35: The Nervous System Flashcards
What are some examples of invertebrate nervous systems?
Some organisms, like sponges, lack a true nervous system. Others, like cnidarians, lack a true brain and instead have a system of separate but connected nerve cells (neurons) called a “nerve net”. Echinoderms have nerve cells that are bundled into fibers called nerves. Flatworms have both a central nervous system (CNS), made up of a small “brain” and two nerve cords, and a peripheral nervous system (PNS) containing a system of nerves that extend throughout the body. The insect nervous system is more complex but also fairly decentralized. It contains a brain, ventral nerve cord, and ganglia (clusters of connected neurons). These ganglia can control movements and behaviors without input from the brain. Octopi may have the most complicated of invertebrate nervous systems—they have neurons that are organized in specialized lobes and eyes that are structurally similar to vertebrate species.
What are some differences between invertebrate and vertebrate nervous systems?
Vertebrate nervous systems are more complex, centralized, and specialized. While there is great diversity among different vertebrate nervous systems, they all share a basic structure: a CNS that contains a brain and spinal cord and a PNS made up of peripheral sensory and motor nerves. The nerve cords of many invertebrates are located ventrally whereas the vertebrate spinal cords are located dorsally. There is debate among evolutionary biologists as to whether these different nervous system plans evolved separately or whether the invertebrate body plan arrangement somehow “flipped” during the evolution of vertebrates.
What are the cell types of the nervous system?
The nervous system is made up of neurons, specialized cells that can receive and transmit chemical or electrical signals, and glia, cells that provide support functions for the neurons by playing an information processing role that is complementary to neurons.
What is an analogy for the nervous system?
A neuron can be compared to an electrical wire—it transmits a signal from one place to another. Glia can be compared to the workers at the electric company who make sure wires go to the right places, maintain the wires, and take down wires that are broken. Although glia have been compared to workers, recent evidence suggests that they also usurp some of the signaling functions of neurons.
What are some examples of neuron count in different organisms?
The nervous system of Drosophila melanogaster contains around 100K neurons, the same as a lobster. A mouse contains around 75M neurons, an octopus around 300M neurons, and the human brain around 86B neurons.
What are dendrites?
Dendrites are tree-like structures that extend away from the cell body to receive messages from other neurons at specialized junctions called synapses. Although some neurons do not have any dendrites, some types of neurons have multiple dendrites. Dendrites can have small protrusions called dendritic spines, which further increase surface area for possible synaptic connections.
What does an axon do?
Once a signal is received by a dendrite, it then travels passively to the cell body. The cell body contains a specialized structure, the axon hillock that integrates signals from multiple synapses and serves as a junction between the cell body and an axon. An axon is a tube-like structure that propagates the integrated signal to specialized endings called axon terminals. These terminals in turn synapse on other neurons, muscle, or target organs. Chemicals released at axon terminals allow signals to be communicated to these other cells. Neurons usually have one or two axons, but some neurons, like amacrine cells in the retina, do not contain any axons.
What is myelin?
Some axons are covered with myelin, which acts as an insulator to minimize dissipation of the electrical signal as it travels down the axon, greatly increasing the speed on conduction. This insulation is important as the axon from a human motor neuron can be as long as a meter—from the base of the spine to the toes. The myelin sheath is not actually part of the neuron. Myelin is produced by glial cells.
What are nodes of Ranvier?
Along the axon there are periodic gaps in the myelin sheath. These gaps are called nodes of Ranvier and are sites where the signal is “recharged” as it travels along the axon.
How do neurons form a network?
A single neuron does not act alone—neuronal communication depends on the connections that neurons make with one another (as well as with other cells, like muscle cells). Dendrites from a single neuron may receive synaptic contact from many other neurons. For example, dendrites from a Purkinje cell in the cerebellum are thought to receive contact from as many as 200,000 other neurons.
What are some examples of different types of neurons?
Examples include a pyramidal cell from the cerebral cortex, a Purkinje cell from the cerebellar cortex, and an olfactory cell from the olfactory epithelium and olfactory bulb.
What are the basic types of neurons?
Neurons are broadly divided into four basic types: unipolar, bipolar, multipolar, and pseudounipolar.
What are unipolar neurons?
Unipolar neurons have only one structure that extends away from the soma. These neurons are not found in vertebrates but are found in insects where they stimulate muscles or glands.
What are bipolar neurons?
A bipolar neuron has one axon and one dendrite extending from the soma. An example of a bipolar neuron is a retinal bipolar cell, which receives signals from photoreceptor cells that are sensitive to light and transmits these signals to ganglion cells that carry the signal to the brain.
What are multipolar neurons?
Multipolar neurons are the most common type of neuron. Each multipolar neuron contains one axon and multiple dendrites. Multipolar neurons can be found in the central nervous system (brain and spinal cord). An example of a multipolar neuron is a Purkinje cell in the cerebellum, which has many branching dendrites but only one axon.
What are pseudounipolar neurons?
Pseudounipolar cells share characteristics with both unipolar and bipolar cells. A pseudounipolar cell has a single process that extends from the soma, like a unipolar cell, but this process later branches into two distinct structures, like a bipolar cell. Most sensory neurons are pseudounipolar and have an axon that branches into two extensions: one connected to dendrites that receive sensory information and another that transmits this information to the spinal cord.
How was neurogenesis discovered?
At one time, scientists believed that people were born with all the neurons they would ever have. Research performed during the last few decades indicates that neurogenesis, the birth of new neurons, continues into adulthood. Neurogenesis was first discovered in songbirds that produce new neurons while learning songs. For mammals, new neurons also play an important role in learning: about 1000 new neurons develop in the hippocampus (a brain structure involved in learning and memory) each day. While most of the new neurons will die, researchers found that an increase in the number of surviving new neurons in the hippocampus correlated with how well rats learned a new task. Both exercise and some antidepressant medications also promote neurogenesis in the hippocampus. Stress has the opposite effect. While neurogenesis is quite limited compared to regeneration in other tissues, research in this area may lead to new treatments for disorders such as Alzheimer’s, stroke, and epilepsy.
How can new neurons be identified?
A compound called bromodeoxyuridine (BrdU) can be injected into the brain of an animal. While all cells will be exposed to BrdU, BrdU will only be incorporated into the DNA of newly generated cells that are in S phase. A technique called immunohistochemistry can be used to attach a fluorescent label to the incorporated BrdU, and a researcher can use fluorescent microscopy to visualize the presence of BrdU, and thus new neurons, in brain tissue.
How can new astrocytes be differentiated from new neurons?
Cells that are actively dividing have bromodeoxyuridine (BrdU) incorporated into their DNA and are labeled in red. Cells that express glial fibrillary acidic protein (GFAP) are labeled in green. Astrocytes, but not neurons, express GFAP. Thus, cells that are labeled both red and green are actively dividing astrocytes, whereas cells labeled red only are actively dividing neurons.
What do glia do?
While glia are often thought of as the supporting cast of the nervous system, the number of glial cells in the brain actually outnumbers the number of neurons by a factor of ten. Neurons would be unable to function without the vital roles that are fulfilled by these glial cells. Glia guide developing neurons to their destinations, buffer ions and chemicals that would otherwise harm neurons, and provide myelin sheaths around axons. Scientists have recently discovered that they also play a role in responding to nerve activity and modulating communication between nerve cells. When glia do not function properly, the result can be disastrous—most brain tumors are caused by mutations in glia.
What do astrocytes do?
Astrocytes make contact with both capillaries and neurons in the CNS. They provide nutrients and other substances to neurons, regulate the concentrations of ions and chemicals in the extracellular fluid, and provide structural support for synapses. Astrocytes also form the blood-brain barrier—a structure that blocks entrance of toxic substances into the brain. Astrocytes, in particular, have been shown through calcium imaging experiments to become active in response to nerve activity, transmit calcium waves between astrocytes, and modulate the activity of surrounding synapses.
What do satellite glia do?
Satellite glia provide nutrients and structural support for neurons in the PNS.
What do microglia do?
Microglia scavenge and degrade dead cells and protect the brain from invading microorganisms.
What do oligodendrocytes do?
Oligodendrocytes form myelin sheaths around axons in the CNS. One axon can be myelinated by several oligodendrocytes, and one oligodendrocyte can provide myelin for multiple neurons.
What do Schwann cells do?
In contrast to oligodendrocytes, in the PNS a single Schwann cell provides myelin for only one axon as the entire Schwann cell surrounds the axon.
What do radial glia do?
Radial glia serve as scaffolds for developing neurons as they migrate to their end destinations.
What do ependymal cells do?
Ependymal cells line fluid-filled ventricles of the brain and the central canal of the spinal cord. They are involved in the production of cerebrospinal fluid, which serves as a cushion for the brain, moves the fluid between the spinal cord and the brain, and is a component for the choroid plexus.
What allows neurons to transmit signals?
These signals are possible because each neuron has a charged cellular membrane (a voltage difference between the inside and outside), and the charge of this membrane can change in response to neurotransmitter molecules released from other neurons and environmental stimuli.
How do charged molecules and ions cross 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. 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.
What are voltage-gated ion channels?
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.
What is membrane potential?
The difference in total charge between the inside and outside of a cell.
When are voltage-gated ion channels inactivated?
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.
What is the 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, however 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.
How is the resting membrane potential established and maintained?
The difference in the number of positively charged potassium ions (K+) inside and outside the cell dominates the resting membrane potential. 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 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. It works by bringing 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. Chloride ions (Cl—) tend to accumulate outside of the cell because they are repelled by negatively-charged proteins within the cytoplasm.
How does a membrane potential change?
At the resting potential, all voltage-gated Na+ channels and most voltage-gated K+ channels are closed. The Na+/K+ transporter pumps K+ ions into the cell and Na+ ions out.
In response to a depolarization, some Na+ channels open, allowing Na+ ions to enter the cell. The membrane starts to depolarize (the charge across the membrane lessens). If the threshold of excitation is reached, all the Na+ channels open.
At the peak action potential, Na+ channels close while K+ channels open. K+ leaves the cell, and the membrane eventually becomes hyperpolarized.
What is an 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.
What happens when a neuron becomes depolarized?
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 the 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 center the cell. 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.
What happens when a neuron becomes hyperpolarized?
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.
How does an action potential spread down an axon?
In response to a signal, the soma end of the axon becomes depolarized.
The depolarization spreads down the axon. Meanwhile, the first part of the membrane repolarizes. Because Na+ channels are inactivated and additional K+ channels have opened, the membrane cannot depolarize again.
The action potential continues to travel down the axon, where the first part of the membrane becomes hyperpolarized as it re-establishes the resting membrane potential.
How is the speed of conduction of an action potential determined?
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.
What does myelin do?
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.
What do nodes of Ranvier do?
The nodes of Ranvier 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.
What do synapses do?
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.
How are neurotransmitters released in a 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.
How do neurotransmitters transmit a signal in a chemical synapse?
Fusion of a vesicle with the presynaptic membrane causes neurotransmitters to be released into the synaptic cleft, the extracellular space between the presynaptic and postsynaptic membranes. The neurotransmitter diffuses across the synaptic cleft and binds to receptor proteins on the postsynaptic membrane.
How are signals transmitted in chemical synapses?
- Action potential arrives at axon terminal.
- Voltage-gated Ca2+ channels open and Ca2+ enters the axon terminal.
- Ca2+ entry causes neurotransmitter-containing synaptic vesicles to release their contents by exocytosis.
- Neurotransmitter diffuses across the synaptic cleft and binds to ligand-gated ion channels on the postsynaptic membrane.
- Binding of neurotransmitter opens ligand-gated ion channels, resulting in graded potentials.
- Reuptake by the presynaptic neuron, enzymatic degradation, and diffusion reduce neurotransmitter levels, terminating the signal.
What happens when a neurotransmitter binds a ligand-gated ion channel?
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.
What is an example of excitatory postsynaptic potential (EPSP)?
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.
What is an example of an inhibitory postsynaptic potential (IPSP)?
Release of neurotransmitter at inhibitory synapses causes inhibitory postsynaptic potentials (IPSPs), a hyperpolarization of the postsynaptic 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.
How are the conditions for signal transmission in a chemical synapse reset?
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.
What is an example of a drug that inhibits neurotransmitter degradation in chemical synapses?
Several drugs act at this step of neurotransmission. For example, some drugs that are given to Alzheimer’s patients works 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.
What are some examples of different chemical neurotransmitters?
Acetylcholine works in the CNS and/or PNS. Biogenic amines such as dopamine, serotonin and norepinephrine work in the CNS and/or PNS. Amino acids such as glycine, glutamate, aspartate and gamma aminobutyric acid work in the CNS. Neuropeptides such as substance P and endorphins work in the CNS and/or PNS.
How do electrical synapses transmit signals?
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 ions that carry this current, other molecules, such as ATP, can diffuse through the large gap junction pores.
What are some 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.
What is 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. 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.
What happens to individuals who suffer from ALS?
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. This 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.
How are machines used to treat ALS?
At the point of paralysis, 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.
What is a brain-computer interface (BCI)?
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. It allows paralyzed patients to control a computer using only their thoughts.
What are some different forms of BCI?
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.
How can BCI be used to treat patients with ALS?
Signals from BCI are 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 email, 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.
What are some limitations of BCI technology?
Despite the advancements in BCI technology, it 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.
What is 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. 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.
How does long-term potentiation (LTP) work?
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. These receptors are normally blocked by magnesium ions; however, when the postsynaptic neuron is depolarized by multiple pre-synaptic inputs in quick succession (either from one neuron or multiple neurons), the magnesium ions are forced out allowing Ca2+ 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.