimes neuropeptides contain other neuropeptides within them! In the case of endorphins, once released, endorphins are cleaved by extracellular enzymes to produce enkephalins, both of which bind to opiod receptors to modulate pain perception in the brain.

The characteristics of the various neurotransmitter systems presented in this section are organized in Table 12.3.

Characteristics of Neurotransmitter Systems (Table 12.3)
SystemCholinergicAmino acidsBiogenic aminesNeuropeptides
NeurotransmittersAcetylcholineGlutamate, glycine, GABASerotonin (5-HT), dopamine, norepinephrine, (epinephrine)Met-enkephalin, beta-endorphin, VIP, Substance P, etc.
ReceptorsNicotinic and muscarinic receptorsGlu receptors, gly receptors, GABA receptors5-HT receptors, D1 and D2 receptors, α-adrenergic and β-adrenergic receptorsReceptors are too numerous to list, but are specific to the peptides.
EliminationDegradation by acetylcholinesteraseReuptake by neurons or gliaReuptake by neuronsDegradation by enzymes called peptidases
Postsynaptic effectNicotinic receptor causes depolarization. Muscarinic receptors can cause both depolarization or hyperpolarization depending on the subtype.Glu receptors cause depolarization. Gly and GABA receptors cause hyperpolarization.Depolarization or hyperpolarization depends on the specific receptor. For example, D1 receptors cause depolarization and D2 receptors cause hyperpolarization.Depolarization or hyperpolarization depends on the specific receptor.

Receptor Mechanism of Action

The important thing to remember about neurotransmitters, and signaling chemicals in general, is that the effect is entirely dependent on the receptor. Neurotransmitters bind to one of two classes of receptors at the cell surface, ionotropic or metabotropic (Figure 12.4.2). Ionotropic receptors are ligand-gated ion channels, such as the nicotinic receptor for acetylcholine or the glycine receptor. A metabotropic receptor involves a complex of proteins that result in metabolic changes within the cell. The receptor complex includes the transmembrane receptor protein, a G protein, and an effector protein. The neurotransmitter, referred to as the first messenger, binds to the receptor protein on the extracellular surface of the cell, and the intracellular side of the protein initiates activity of the G protein. The G protein is a guanosine triphosphate (GTP) hydrolase that physically moves from the receptor protein to the effector protein to activate the latter. An effector protein is an enzyme that catalyzes the generation of a new molecule, which acts as the intracellular mediator, or the second messenger.

Different receptors use different second messengers. Two common examples of second messengers are cyclic adenosine monophosphate (cAMP) and inositol triphosphate (IP3). The enzyme adenylate cyclase (an example of an effector protein) makes cAMP, and phospholipase C is the enzyme that makes IP3. Second messengers, after they are produced by the effector protein, cause metabolic changes within the cell. These changes are most likely the activation of other enzymes in the cell. In neurons, they often modify ion channels, either opening or closing them. These enzymes can also cause changes in the cell, such as the activation of genes in the nucleus, and therefore the increased synthesis of proteins. In neurons, these kinds of changes are often the basis of stronger connections between cells at the synapse and may be the basis of learning and memory.

This diagram contains two images, labeled A and B. Both images show a cross section of a postsynaptic membrane. There are two proteins embedded in each of the two membrane cross sections. In diagram A, direct activation brings about an immediate response. Here, both of the membrane proteins are ion channels. Several hexagonal neurotransmitters bind to ionotropic receptors on the extracellular fluid side of the channels. The binding of neurotransmitters causes the channels to open, allowing ions to flow from the extracellular fluid into the cytosol. Image B shows indirect activation, which involves a prolonged response, amplified over time. Here, one of the cell membrane proteins is solid while the other is a channel. Neurotransmitters bind to metabotropic receptors on the extracellular side of the solid protein. This triggers the solid protein to activate a G protein in the cytoplasm. The G protein binds to an effector protein in the cytoplasm, which results in the production of several second messenger particles. The second messenger activates enzymes that open the channel protein, allowing ions to enter the cytoplasm.
Figure 12.4.2 – Receptor Types: (a) An ionotropic receptor is a channel that opens when the neurotransmitter binds to it. (b) A metabotropic receptor is a complex that causes metabolic changes in the cell when the neurotransmitter binds to it (1). After binding, the G protein hydrolyzes GTP and moves to the effector protein (2). When the G protein contacts the effector protein, a second messenger is generated, such as cAMP (3). The second messenger can then go on to cause changes in the neuron, such as opening or closing ion channels, metabolic changes, and changes in gene transcription.

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Watch this video to learn about the release of a neurotransmitter. The action potential reaches the end of the axon, called the axon terminal, and a chemical signal is released to tell the target cell to do something—either to initiate a new action potential, or to suppress that activity. In a very short space, the electrical signal of the action potential is changed into the chemical signal of a neurotransmitter and then back to electrical changes in the target cell membrane. What is the importance of voltage-gated calcium channels in the release of neurotransmitters?

Graded Potentials

Local changes in the membrane potential away from resting levels are called graded potentials and are usually associated with opening gated channels on the membrane a neuron. The type and amount of change in the membrane potential is determined by the ion that crosses the membrane, how many ions cross and for how long. Graded potentials can be of two sorts, either they are depolarizing (above resting membrane potential) or hyperpolarizing (below resting membrane potential) (Figure 12.4.3). Depolarizing graded potentials are often the result of Na+ or Ca2+ entering the cell. Both of these ions have higher concentrations outside the cell than inside; because they have a positive charge, when they move into the cell the membrane becomes less negative inside relative to the outside. Hyperpolarizing graded potentials can be caused by K+ leaving the cell or Cl– entering the cell. The membrane becomes more negative if a positive charge moves out of a cell or if a negative charge enters the cell. Graded potentials are transient and are dissipated as they move away from the site of the initial stimulus.

When ion channels are left open longer or more channels are opened (for the same ion), the stimulus affecting a neuron is bigger. A “bigger stimulus” occurs due to a more painful stimulus, a heavier load, a brighter light etc. These larger stimuli induce larger graded potentials of longer duration in neurons and can be either depolarizing or hyperpolarizing.

The graph has membrane potential, in millivolts, on the X axis, ranging from negative 90 to positive 30. Time is on the X axis. The left half of the plot line is labeled the depolarizing graded potential. The plot has four progressively larger peaks, with each starting at the resting membrane potential of negative 70. The lowest peak reaches to about negative 65 and is narrow in width, as this represents a small stimulus that causes a small depolarization of the cell membrane. The second peak reaches to about negative 60 but is still narrow. This represents a larger stimulus causing more depolarization. The third peak also reaches to negative 60, but is about twice as wide as the other two peaks. This represents a stimulus of longer duration, which causes a longer lasting depolarization. However, this stimulus is not greater in strength than the previous stimulus. The rightmost peak among the depolarizing graded potentials reaches above the threshold line to about negative 51. This represents a stimulus of sufficient strength to trigger an action potential. The right half of the plot is labeled the hyperpolarizing graded potential. The plot line in this half begins at the resting potential of negative 70, but then drops to more negative membrane potentials. The first peak drops to negative 75 EV, the second peak drops to negative 80 EV and the third peak drops to negative 88 EV. These peaks represent a stimulus that results in hyperpolarization, which is triggered by the activation of specific ion channels in the cell membrane.
Figure 12.4.3 – Graded Potentials: Graded potentials are temporary changes in the membrane voltage, the characteristics of which depend on the size of the stimulus. Some types of stimuli cause depolarization of the membrane, whereas others cause hyperpolarization. It depends on the specific ion channels that are activated in the cell membrane.

For the unipolar cells of sensory neurons—both those with free nerve endings and those within encapsulations—graded potentials develop in the dendrites and influence the generation of an action potential in the axon of the same cell. This is called a generator potential. For other sensory receptor cells which are not neurons, such as taste cells or photoreceptors of the retina, graded potentials in receptor cell membranes result in the release of neurotransmitters at synapses with sensory neurons. This is called a receptor potential, and we will consider this type of graded potential during a discussion of the special senses.

A postsynaptic potential (PSP) is the graded potential in the dendrites or cell body of a neuron that is receiving synapses from other cells. Postsynaptic potentials can be depolarizing or hyperpolarizing. Depolarization in a postsynaptic potential is called an excitatory postsynaptic potential (EPSP) because it causes the membrane potential to move toward threshold. Hyperpolarization in a postsynaptic potential is an inhibitory postsynaptic potential (IPSP) because it causes the membrane potential to move away from threshold.

Summation

All types of graded potentials will result in small changes (either depolarization or hyperpolarization) in the voltage of a membrane. These changes can lead to the neuron reaching threshold if the changes add together, or summate. The combined effects of different types of graded potentials are illustrated in Figure 12.4.4. If the total change in voltage that reaches the initial segment (or trigger zone) is a positive 15 mV, meaning that the membrane depolarizes from -70 mV (resting membrane potential) to -55 mV (threshold), then the graded potentials will result in the initiation of an action potential.

Graded potentials summate at a specific location at the beginning of the axon to initiate the action potential, namely the initial segment. For sensory neurons, the initial segment is directly adjacent to the dendritic endings (since the cell body is located more proximally). For all other neurons, the initial segment of the axon is found at the axon hillock and it is where summation takes place. These locations have a high density of voltage-gated Na+ channels that initiate the depolarizing phase of the action potential and is often referred as the trigger zone.

Summation can be spatial or temporal, meaning it can be the result of multiple graded potentials occurring simultaneously at different locations on the neuron (spatial), or all at the same place but in rapid succession (temporal). Spatial and temporal summation can act together, as well. Since graded potentials dissipated with distance and time, summation is the total change in voltage due to all spatial and temporal graded potentials that reach the trigger zone or initial segment at each moment.

This graph has membrane potential, in millivolts, on the X axis, ranging from negative 90 to negative 40. Time is on the X axis. The plot line is moving up and down between the resting membrane potential of minus 70 EV and the threshold potential of minus 55 EV. An EPSP causes the plot line to move higher, closer to the threshold potential. An IPSP causes the plot line to move lower, further away from the threshold potential. Toward the right side of the graph, the neuron receives an EPSP that pushes the membrane potential above the threshold, triggering an action potential that causes the plot line to quickly rise above positive 30 EV. The plot line then quickly drops back below minus 70 EV but then gradually increases back to minus 70. A picture of a neuron indicates that excitatory post synaptic potentials are commonly provided by synapses on the neuron’s dendrites. Inhibitory post synaptic potentials are commonly provided by synapses near the neuron’s axon hillock.
Figure 12.4.4 – Postsynaptic Potential Summation: The result of summation of postsynaptic potentials is the overall change in the membrane potential. At point A, several different excitatory postsynaptic potentials add up to a large depolarization. At point B, a mix of excitatory and inhibitory postsynaptic potentials result in a different end result for the membrane potential.

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Watch this video to learn about summation. The process of converting electrical signals to chemical signals and back requires subtle changes that can result in transient increases or decreases in membrane voltage. To cause a lasting change in the target cell, multiple signals are usually added together, or summated. Does spatial summation have to happen all at once, or can the separate signals arrive on the postsynaptic neuron at slightly different times? Explain your answer.

Disorders of the Nervous System

The underlying cause of some neurodegenerative diseases, such as Alzheimer’s and Parkinson’s, appears to be related to proteins—specifically, to proteins behaving badly. One of the strongest theories of what causes Alzheimer’s disease is based on the accumulation of beta-amyloid plaques, dense conglomerations of a protein that is not functioning correctly. Parkinson’s disease is linked to an increase in a protein known as alpha-synuclein that is toxic to the cells of the substantia nigra nucleus in the midbrain.

For proteins to function correctly, they are dependent on their three-dimensional shape. The linear sequence of amino acids folds into a three-dimensional shape that is based on the interactions between and among those amino acids. When the folding is disturbed, and proteins take on a different shape, they stop functioning correctly. But the disease is not necessarily the result of functional loss of these proteins; rather, these altered proteins start to accumulate and may become toxic. For example, in Alzheimer’s, the hallmark of the disease is the accumulation of these amyloid plaques in the cerebral cortex. The term coined to describe this sort of disease is “proteopathy” and it includes other diseases. Creutzfeld-Jacob disease, the human variant of the prion disease known as mad cow disease in the bovine, also involves the accumulation of amyloid plaques, similar to Alzheimer’s. Diseases of other organ systems can fall into this group as well, such as cystic fibrosis or type 2 diabetes. Recognizing the relationship between these diseases has suggested new therapeutic possibilities. Interfering with the accumulation of the proteins, and possibly as early as their original production within the cell, may unlock new ways to alleviate these devastating diseases.

Chapter Review

The basis of the electrical signal within a neuron is the action potential that propagates down the axon. For a neuron to generate an action potential, it needs to receive input from another source, either another neuron or a sensory stimulus. That input will result in opening ion channels in the neuron, resulting in a graded potential based on the strength of the stimulus. Graded potentials can be depolarizing or hyperpolarizing and can summate to affect the probability of the neuron reaching threshold at the initial segment or trigger zone. Graded potentials produced by interactions between neurons at synapses are called postsynaptic potentials (PSPs). A depolarizing graded potential at a synapse is called an excitatory PSP, and a hyperpolarizing graded potential at a synapse is called an inhibitory PSP.

Synapses are the contacts between neurons, which can either be chemical or electrical in nature. Chemical synapses are far more common. At a chemical synapse, neurotransmitter is released from the presynaptic element and diffuses across the synaptic cleft. The neurotransmitter binds to a receptor protein and causes a change in the postsynaptic membrane (the PSP). The neurotransmitter must be inactivated or removed from the synaptic cleft so that the stimulus is limited in time.

The particular characteristics of a synapse vary based on the neurotransmitter system produced by that neuron. The cholinergic system is found at the neuromuscular junction and in certain places within the nervous system. Amino acids, such as glutamate, glycine, and gamma-aminobutyric acid (GABA) are used as neurotransmitters. Other neurotransmitters are the result of amino acids being enzymatically changed, as in the biogenic amines, or being covalently bonded together, as in the neuropeptides.

Interactive Link Questions

Watch this video to learn about summation. The process of converting electrical signals to chemical signals and back requires subtle changes that can result in transient increases or decreases in membrane voltage. To cause a lasting change in the target cell, multiple signals are usually added together, or summated. Does spatial summation have to happen all at once, or can the separate signals arrive on the postsynaptic neuron at slightly different times? Explain your answer.

A second signal from a separate presynaptic neuron can arrive slightly later, as long as it arrives before the first one dies off, or dissipates.

Watch this video to learn about the release of a neurotransmitter. The action potential reaches the end of the axon, called the axon terminal, and a chemical signal is released to tell the target cell to do something, either initiate a new action potential, or to suppress that activity. In a very short space, the electrical signal of the action potential is changed into the chemical signal of a neurotransmitter, and then back to electrical changes in the target cell membrane. What is the importance of voltage-gated calcium channels in the release of neurotransmitters?

The action potential depolarizes the cell membrane of the axon terminal, which contains the voltage-gated Ca2+ channel. That voltage change opens the channel so that Ca2+ can enter the axon terminal. Calcium ions make it possible for synaptic vesicles to release their contents through exocytosis.

Review Questions

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An interactive H5P element has been excluded from this version of the text. You can view it online here:
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An interactive H5P element has been excluded from this version of the text. You can view it online here:
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An interactive H5P element has been excluded from this version of the text. You can view it online here:
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An interactive H5P element has been excluded from this version of the text. You can view it online here:
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Critical Thinking Questions

1. If a postsynaptic cell has synapses from five different cells, and three cause EPSPs and two of them cause IPSPs, give an example of a series of depolarizations and hyperpolarizations that would result in the neuron reaching threshold.

2. Why is the receptor the important element determining the effect a neurotransmitter has on a target cell?

Glossary

biogenic amine
class of neurotransmitters that are enzymatically derived from amino acids but no longer contain a carboxyl group
chemical synapse
connection between two neurons, or between a neuron and its target, where a neurotransmitter diffuses across a very short distance
cholinergic system
neurotransmitter system of acetylcholine, which includes its receptors and the enzyme acetylcholinesterase
effector protein
enzyme that catalyzes the generation of a new molecule, which acts as the intracellular mediator of the signal that binds to the receptor
electrical synapse
connection between two neurons, or any two electrically active cells, where ions flow directly through channels spanning their adjacent cell membranes
excitatory postsynaptic potential (EPSP)
graded potential in the postsynaptic membrane that is the result of depolarization and makes an action potential more likely to occur
generator potential
graded potential from dendrites of a unipolar cell which generates the action potential in the initial segment of that cell’s axon
G protein
guanosine triphosphate (GTP) hydrolase that physically moves from the receptor protein to the effector protein to activate the latter
inhibitory postsynaptic potential (IPSP)
graded potential in the postsynaptic membrane that is the result of hyperpolarization and makes an action potential less likely to occur
metabotropic receptor
neurotransmitter receptor that involves a complex of proteins that cause metabolic changes in a cell
muscarinic receptor
type of acetylcholine receptor protein that is characterized by also binding to muscarine and is a metabotropic receptor
neuropeptide
neurotransmitter type that includes protein molecules and shorter chains of amino acids
nicotinic receptor
type of acetylcholine receptor protein that is characterized by also binding to nicotine and is an ionotropic receptor
postsynaptic potential (PSP)
graded potential in the postsynaptic membrane caused by the binding of neurotransmitter to protein receptors
receptor potential
graded potential in a specialized sensory cell that directly causes the release of neurotransmitter without an intervening action potential
spatial summation
combination of graded potentials across the neuronal cell membrane caused by signals from separate presynaptic elements that add up to initiate an action potential
summate
to add together, as in the cumulative change in postsynaptic potentials toward reaching threshold in the membrane, either across a span of the membrane or over a certain amount of time
synapse
synapse is the site of communication between a neuron and another cell (target cell, not necessarily another neuron)
synaptic cleft
small gap between cells in a chemical synapse where neurotransmitter diffuses from the presynaptic element to the postsynaptic element
temporal summation
combination of graded potentials at the same location on a neuron resulting in a strong signal from one input

Solutions

Answers for Critical Thinking Questions

  1. EPSP1 = +5 mV, EPSP2 = +7 mV, EPSP 3 = +10 mV, IPSP1 = -4 mV, IPSP2 = -3 mV. 5 + 7 + 10 – 4 – 3 = +15 mV.
  2. Different neurotransmitters have different receptors. Thus, the type of receptor in the postsynaptic cell is what determines which ion channels open. Acetylcholine binding to the nicotinic receptor causes cations to cross the membrane. GABA binding to its receptor causes the anion chloride to cross the membrane.

Annotate

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12.5 The Action Potential
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Anatomy and Physiology
Copyright © 2019 by Lindsay M. Biga, Sierra Dawson, Amy Harwell, Robin Hopkins, Joel Kaufmann, Mike LeMaster, Philip Matern, Katie Morrison-Graham, Devon Quick & Jon Runyeon

Anatomy & Physiology by Lindsay M. Biga, Sierra Dawson, Amy Harwell, Robin Hopkins, Joel Kaufmann, Mike LeMaster, Philip Matern, Katie Morrison-Graham, Devon Quick & Jon Runyeon is licensed under a Creative Commons Attribution-ShareAlike 4.0 International License, except where otherwise noted.

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