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Biology 2e

35.2 How Neurons Communicate

Biology 2e35.2 How Neurons Communicate
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  1. Preface
  2. The Chemistry of Life
    1. 1 The Study of Life
      1. Introduction
      2. 1.1 The Science of Biology
      3. 1.2 Themes and Concepts of Biology
      4. Key Terms
      5. Chapter Summary
      6. Visual Connection Questions
      7. Review Questions
      8. Critical Thinking Questions
    2. 2 The Chemical Foundation of Life
      1. Introduction
      2. 2.1 Atoms, Isotopes, Ions, and Molecules: The Building Blocks
      3. 2.2 Water
      4. 2.3 Carbon
      5. Key Terms
      6. Chapter Summary
      7. Visual Connection Questions
      8. Review Questions
      9. Critical Thinking Questions
    3. 3 Biological Macromolecules
      1. Introduction
      2. 3.1 Synthesis of Biological Macromolecules
      3. 3.2 Carbohydrates
      4. 3.3 Lipids
      5. 3.4 Proteins
      6. 3.5 Nucleic Acids
      7. Key Terms
      8. Chapter Summary
      9. Visual Connection Questions
      10. Review Questions
      11. Critical Thinking Questions
  3. The Cell
    1. 4 Cell Structure
      1. Introduction
      2. 4.1 Studying Cells
      3. 4.2 Prokaryotic Cells
      4. 4.3 Eukaryotic Cells
      5. 4.4 The Endomembrane System and Proteins
      6. 4.5 The Cytoskeleton
      7. 4.6 Connections between Cells and Cellular Activities
      8. Key Terms
      9. Chapter Summary
      10. Visual Connection Questions
      11. Review Questions
      12. Critical Thinking Questions
    2. 5 Structure and Function of Plasma Membranes
      1. Introduction
      2. 5.1 Components and Structure
      3. 5.2 Passive Transport
      4. 5.3 Active Transport
      5. 5.4 Bulk Transport
      6. Key Terms
      7. Chapter Summary
      8. Visual Connection Questions
      9. Review Questions
      10. Critical Thinking Questions
    3. 6 Metabolism
      1. Introduction
      2. 6.1 Energy and Metabolism
      3. 6.2 Potential, Kinetic, Free, and Activation Energy
      4. 6.3 The Laws of Thermodynamics
      5. 6.4 ATP: Adenosine Triphosphate
      6. 6.5 Enzymes
      7. Key Terms
      8. Chapter Summary
      9. Visual Connection Questions
      10. Review Questions
      11. Critical Thinking Questions
    4. 7 Cellular Respiration
      1. Introduction
      2. 7.1 Energy in Living Systems
      3. 7.2 Glycolysis
      4. 7.3 Oxidation of Pyruvate and the Citric Acid Cycle
      5. 7.4 Oxidative Phosphorylation
      6. 7.5 Metabolism without Oxygen
      7. 7.6 Connections of Carbohydrate, Protein, and Lipid Metabolic Pathways
      8. 7.7 Regulation of Cellular Respiration
      9. Key Terms
      10. Chapter Summary
      11. Visual Connection Questions
      12. Review Questions
      13. Critical Thinking Questions
    5. 8 Photosynthesis
      1. Introduction
      2. 8.1 Overview of Photosynthesis
      3. 8.2 The Light-Dependent Reactions of Photosynthesis
      4. 8.3 Using Light Energy to Make Organic Molecules
      5. Key Terms
      6. Chapter Summary
      7. Visual Connection Questions
      8. Review Questions
      9. Critical Thinking Questions
    6. 9 Cell Communication
      1. Introduction
      2. 9.1 Signaling Molecules and Cellular Receptors
      3. 9.2 Propagation of the Signal
      4. 9.3 Response to the Signal
      5. 9.4 Signaling in Single-Celled Organisms
      6. Key Terms
      7. Chapter Summary
      8. Visual Connection Questions
      9. Review Questions
      10. Critical Thinking Questions
    7. 10 Cell Reproduction
      1. Introduction
      2. 10.1 Cell Division
      3. 10.2 The Cell Cycle
      4. 10.3 Control of the Cell Cycle
      5. 10.4 Cancer and the Cell Cycle
      6. 10.5 Prokaryotic Cell Division
      7. Key Terms
      8. Chapter Summary
      9. Visual Connection Questions
      10. Review Questions
      11. Critical Thinking Questions
  4. Genetics
    1. 11 Meiosis and Sexual Reproduction
      1. Introduction
      2. 11.1 The Process of Meiosis
      3. 11.2 Sexual Reproduction
      4. Key Terms
      5. Chapter Summary
      6. Visual Connection Questions
      7. Review Questions
      8. Critical Thinking Questions
    2. 12 Mendel's Experiments and Heredity
      1. Introduction
      2. 12.1 Mendel’s Experiments and the Laws of Probability
      3. 12.2 Characteristics and Traits
      4. 12.3 Laws of Inheritance
      5. Key Terms
      6. Chapter Summary
      7. Visual Connection Questions
      8. Review Questions
      9. Critical Thinking Questions
    3. 13 Modern Understandings of Inheritance
      1. Introduction
      2. 13.1 Chromosomal Theory and Genetic Linkage
      3. 13.2 Chromosomal Basis of Inherited Disorders
      4. Key Terms
      5. Chapter Summary
      6. Visual Connection Questions
      7. Review Questions
      8. Critical Thinking Questions
    4. 14 DNA Structure and Function
      1. Introduction
      2. 14.1 Historical Basis of Modern Understanding
      3. 14.2 DNA Structure and Sequencing
      4. 14.3 Basics of DNA Replication
      5. 14.4 DNA Replication in Prokaryotes
      6. 14.5 DNA Replication in Eukaryotes
      7. 14.6 DNA Repair
      8. Key Terms
      9. Chapter Summary
      10. Visual Connection Questions
      11. Review Questions
      12. Critical Thinking Questions
    5. 15 Genes and Proteins
      1. Introduction
      2. 15.1 The Genetic Code
      3. 15.2 Prokaryotic Transcription
      4. 15.3 Eukaryotic Transcription
      5. 15.4 RNA Processing in Eukaryotes
      6. 15.5 Ribosomes and Protein Synthesis
      7. Key Terms
      8. Chapter Summary
      9. Visual Connection Questions
      10. Review Questions
      11. Critical Thinking Questions
    6. 16 Gene Expression
      1. Introduction
      2. 16.1 Regulation of Gene Expression
      3. 16.2 Prokaryotic Gene Regulation
      4. 16.3 Eukaryotic Epigenetic Gene Regulation
      5. 16.4 Eukaryotic Transcription Gene Regulation
      6. 16.5 Eukaryotic Post-transcriptional Gene Regulation
      7. 16.6 Eukaryotic Translational and Post-translational Gene Regulation
      8. 16.7 Cancer and Gene Regulation
      9. Key Terms
      10. Chapter Summary
      11. Visual Connection Questions
      12. Review Questions
      13. Critical Thinking Questions
    7. 17 Biotechnology and Genomics
      1. Introduction
      2. 17.1 Biotechnology
      3. 17.2 Mapping Genomes
      4. 17.3 Whole-Genome Sequencing
      5. 17.4 Applying Genomics
      6. 17.5 Genomics and Proteomics
      7. Key Terms
      8. Chapter Summary
      9. Visual Connection Questions
      10. Review Questions
      11. Critical Thinking Questions
  5. Evolutionary Processes
    1. 18 Evolution and the Origin of Species
      1. Introduction
      2. 18.1 Understanding Evolution
      3. 18.2 Formation of New Species
      4. 18.3 Reconnection and Speciation Rates
      5. Key Terms
      6. Chapter Summary
      7. Visual Connection Questions
      8. Review Questions
      9. Critical Thinking Questions
    2. 19 The Evolution of Populations
      1. Introduction
      2. 19.1 Population Evolution
      3. 19.2 Population Genetics
      4. 19.3 Adaptive Evolution
      5. Key Terms
      6. Chapter Summary
      7. Visual Connection Questions
      8. Review Questions
      9. Critical Thinking Questions
    3. 20 Phylogenies and the History of Life
      1. Introduction
      2. 20.1 Organizing Life on Earth
      3. 20.2 Determining Evolutionary Relationships
      4. 20.3 Perspectives on the Phylogenetic Tree
      5. Key Terms
      6. Chapter Summary
      7. Visual Connection Questions
      8. Review Questions
      9. Critical Thinking Questions
  6. Biological Diversity
    1. 21 Viruses
      1. Introduction
      2. 21.1 Viral Evolution, Morphology, and Classification
      3. 21.2 Virus Infections and Hosts
      4. 21.3 Prevention and Treatment of Viral Infections
      5. 21.4 Other Acellular Entities: Prions and Viroids
      6. Key Terms
      7. Chapter Summary
      8. Visual Connection Questions
      9. Review Questions
      10. Critical Thinking Questions
    2. 22 Prokaryotes: Bacteria and Archaea
      1. Introduction
      2. 22.1 Prokaryotic Diversity
      3. 22.2 Structure of Prokaryotes: Bacteria and Archaea
      4. 22.3 Prokaryotic Metabolism
      5. 22.4 Bacterial Diseases in Humans
      6. 22.5 Beneficial Prokaryotes
      7. Key Terms
      8. Chapter Summary
      9. Visual Connection Questions
      10. Review Questions
      11. Critical Thinking Questions
    3. 23 Protists
      1. Introduction
      2. 23.1 Eukaryotic Origins
      3. 23.2 Characteristics of Protists
      4. 23.3 Groups of Protists
      5. 23.4 Ecology of Protists
      6. Key Terms
      7. Chapter Summary
      8. Visual Connection Questions
      9. Review Questions
      10. Critical Thinking Questions
    4. 24 Fungi
      1. Introduction
      2. 24.1 Characteristics of Fungi
      3. 24.2 Classifications of Fungi
      4. 24.3 Ecology of Fungi
      5. 24.4 Fungal Parasites and Pathogens
      6. 24.5 Importance of Fungi in Human Life
      7. Key Terms
      8. Chapter Summary
      9. Visual Connection Questions
      10. Review Questions
      11. Critical Thinking Questions
    5. 25 Seedless Plants
      1. Introduction
      2. 25.1 Early Plant Life
      3. 25.2 Green Algae: Precursors of Land Plants
      4. 25.3 Bryophytes
      5. 25.4 Seedless Vascular Plants
      6. Key Terms
      7. Chapter Summary
      8. Visual Connection Questions
      9. Review Questions
      10. Critical Thinking Questions
    6. 26 Seed Plants
      1. Introduction
      2. 26.1 Evolution of Seed Plants
      3. 26.2 Gymnosperms
      4. 26.3 Angiosperms
      5. 26.4 The Role of Seed Plants
      6. Key Terms
      7. Chapter Summary
      8. Visual Connection Questions
      9. Review Questions
      10. Critical Thinking Questions
    7. 27 Introduction to Animal Diversity
      1. Introduction
      2. 27.1 Features of the Animal Kingdom
      3. 27.2 Features Used to Classify Animals
      4. 27.3 Animal Phylogeny
      5. 27.4 The Evolutionary History of the Animal Kingdom
      6. Key Terms
      7. Chapter Summary
      8. Visual Connection Questions
      9. Review Questions
      10. Critical Thinking Questions
    8. 28 Invertebrates
      1. Introduction
      2. 28.1 Phylum Porifera
      3. 28.2 Phylum Cnidaria
      4. 28.3 Superphylum Lophotrochozoa: Flatworms, Rotifers, and Nemerteans
      5. 28.4 Superphylum Lophotrochozoa: Molluscs and Annelids
      6. 28.5 Superphylum Ecdysozoa: Nematodes and Tardigrades
      7. 28.6 Superphylum Ecdysozoa: Arthropods
      8. 28.7 Superphylum Deuterostomia
      9. Key Terms
      10. Chapter Summary
      11. Visual Connection Questions
      12. Review Questions
      13. Critical Thinking Questions
    9. 29 Vertebrates
      1. Introduction
      2. 29.1 Chordates
      3. 29.2 Fishes
      4. 29.3 Amphibians
      5. 29.4 Reptiles
      6. 29.5 Birds
      7. 29.6 Mammals
      8. 29.7 The Evolution of Primates
      9. Key Terms
      10. Chapter Summary
      11. Visual Connection Questions
      12. Review Questions
      13. Critical Thinking Questions
  7. Plant Structure and Function
    1. 30 Plant Form and Physiology
      1. Introduction
      2. 30.1 The Plant Body
      3. 30.2 Stems
      4. 30.3 Roots
      5. 30.4 Leaves
      6. 30.5 Transport of Water and Solutes in Plants
      7. 30.6 Plant Sensory Systems and Responses
      8. Key Terms
      9. Chapter Summary
      10. Visual Connection Questions
      11. Review Questions
      12. Critical Thinking Questions
    2. 31 Soil and Plant Nutrition
      1. Introduction
      2. 31.1 Nutritional Requirements of Plants
      3. 31.2 The Soil
      4. 31.3 Nutritional Adaptations of Plants
      5. Key Terms
      6. Chapter Summary
      7. Visual Connection Questions
      8. Review Questions
      9. Critical Thinking Questions
    3. 32 Plant Reproduction
      1. Introduction
      2. 32.1 Reproductive Development and Structure
      3. 32.2 Pollination and Fertilization
      4. 32.3 Asexual Reproduction
      5. Key Terms
      6. Chapter Summary
      7. Visual Connection Questions
      8. Review Questions
      9. Critical Thinking Questions
  8. Animal Structure and Function
    1. 33 The Animal Body: Basic Form and Function
      1. Introduction
      2. 33.1 Animal Form and Function
      3. 33.2 Animal Primary Tissues
      4. 33.3 Homeostasis
      5. Key Terms
      6. Chapter Summary
      7. Visual Connection Questions
      8. Review Questions
      9. Critical Thinking Questions
    2. 34 Animal Nutrition and the Digestive System
      1. Introduction
      2. 34.1 Digestive Systems
      3. 34.2 Nutrition and Energy Production
      4. 34.3 Digestive System Processes
      5. 34.4 Digestive System Regulation
      6. Key Terms
      7. Chapter Summary
      8. Visual Connection Questions
      9. Review Questions
      10. Critical Thinking Questions
    3. 35 The Nervous System
      1. Introduction
      2. 35.1 Neurons and Glial Cells
      3. 35.2 How Neurons Communicate
      4. 35.3 The Central Nervous System
      5. 35.4 The Peripheral Nervous System
      6. 35.5 Nervous System Disorders
      7. Key Terms
      8. Chapter Summary
      9. Visual Connection Questions
      10. Review Questions
      11. Critical Thinking Questions
    4. 36 Sensory Systems
      1. Introduction
      2. 36.1 Sensory Processes
      3. 36.2 Somatosensation
      4. 36.3 Taste and Smell
      5. 36.4 Hearing and Vestibular Sensation
      6. 36.5 Vision
      7. Key Terms
      8. Chapter Summary
      9. Visual Connection Questions
      10. Review Questions
      11. Critical Thinking Questions
    5. 37 The Endocrine System
      1. Introduction
      2. 37.1 Types of Hormones
      3. 37.2 How Hormones Work
      4. 37.3 Regulation of Body Processes
      5. 37.4 Regulation of Hormone Production
      6. 37.5 Endocrine Glands
      7. Key Terms
      8. Chapter Summary
      9. Visual Connection Questions
      10. Review Questions
      11. Critical Thinking Questions
    6. 38 The Musculoskeletal System
      1. Introduction
      2. 38.1 Types of Skeletal Systems
      3. 38.2 Bone
      4. 38.3 Joints and Skeletal Movement
      5. 38.4 Muscle Contraction and Locomotion
      6. Key Terms
      7. Chapter Summary
      8. Visual Connection Questions
      9. Review Questions
      10. Critical Thinking Questions
    7. 39 The Respiratory System
      1. Introduction
      2. 39.1 Systems of Gas Exchange
      3. 39.2 Gas Exchange across Respiratory Surfaces
      4. 39.3 Breathing
      5. 39.4 Transport of Gases in Human Bodily Fluids
      6. Key Terms
      7. Chapter Summary
      8. Visual Connection Questions
      9. Review Questions
      10. Critical Thinking Questions
    8. 40 The Circulatory System
      1. Introduction
      2. 40.1 Overview of the Circulatory System
      3. 40.2 Components of the Blood
      4. 40.3 Mammalian Heart and Blood Vessels
      5. 40.4 Blood Flow and Blood Pressure Regulation
      6. Key Terms
      7. Chapter Summary
      8. Visual Connection Questions
      9. Review Questions
      10. Critical Thinking Questions
    9. 41 Osmotic Regulation and Excretion
      1. Introduction
      2. 41.1 Osmoregulation and Osmotic Balance
      3. 41.2 The Kidneys and Osmoregulatory Organs
      4. 41.3 Excretion Systems
      5. 41.4 Nitrogenous Wastes
      6. 41.5 Hormonal Control of Osmoregulatory Functions
      7. Key Terms
      8. Chapter Summary
      9. Visual Connection Questions
      10. Review Questions
      11. Critical Thinking Questions
    10. 42 The Immune System
      1. Introduction
      2. 42.1 Innate Immune Response
      3. 42.2 Adaptive Immune Response
      4. 42.3 Antibodies
      5. 42.4 Disruptions in the Immune System
      6. Key Terms
      7. Chapter Summary
      8. Visual Connection Questions
      9. Review Questions
      10. Critical Thinking Questions
    11. 43 Animal Reproduction and Development
      1. Introduction
      2. 43.1 Reproduction Methods
      3. 43.2 Fertilization
      4. 43.3 Human Reproductive Anatomy and Gametogenesis
      5. 43.4 Hormonal Control of Human Reproduction
      6. 43.5 Human Pregnancy and Birth
      7. 43.6 Fertilization and Early Embryonic Development
      8. 43.7 Organogenesis and Vertebrate Formation
      9. Key Terms
      10. Chapter Summary
      11. Visual Connection Questions
      12. Review Questions
      13. Critical Thinking Questions
  9. Ecology
    1. 44 Ecology and the Biosphere
      1. Introduction
      2. 44.1 The Scope of Ecology
      3. 44.2 Biogeography
      4. 44.3 Terrestrial Biomes
      5. 44.4 Aquatic Biomes
      6. 44.5 Climate and the Effects of Global Climate Change
      7. Key Terms
      8. Chapter Summary
      9. Visual Connection Questions
      10. Review Questions
      11. Critical Thinking Questions
    2. 45 Population and Community Ecology
      1. Introduction
      2. 45.1 Population Demography
      3. 45.2 Life Histories and Natural Selection
      4. 45.3 Environmental Limits to Population Growth
      5. 45.4 Population Dynamics and Regulation
      6. 45.5 Human Population Growth
      7. 45.6 Community Ecology
      8. 45.7 Behavioral Biology: Proximate and Ultimate Causes of Behavior
      9. Key Terms
      10. Chapter Summary
      11. Visual Connection Questions
      12. Review Questions
      13. Critical Thinking Questions
    3. 46 Ecosystems
      1. Introduction
      2. 46.1 Ecology of Ecosystems
      3. 46.2 Energy Flow through Ecosystems
      4. 46.3 Biogeochemical Cycles
      5. Key Terms
      6. Chapter Summary
      7. Visual Connection Questions
      8. Review Questions
      9. Critical Thinking Questions
    4. 47 Conservation Biology and Biodiversity
      1. Introduction
      2. 47.1 The Biodiversity Crisis
      3. 47.2 The Importance of Biodiversity to Human Life
      4. 47.3 Threats to Biodiversity
      5. 47.4 Preserving Biodiversity
      6. Key Terms
      7. Chapter Summary
      8. Visual Connection Questions
      9. Review Questions
      10. Critical Thinking Questions
  10. A | The Periodic Table of Elements
  11. B | Geological Time
  12. C | Measurements and the Metric System
  13. Index
By the end of this section, you will be able to do the following:
  • Describe the basis of the resting membrane potential
  • Explain the stages of an action potential and 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 or a 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 committee, one neuron usually receives and synthesizes messages from multiple other neurons before “making the decision” to send the message 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 are possible because each neuron has a charged cellular membrane (a voltage difference between the inside and the outside), and the charge of this membrane can change in response to neurotransmitter molecules released from other neurons and environmental stimuli. To understand how neurons communicate, one must first understand the basis of the baseline or ‘resting’ membrane charge.

Neuronal Charged Membranes

The lipid bilayer membrane that surrounds a neuron is impermeable to charged molecules or ions. To enter or exit the neuron, ions must pass through special proteins called ion channels that span the membrane. Ion channels have different configurations: open, closed, and inactive, as illustrated in Figure 35.9. Some ion channels need to be activated in order to open and allow ions to pass into or out of the cell. These ion channels are sensitive to the environment and can change their shape accordingly. Ion channels that change their structure in response to voltage changes are called voltage-gated ion channels. Voltage-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 cell is called the membrane potential.

The first image shows a voltage-gated sodium channel that is closed at the resting potential. In response to a nerve impulse the channel opens, allowing sodium to enter the cell. After the impulse the channel enters an inactive state. The channel closes by a different mechanism and, for a brief period does not reopen in response to a new nerve impulse.
Figure 35.9 Voltage-gated ion channels open in response to changes in membrane voltage. After activation, they become inactivated for a brief period and will no longer open in response to a signal.

Link to Learning

This video discusses the basis of the resting membrane potential.

Resting Membrane Potential

A neuron at rest is negatively charged: the inside of a 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; it is caused by differences in the concentrations of ions inside and outside the cell. If the membrane were equally permeable to all ions, each type of ion would flow across the membrane and the system would reach equilibrium. Because ions cannot simply cross the membrane at will, there are different concentrations of several ions inside and outside the cell, as shown in Table 35.1. The difference in the number of positively charged potassium ions (K+) inside and outside the cell dominates the resting membrane potential (Figure 35.10). When the membrane is at rest, K+ ions accumulate inside the cell due to a net movement with the concentration gradient. The negative resting membrane potential is created and maintained by increasing the concentration of cations outside the cell (in the extracellular fluid) relative to inside the cell (in the cytoplasm). 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 of the cell. The cell possesses potassium and sodium leakage 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, potassium diffuses out of the cell at a much faster rate than sodium leaks in. Because more cations are leaving the cell than are entering, this causes the interior of the cell to be negatively charged relative to the outside of the cell. The actions of the sodium potassium pump help to maintain the resting potential, once established. Recall that sodium potassium pumps brings two K+ ions into the cell while removing three Na+ ions per ATP consumed. As more cations are expelled from the cell than taken in, the inside of the cell remains negatively charged relative to the extracellular fluid. It should be noted that chloride ions (Cl) tend to accumulate outside of the cell because they are repelled by negatively-charged proteins within the cytoplasm.

Ion Concentration Inside and Outside Neurons
Ion Extracellular concentration (mM) Intracellular concentration (mM) Ratio outside/inside
Na+ 145 12 12
K+ 4 155 0.026
Cl 120 4 30
Organic anions (A−) 100
Table 35.1 The resting membrane potential is a result of different concentrations inside and outside the cell.
The resting membrane potential of minus seventy volts is maintained by a sodium/potassium transporter that transports sodium ions out of the cell and potassium ions in. Voltage gated sodium and potassium channels are closed. In response to a nerve impulse, some sodium channels open, allowing sodium ions to enter the cell. The membrane starts to depolarize; in other words, the charge across the membrane lessens. If the membrane potential increases to the threshold of excitation, all the sodium channels open. At the peak action potential, potassium channels open and potassium ions leave the cell. The membrane eventually becomes hyperpolarized.
Figure 35.10 The (a) resting membrane potential is a result of different concentrations of Na+ and K+ ions inside and outside the cell. A nerve impulse causes Na+ to enter the cell, resulting in (b) depolarization. At the peak action potential, K+ channels open and the cell becomes (c) hyperpolarized.

Action Potential

A neuron can receive input from other neurons and, if this input is strong enough, send the signal to downstream neurons. Transmission of a signal between neurons is generally carried by a chemical called a neurotransmitter. Transmission of a signal within a neuron (from dendrite to axon terminal) is carried by a brief reversal of the resting membrane potential called an action potential. When neurotransmitter molecules bind to receptors located on a neuron’s dendrites, ion channels open. At excitatory synapses, this opening allows positive ions to enter the neuron and results in depolarization of the membrane—a decrease in the difference in voltage between the inside and outside of the neuron. A stimulus from a sensory cell or another neuron depolarizes the target neuron to its threshold potential (-55 mV). Na+ channels in the axon hillock open, allowing positive ions to enter the cell (Figure 35.10 and Figure 35.11). Once the sodium channels open, the neuron completely depolarizes to a 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 to the resting potential. To accomplish this, the Na+ channels close and cannot be opened. This begins the neuron's refractory period, in which it cannot produce another action potential because its sodium channels will not open. At the same time, voltage-gated K+ channels open, allowing K+ to leave the cell. As K+ ions leave the cell, the membrane potential once again becomes negative. The diffusion of K+ out of the cell actually hyperpolarizes the cell, in that the membrane potential becomes more negative than the cell's normal resting potential. At this point, the sodium channels will return to their resting state, meaning they are ready to open again if the membrane potential again exceeds the threshold potential. Eventually the extra K+ ions diffuse out of the cell through the potassium leakage channels, bringing the cell from its hyperpolarized state, back to its resting membrane potential.

Visual Connection

Graph plots membrane potential in millivolts versus time. The membrane remains at the resting potential of negative 70 millivolts until a nerve impulse occurs in step 1. Some sodium channels open, and the potential begins to rapidly climb past the threshold of excitation of negative 55 millivolts, at which point all the sodium channels open. At the peak action potential, the potential begins to rapidly drop as potassium channels open and sodium channels close. As a result, the membrane repolarizes past the resting membrane potential and becomes hyperpolarized. The membrane potential then gradually returns to normal.
Figure 35.11 The formation of an action potential can be divided into five steps: (1) A stimulus from a sensory cell or another neuron causes the target cell to depolarize toward the threshold potential. (2) If the threshold of excitation is reached, all Na+ channels open and the membrane depolarizes. (3) At the peak action potential, K+ channels open and K+ begins to leave the cell. At the same time, Na+ channels close. (4) The membrane becomes hyperpolarized as K+ ions continue to leave the cell. The hyperpolarized membrane is in a refractory period and cannot fire. (5) The K+ channels close and the Na+/K+ transporter restores the resting potential.

Potassium channel blockers, such as amiodarone and procainamide, which are used to treat abnormal electrical activity in the heart, called cardiac dysrhythmia, impede the movement of K+ through voltage-gated K+ channels. Which part of the action potential would you expect potassium channels to affect?

The action potential travels from the soma down the axon to the axon terminal. The action potential is initiated when a signal from the soma causes the soma-end of the axon membrane to depolarize. The depolarization spreads down the axon. Meanwhile, the membrane at the start of the axon repolarizes. Because potassium channels are open, the membrane cannot depolarize again. The action potential continues to spread down the axon this way.
Figure 35.12 The action potential is conducted down the axon as the axon membrane depolarizes, then repolarizes.

Link to Learning

This video presents an overview of action potential.

Myelin and the Propagation of the Action Potential

For an action potential to communicate information to another neuron, it must travel along the axon and reach the axon terminals where it can initiate neurotransmitter release. The speed of conduction of an action potential along an axon is influenced by both the diameter of the axon and the axon’s resistance to current leak. Myelin acts as an insulator that prevents current from leaving the axon; this increases 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, illustrated in Figure 35.13 are gaps in the myelin sheath along the axon. These unmyelinated spaces are about one micrometer long and contain voltage-gated Na+ and K+ channels. Flow of ions through these channels, particularly the Na+ channels, regenerates the action potential over and over again along the axon. This ‘jumping’ of the action potential from one node to the next is called saltatory conduction. If nodes of Ranvier were not present along an axon, the action potential would propagate very slowly since Na+ and K+ channels would have to continuously regenerate action potentials at every point along the axon instead of at specific points. Nodes of Ranvier also save energy for the neuron since the channels only need to be present at the nodes and not along the entire axon.

Illustration shows an axon covered in three bands of myelin sheath. Between the sheath coverings the axon is exposed. The uncovered parts of the axon are called nodes of Ranvier. In the illustration, the left node of Ranvier is depolarized such that the membrane potential is positive inside and negative outside. The right membrane of the right node is at the resting potential, negative inside and positive outside. An arrow indicates that the depolarization jumps from the left node to the right, so that the right node becomes depolarized.
Figure 35.13 Nodes of Ranvier are gaps in myelin coverage along axons. Nodes contain voltage-gated K+ and Na+ channels. Action potentials travel down the axon by jumping from one node to the next.

Synaptic Transmission

The synapse or “gap” is the place where information is transmitted from one neuron to another. Synapses usually form between axon terminals and dendritic spines, but this is not universally true. There are also axon-to-axon, dendrite-to-dendrite, and axon-to-cell body synapses. The neuron transmitting the signal is called the presynaptic neuron, and the neuron receiving the signal is called the postsynaptic neuron. Note that these designations are relative to a particular synapse—most neurons are both presynaptic and postsynaptic. There are two types of synapses: chemical and electrical.

Chemical Synapse

When an action potential reaches the axon terminal it depolarizes the membrane and opens voltage-gated Na+ channels. Na+ ions enter the cell, further depolarizing the presynaptic membrane. This depolarization causes voltage-gated Ca2+ channels to open. Calcium ions entering the cell initiate a signaling cascade that causes small membrane-bound vesicles, called synaptic vesicles, containing neurotransmitter molecules to fuse with the presynaptic membrane. Synaptic vesicles are shown in Figure 35.14, which is an image from a scanning electron microscope.

The axon terminal is spherical. A section is sliced off, revealing small blue and orange vesicles just inside.
Figure 35.14 This pseudocolored image taken with a scanning electron microscope shows an axon terminal that was broken open to reveal synaptic vesicles (blue and orange) inside the neuron. (credit: modification of work by Tina Carvalho, NIH-NIGMS; scale-bar data from Matt Russell)

Fusion of a vesicle with the presynaptic membrane causes neurotransmitter to be released into the synaptic cleft, the extracellular space between the presynaptic and postsynaptic membranes, as illustrated in Figure 35.15. The neurotransmitter diffuses across the synaptic cleft and binds to receptor proteins on the postsynaptic membrane.

Illustration shows a narrow axon of a presynaptic cell widening into a bulb-like axon terminal. A narrow synaptic cleft separates the axon terminal of the presynaptic cell from the postsynaptic cell. In step 1, an action potential arrives at the axon terminal. In step 2, the action potential causes voltage-gated calcium channels in the axon terminal open, allowing calcium to enter. In step 3, calcium influx causes neurotransmitter-containing synaptic vesicles to fuse with the plasma membrane. Contents of the vesicles are released into the synaptic cleft by exocytosis. In step 4, neurotransmitter diffuses across the synaptic cleft and binds ligand-gated ion channels on the postsynaptic membrane, causing the channels to open. In step 5, the open channels cause ion movement into or out of the cell, resulting in a localized change in membrane potential. In step 6, reuptake by the presynaptic neuron, enzymatic degradation and diffusion reduce neurotransmitter levels, terminating the signal.
Figure 35.15 Communication at chemical synapses requires release of neurotransmitters. When the presynaptic membrane is depolarized, voltage-gated Ca2+ channels open and allow Ca2+ to enter the cell. The calcium entry causes synaptic vesicles to fuse with the membrane and release neurotransmitter molecules into the synaptic cleft. The neurotransmitter diffuses across the synaptic cleft and binds to ligand-gated ion channels in the postsynaptic membrane, resulting in a localized depolarization or hyperpolarization of the postsynaptic neuron.

The binding of a specific neurotransmitter causes particular ion channels, in this case ligand-gated channels, on the postsynaptic membrane to open. Neurotransmitters can either have excitatory or inhibitory effects on the postsynaptic membrane, as detailed in Table 35.1. For example, when acetylcholine is released at the synapse between a nerve and muscle (called the neuromuscular junction) by a presynaptic neuron, it causes postsynaptic Na+ channels to open. Na+ enters the postsynaptic cell and causes the postsynaptic membrane to 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 (IPSPs), a hyperpolarization of the presynaptic membrane. For example, when the neurotransmitter GABA (gamma-aminobutyric acid) is released from a presynaptic neuron, it binds to and opens Cl- channels. Cl- ions enter the cell and hyperpolarizes the membrane, making the neuron less likely to fire an action potential.

Once neurotransmission has occurred, the neurotransmitter 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 cleft, it can be degraded by enzymes in the synaptic cleft, or it 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 acetylcholinesterase, the enzyme that degrades acetylcholine. This inhibition of the enzyme essentially increases neurotransmission at synapses that release acetylcholine. Once released, the acetylcholine stays in the cleft and can continually bind and unbind to postsynaptic receptors.

Neurotransmitter Function and Location
Neurotransmitter Example Location
Acetylcholine CNS and/or PNS
Biogenic amine Dopamine, serotonin, norepinephrine CNS and/or PNS
Amino acid Glycine, glutamate, aspartate, gamma aminobutyric acid CNS
Neuropeptide Substance P, endorphins CNS and/or PNS
Table 35.2

Electrical Synapse

While electrical synapses are fewer in number than chemical synapses, they are found in all nervous systems and play important and unique roles. The mode of neurotransmission in electrical synapses is quite different from that in chemical synapses. In an electrical synapse, the presynaptic and postsynaptic membranes are very close together and are actually physically connected by channel proteins forming gap junctions. Gap junctions allow current to pass directly from one cell to the next. In addition to the ions that carry this current, 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 on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is 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 are bidirectional. Electrical synapses are also more reliable as they are less likely to be blocked, and they are important for synchronizing the electrical activity of a group of neurons. For example, electrical synapses in the thalamus are thought to regulate slow-wave sleep, and disruption of these synapses can cause seizures.

Signal Summation

Sometimes a single EPSP is strong enough to induce an action potential in the postsynaptic neuron, but often multiple presynaptic inputs must create EPSPs around the same time for the postsynaptic neuron to be sufficiently depolarized to fire an action potential. This process is called summation and occurs at the axon hillock, as illustrated in Figure 35.16. Additionally, one neuron often has inputs from many presynaptic neurons—some excitatory and some inhibitory—so IPSPs can cancel out EPSPs and vice versa. It is the net change in postsynaptic membrane voltage that determines whether the postsynaptic cell has reached its threshold of excitation needed to fire an action potential. Together, synaptic summation and the threshold for excitation act as a filter so that random “noise” in the system is not transmitted as important information.

Illustration shows the location of the axon hillock, which is the area connecting the neuron body to the axon. A graph shows the summation of membrane potentials at the axon hillock, plotted as membrane potential in millivolts versus time. Initially, the membrane potential at the axon hillock is minus 70 millivolts. A series of E P S Ps and I P S Ps cause the potential to rise and fall. Eventually, the potential increases to the threshold of excitation. At this point the nerve fires, resulting in a sharp increase in membrane potential, followed by a rapid decrease. The hillock becomes hyperpolarized such that the membrane potential is lower than the resting potential. The hillock then gradually returns to the resting potential.
Figure 35.16 A single neuron can receive both excitatory and inhibitory inputs from multiple neurons, resulting in local membrane depolarization (EPSP input) and hyperpolarization (IPSP input). All these inputs are added together at the axon hillock. If the EPSPs are strong enough to overcome the IPSPs and reach the threshold of excitation, the neuron will fire.

Everyday Connection

Brain-computer interface

Amyotrophic lateral sclerosis (ALS, also called Lou Gehrig’s Disease) is a neurological disease characterized by the degeneration of the motor neurons that control voluntary movements. The disease begins with muscle weakening and lack 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 of the world. One technology, for example, allows patients to type out sentences by twitching their cheek. These sentences can then be read aloud by a computer.

A relatively 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 (BCI) 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 several forms of BCI. Some forms use EEG recordings from electrodes taped onto the skull. These recordings contain information from large populations of neurons that can be decoded by a computer. Other forms of BCI require the implantation of an array of electrodes smaller than a postage stamp in the arm and hand area of the motor cortex. This form of BCI, while more invasive, is very powerful as each electrode can record actual action potentials from one or more neurons. These signals are then sent to a computer, which has been trained to decode the signal and feed it to a tool—such as a cursor on a computer screen. 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 (even though 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 a robotic arm and even to feed herself coffee using BCI technology.

Despite the amazing advancements in BCI technology, it also has limitations. The technology can require many hours of training and long periods of intense concentration for the patient; it can also require brain surgery to implant the devices.

Illustration shows a person in a wheelchair, facing a computer screen. An arrow indicates that neural signals travel from the brain of the paralyzed person to the computer.
Figure 35.17 With brain-computer interface technology, neural signals from a paralyzed patient are collected, decoded, and then fed to a tool, such as a computer, a wheelchair, or a robotic arm.

Link to Learning

Watch this video 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 in action.

Synaptic Plasticity

Synapses are not static structures. They can be weakened or strengthened. They can be broken, and new synapses can be made. Synaptic plasticity allows for these changes, which are all needed for a functioning nervous system. In fact, synaptic plasticity is the basis of learning and memory. Two processes in particular, long-term potentiation (LTP) and long-term depression (LTD) are important forms of synaptic plasticity that occur in synapses in the hippocampus, a brain region that is involved in storing memories.

Long-term Potentiation (LTP)

Long-term potentiation (LTP) is a persistent strengthening of a synaptic connection. LTP is based on the Hebbian principle: cells that fire together wire together. There are various mechanisms, none fully understood, behind the synaptic strengthening seen with LTP. One known mechanism involves a type of postsynaptic glutamate receptor, called NMDA (N-Methyl-D-aspartate) receptors, shown in Figure 35.18. These receptors are normally blocked by magnesium ions; however, when the postsynaptic neuron is depolarized by multiple presynaptic inputs in quick succession (either from one neuron or multiple neurons), the magnesium ions are forced out allowing Ca ions to pass into the postsynaptic cell. Next, Ca2+ ions entering the cell initiate a signaling cascade that causes a different type of glutamate receptor, called AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) receptors, to be inserted into the postsynaptic membrane, since activated AMPA receptors allow positive ions to enter the cell. So, the next time glutamate is released from the presynaptic membrane, it will have a larger excitatory effect (EPSP) on the postsynaptic cell because the binding of glutamate to these AMPA receptors will allow more positive ions into the cell. The insertion of additional AMPA receptors strengthens the synapse and means that the postsynaptic neuron is more likely to fire in response to presynaptic neurotransmitter release. Some drugs of abuse co-opt the LTP pathway, and this synaptic strengthening can lead to addiction.

Long-term Depression (LTD)

Long-term depression (LTD) is essentially the reverse of LTP: it is a long-term weakening of a synaptic connection. One mechanism known to cause LTD also involves AMPA receptors. In this situation, calcium that enters through NMDA receptors initiates a different signaling cascade, which results in the removal of AMPA receptors from the postsynaptic membrane, as illustrated in Figure 35.18. The decrease in AMPA receptors in the membrane makes the postsynaptic neuron less responsive to glutamate released from the presynaptic neuron. While it may seem counterintuitive, LTD may be just as important for learning and memory as LTP. The weakening and pruning of unused synapses allows for unimportant connections to be lost and makes the synapses that have undergone LTP that much stronger by comparison.

Illustration shows the mechanism of L T P and L T D. Normally, the N M D A receptor in the postsynaptic neuron is activated by glutamate binding, but only after depolarization removes an inhibitory magnesium ion. Once the magnesium is removed, calcium can enter the cell. In response to an increase in intracellular calcium, A M P A receptors are inserted into the plasma membrane, which amplifies the signal resulting in L T P. L D P occurs when low-frequency stimulation results in the activation of a different calcium-signaling cascade that causes A M P A receptors to be removed from the plasma membrane. As a result, the nerve cell becomes less responsive to glutamate.
Figure 35.18 Calcium entry through postsynaptic NMDA receptors can initiate two different forms of synaptic plasticity: long-term potentiation (LTP) and long-term depression (LTD). LTP arises when a single synapse is repeatedly stimulated. This stimulation causes a calcium- and CaMKII-dependent cellular cascade, which results in the insertion of more AMPA receptors into the postsynaptic membrane. The next time glutamate is released from the presynaptic cell, it will bind to both NMDA and the newly inserted AMPA receptors, thus depolarizing the membrane more efficiently. LTD occurs when few glutamate molecules bind to NMDA receptors at a synapse (due to a low firing rate of the presynaptic neuron). The calcium that does flow through NMDA receptors initiates a different calcineurin and protein phosphatase 1-dependent cascade, which results in the endocytosis of AMPA receptors. This makes the postsynaptic neuron less responsive to glutamate released from the presynaptic neuron.
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