Chapter 16. The Nervous System
learning goals
At the end of this section you can:
- Describe the basis of the resting membrane potential.
- Explain the stages of an action potential and how action potentials propagate.
- Explain the similarities and differences between chemical and electrical synapses.
- Describe long-term potentiation and long-term depression.
All the functions carried out by the nervous system, from a simple motor reflex to more advanced functions such as remembering or making a decision, require neurons to communicate with each other. While humans use words and body language to communicate, neurons use electrical and chemical signals. Like a person in a committee, a neuron normally receives and synthesizes messages from several other neurons before "making the decision" to send the message 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 cell membrane (a voltage difference between the inside and the outside) and the charge on this membrane can change in response to neurotransmitter molecules released by other neurons and environmental stimuli. To understand how neurons communicate, one must first understand the baseline or "resting" membrane charge basis.
Neural charged membranes
The lipid bilayer membrane that surrounds a neuron is impermeable to charged molecules or ions. To enter or leave 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 shown in Figure 16.9. Some ion channels must be activated to open and allow ions to enter or leave the cell. These ion channels are sensitive to the environment and can change 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 total charge difference between the inside and outside of the cell is called Membrane potential.
concept in action
go deadVideodiscusses the basis of the resting membrane potential.
Ruhemembranpotencial
A resting neuron is negatively charged: the inside of a cell is about 70 millivolts more negative than the outside (−70 mV, note that this number varies by neuron type and species). This voltage is called the resting membrane potential; it is caused by differences in ion concentrations inside and outside the cell. If the membrane were equally permeable to all ions, any type of ion would flow through the membrane and the system would reach equilibrium. Because ions cannot simply cross the membrane at will, different concentrations of multiple ions exist inside and outside the cell, as shown in FIG.Tabla 16.1. The difference in the number of positively charged potassium ions (K+) inside and outside the cell is dominated by the resting membrane potential (Figure 16.10). When the membrane is at rest, K+Ions accumulate within the cell due to net movement down 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 inside the cell is created because the cell membrane is more permeable to the movement of potassium ions than to the movement of sodium ions. In neurons, potassium ions are held in high concentrations inside the cell, while sodium ions are held in high concentrations outside of the cell. The cell has potassium and sodium leakage channels that allow the two cations to diffuse down their concentration gradient. However, neurons have many more potassium leak channels than sodium leak channels. Therefore, potassium diffuses out of the cell much faster than sodium enters it. Since more cations leave the cell than enter, this makes the inside of the cell negatively charged relative to the outside of the cell. The actions of the sodium-potassium pump help maintain the resting potential once established. Remember that sodium-potassium pumps bring two K+-ions in the cell while three Na are removed+ions per ATP consumed. Because more cations are expelled from the cell than are taken up, the interior of the cell remains negatively charged relative to the extracellular fluid. It should be noted that calcium ions (Cl–) tend to accumulate outside the cell as they are repelled by negatively charged proteins in the cytoplasm.
| Ion concentration inside and outside neurons. | |||
|---|---|---|---|
| Ion | Extracellular concentration (mM) | Intracellular concentration (mM) | outside/inside relationship |
| nice+ | 145 | 12 | 12 |
| K+ | 4 | 155 | 0,026 |
| Kl− | 120 | 4 | 30 |
| Organic anions (A−) | — | 100 | |
action potential
A neuron can receive information from other neurons and, if that information is strong enough, transmit the signal to subsequent neurons. Transmission of a signal between neurons is usually accomplished by a chemical called a neurotransmitter. The transmission of a signal within a neuron (from the dendrite to the axon terminal) occurs through a brief reversal of the resting membrane potential, called firing. action potential. When neurotransmitter molecules bind to receptors located on the dendrites of a neuron, ion channels open. In excitatory synapses, this opening allows positive ions to enter the neuron and leads to depolarizationmembrane - a decrease in the voltage difference 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). N/A+Channels in the axon hillock open, allowing positive ions to enter the cell (Figure 16.10yFigure 16.11). Once the sodium channels open, the neuron is fully depolarized to a membrane potential of about +40 mV. Action potentials are considered an "all or nothing" event because the neuron always fully depolarizes upon reaching the threshold potential. After depolarization is complete, the cell must now "reset" its membrane voltage to the resting potential. To achieve this, the Na+The channels are closed and cannot be opened. Here begins the neuron refractory period, in which it cannot generate another action potential because its sodium channels do not open. K voltage controlled simultaneously+Open channels, causing K+to get out of the cell. Questions+ions leave the cell, the membrane potential returns to negative. The spread of K+actually out of cell hyperpolarizedof the cell by making the membrane potential more negative than the normal resting potential of the cell. At this point, the sodium channels return to their quiescent state, which means that they are ready to open again when the membrane potential crosses the threshold potential again. Finally the extra K+Ions diffuse out of the cell through potassium leak channels, bringing the cell from its hyperpolarized state to its resting membrane potential.
Potassium channel blockers, such as amiodarone and procainamide, which are used to treat abnormal electrical activity in the heart called arrhythmia, prevent the movement of K+by controlled voltage K+channels. What part of the action potential would you expect from potassium channels?
concept in action
go deadVideogives an overview of action potentials.
Myelin and propagation of the action potential.
For an action potential to transmit information to another neuron, it must travel down the axon and reach the axon terminals, where it can initiate neurotransmitter release. The conduction velocity of an action potential down an axon is affected by both the diameter of the axon and the resistance of the axon to leakage current. Myelin acts as an insulator preventing current from leaving the axon; This increases the conduction velocity of the action potential. In demyelinating diseases such as multiple sclerosis, action potential conduction slows because current leaks from previously isolated areas of axons. Ranvier's knots illustrated inFigure 16.13are gaps in the myelin sheath along the axon. These myelinated spaces are approximately one micron in length and contain voltage-gated Na.+yk+channels. Ion flow through these channels, especially Na+channels, the action potential is repeatedly regenerated along the length of the axon. This "jump" of the action potential from one node to the next is called a "jump." saltatory line. If there were no Ranvier nodes along an axon, the action potential would propagate very slowly because Na+yk+The channels would need to continually regenerate action potentials at every point along the axon, rather than at specific points. Ranvier's nodes also conserve energy for the neuron because the channels only need to be present in the nodes rather than along the entire length of the axon.
synaptic transmission
The synapse, or "gap," is the place where information is passed from one neuron to another. Synapses generally 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 that sends the signal is called the presynaptic neuron and the neuron that receives the signal is called the postsynaptic neuron. Note that these terms refer to a specific synapse: most neurons are both presynaptic and postsynaptic. There are two types of synapses: chemical and electrical.
When an action potential reaches the axon terminal, it depolarizes the membrane and opens voltage-dependent Na.+channels. Y+The ions enter the cell and further depolarize the presynaptic membrane. This depolarization causes voltage-dependent Ca2+to open channels. Calcium ions entering the cell initiate a signaling cascade that causes small membrane-bound vesicles called synaptic vesicle, which contains neurotransmitter molecules to fuse with the presynaptic membrane. Synaptic vesicles are shown inFigure 16.14, which is an image from a scanning electron microscope.
Fusion of a vesicle with the presynaptic membrane causes neurotransmitters to be released across the membrane. synaptic cleft, the extracellular space between the presynaptic and postsynaptic membranes, as shown inFigure 16.15. The neurotransmitter diffuses across the synaptic cleft and binds to receptor proteins on the postsynaptic membrane.
Binding of a specific neurotransmitter opens specific ion channels, in this case ligand-gated channels, in the postsynaptic membrane. Neurotransmitters can have excitatory or inhibitory effects on the postsynaptic membrane, as detailed inTabla 16.2. For example, when acetylcholine is released from a presynaptic neuron at the synapse between a nerve and a muscle (called the neuromuscular junction), it causes postsynaptic Na+to open channels. N/A+enters the postsynaptic cell and causes depolarization of the postsynaptic membrane. This depolarization is called Exzitatorisches postsynaptisches Potencial (EPSP)and increases the likelihood that the postsynaptic neuron will fire an action potential. release of neurotransmitters at inhibitory synapses 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 Cl and opens it.–channels. class–The ions enter the cell and hyperpolarize 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 to allow the postsynaptic membrane to "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 work on this step of neurotransmission. For example, some medications given to Alzheimer's patients work by inhibiting acetylcholinesterase, the enzyme that breaks down acetylcholine. This enzyme inhibition essentially increases neurotransmission at synapses that release acetylcholine. Once released, acetylcholine remains in the cleft and can continually bind and unbind from postsynaptic receptors.
| neurotransmitter | example | ort |
|---|---|---|
| acetylcholine | — | SNC y/o SNP |
| Amin Biogenes | Dopamina, Serotonina, Noradrenalina | SNC y/o SNP |
| amino acids | Glycine, glutamate, aspartate, gamma-aminobutyric acid | ZNS |
| neuropeptide | substance P, endorphins | SNC y/o SNP |
electrical synapse
Although electrical synapses are less numerous than chemical synapses, they are found in all nervous systems and play an important and unique role. The nature of neurotransmission at electrical synapses is quite different from that at chemical synapses. In an electrical synapse, the presynaptic and postsynaptic membranes are close together and are actually physically connected by channel proteins that form gap junctions. Open junctions allow current to flow 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 pores of the gap junctions.
There are key differences between chemical and electrical synapses. Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to propagate their signal, there is a delay of about a millisecond between the time the axon's potential reaches the presynaptic end and the time the axon is released. neurotransmitter begins to open postsynaptic ion channels. Also, this signage is one-way. By contrast, signaling at electrical synapses is nearly instantaneous (which is important for synapses involved in cue reflexes), and some electrical synapses are bidirectional. Electrical synapses are also more reliable because they are less likely to block and are important in synchronizing the electrical activity of a group of neurons. For example, electrical synapses in the thalamus are thought to regulate deep sleep, and disruption of these synapses can cause seizures.
sum of signals
Sometimes a single EPSP is strong enough to induce an action potential in the postsynaptic neuron, but often multiple presynaptic inputs must generate EPSPs at approximately the same time for the postsynaptic neuron to depolarize enough to elicit an action potential. action. This process is called totaland occurs in the axon hillock as shown inFigure 16.16. Also, a neuron often receives inputs from many presynaptic neurons, some excitatory and some inhibitory, so IPSPs can cancel EPSPs and vice versa. It is the net change in the postsynaptic membrane voltage that determines whether the postsynaptic cell has reached the excitation threshold necessary to initiate an action potential. Synaptic summation and arousal threshold work together as a filter so that random "noise" in the system is not transmitted as important information.
brain-computer interface
Amyotrophic lateral sclerosis (ALS, also known as Lou Gehrig's disease) is a neurological disorder characterized by degeneration of motor neurons that control voluntary movement. The disease begins with muscle weakness and incoordination, eventually destroying neurons that control speech, breathing, and swallowing; In the end, the disease can lead to paralysis. At this point, patients need the help of machines to breathe and communicate. Various specialized technologies have been developed to allow "locked-out" patients to communicate with the rest of the world. For example, one technology allows patients to write sentences by moving their cheeks. These sentences can then be read by a computer.
A relatively new line of research that is helping paralyzed patients, including those with ALS, to communicate and maintain some level of self-sufficiency is called brain-computer interface (BCI) technology and is illustrated inFigure 16.17. This technology sounds like science fiction: it allows paralyzed patients to control a computer with just their thoughts. There are different forms of BCI. Some forms use EEG recordings from electrodes attached to 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 into the motor cortex of the arm and hand. Although more invasive, this form of BCI is very powerful because each electrode can record the actual action potentials of one or more neurons. These signals are then sent to a computer, which has been trained to decode the signal and send it to a tool, such as a cursor on a computer screen. This means that an ALS patient can use email, read the Internet, and communicate with others by remembering to move their hand or arm (even if the paralyzed patient cannot make that body movement). Recent advances have allowed a paralyzed incarcerated patient who suffered a stroke 15 years ago to control a robotic arm and even use BCI technology to feed herself coffee.
Despite the incredible advances in BCI technology, it also has limitations. The technology can require many hours of training and long periods of intense concentration for the patient; Brain surgery may also be required to implant the devices.
concept in action
clockIt's videoin which a paralyzed woman uses a brain-controlled robotic arm to pop a drink into 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 destroy and form new synapses. Synaptic plasticity enables these changes, all of which are necessary for the functioning of the 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 at synapses in the hippocampus, a brain region involved in memory storage.
Long Term Potentiation (LTP)
Long Term Potentiation (LTP)it is a sustained reinforcement of a synaptic connection. LTP is based on the Hebbian principle: cells that fire together connect. There are several mechanisms, none of which are fully understood, behind the observed synaptic enhancement in LTP. One known mechanism involves a type of postsynaptic glutamate receptor called the NMDA (N-methyl-D-aspartate) receptor, shown inFigure 16.18. These receptors are normally blocked by magnesium ions; However, when the postsynaptic neuron is depolarized by multiple presynaptic inputs in rapid succession (either from one or several neurons), magnesium ions are ejected, allowing Ca ions to enter the postsynaptic cell. Next approx.2+Ions entering the cell initiate a signaling cascade that causes another class of glutamate receptors, called AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) receptors, to insert into the postsynaptic membrane. , as AMPA is activated. Receptors allow positive ions to enter the cell. So the next time glutamate is released from the presynaptic membrane, it will have a greater excitatory effect (EPSP) on the postsynaptic cell because glutamate binding to these AMPA receptors allows more positive ions to enter 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 the release of presynaptic neurotransmitters. 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)it is essentially the opposite of LTP: it is a long-term weakening of a synaptic connection. A mechanism known to cause LTD also involves AMPA receptors. In this situation, calcium entering through NMDA receptors initiates another signaling cascade that leads to removal of AMPA receptors from the postsynaptic membrane, as shown in FIG.Figure 16.18. The decrease in AMPA receptors on the membrane makes the postsynaptic neuron less sensitive to glutamate released by the presynaptic neuron. While it may seem counterintuitive, LTD may be just as important as LTP for learning and memory. The weakening and pruning of unused synapses allows for the loss of insignificant connections and makes synapses that have undergone LTP much stronger in comparison.
abstract
Neurons have charged membranes because there are different concentrations of ions inside and outside the cell. Voltage-gated ion channels control the movement of ions in and out of a neuron. When a neuronal membrane depolarizes to at least the excitation threshold, an action potential is triggered. The action potential then propagates along a myelinated axon to the axon terminals. In a chemical synapse, the action potential causes the release of neurotransmitter molecules into the synaptic cleft. By binding to postsynaptic receptors, the neurotransmitter can induce excitatory or inhibitory postsynaptic potentials by depolarizing or hyperpolarizing the postsynaptic membrane. At electrical synapses, the action potential is communicated directly to the postsynaptic cell via gap junctions, large channel proteins that connect the presynaptic and postsynaptic membranes. Synapses are not static structures and can grow stronger and weaker. Two mechanisms of synaptic plasticity are long-term potentiation and long-term depression.
training
- Potassium channel blockers, such as amiodarone and procainamide, which are used to treat abnormal electrical activity in the heart called arrhythmia, prevent the movement of K+ through voltage-gated K+ channels. What part of the action potential would you expect from potassium channels?
- For a neuron to fire an action potential, its membrane must reach ________.
- hyperpolarization
- arousal threshold
- the refractory period
- Inhibitory postsynaptic potential
- After an action potential, the opening of additional voltage-gated ________ channels and the inactivation of sodium channels cause the membrane to return to its resting membrane potential.
- Sodium
- Potassium
- soccer
- Chloride
- What do you call the protein channels that connect two neurons in an electrical synapse?
- synaptic vesicle
- voltage gated ion channels
- Gap-Junction-Protein
- Sodium and potassium exchange pumps
- How does myelin support the propagation of an action potential down an axon? How do Ranvier nodes support this process?
- What are the main steps in chemical neurotransmission?
answers
- Potassium channel blockers slow down the repolarization phase but have no effect on depolarization.
- B
- B
- C
- Myelin prevents current from leaving the axon. Ranvier's nodes allow action potential regeneration at specific points along the axon. They also conserve energy for the cell because voltage-gated ion channels and sodium and potassium transporters are not needed along the myelinated portions of the axon.
- An action potential travels down an axon until it depolarizes the membrane at one axon terminal. Membrane depolarization causes voltage-dependent Ca2+Open channels and ca2+to enter the cell. Intracellular calcium influx causes synaptic vesicles containing neurotransmitters to fuse with the presynaptic membrane. The neurotransmitter diffuses across the synaptic cleft and binds to receptors on the postsynaptic membrane. Depending on the specific neurotransmitter and postsynaptic receptor, this action can result in the entry of positive (excitatory postsynaptic potential) or negative (inhibitory postsynaptic potential) ions into the cell.
glossary
- action potential
- transient self-propagating change in electrical potential across the membrane of a neuron (or muscle)
- depolarization
- Change in membrane potential to a less negative value
- Exzitatorisches postsynaptisches Potencial (EPSP)
- Depolarization of a postsynaptic membrane caused by neurotransmitter molecules released from a presynaptic cell
- hyperpolarization
- Change in membrane potential to a more negative value
- Inhibitory postsynaptic potential (IPSP)
- Hyperpolarization of a postsynaptic membrane caused by neurotransmitter molecules released from a presynaptic cell
- Long-term depression (LTD)
- prolonged decrease in synaptic coupling between a pre- and post-synaptic cell
- Membrane potential
- Difference in electrical potential between the inside and outside of a cell
- refractory period
- Period of time after an action potential when it is most difficult or impossible to trigger an action potential; caused by inactivation of sodium channels and activation of additional membrane potassium channels
- saltatory line
- "Jumping" of an action potential along an axon from one Ranvier node to the next
- total
- Process of multiple presynaptic inputs that generate EPSPs at approximately the same time so that the postsynaptic neuron depolarizes enough to initiate an action potential.
- synaptic cleft
- Gap between the presynaptic and postsynaptic membrane
- synaptic vesicle
- spherical structure that contains a neurotransmitter