35: The Nervous System Flashcards

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1
Q

What are some examples of invertebrate nervous systems?

A

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.

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2
Q

What are some differences between invertebrate and vertebrate nervous systems?

A

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.

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3
Q

What are the cell types of the nervous system?

A

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.

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4
Q

What is an analogy for the nervous system?

A

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.

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5
Q

What are some examples of neuron count in different organisms?

A

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.

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6
Q

What are dendrites?

A

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.

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7
Q

What does an axon do?

A

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.

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8
Q

What is myelin?

A

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.

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9
Q

What are nodes of Ranvier?

A

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.

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10
Q

How do neurons form a network?

A

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.

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11
Q

What are some examples of different types of neurons?

A

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.

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12
Q

What are the basic types of neurons?

A

Neurons are broadly divided into four basic types: unipolar, bipolar, multipolar, and pseudounipolar.

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13
Q

What are unipolar neurons?

A

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.

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14
Q

What are bipolar neurons?

A

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.

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15
Q

What are multipolar neurons?

A

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.

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16
Q

What are pseudounipolar neurons?

A

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.

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17
Q

How was neurogenesis discovered?

A

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.

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18
Q

How can new neurons be identified?

A

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.

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19
Q

How can new astrocytes be differentiated from new neurons?

A

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.

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20
Q

What do glia do?

A

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.

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21
Q

What do astrocytes do?

A

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.

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22
Q

What do satellite glia do?

A

Satellite glia provide nutrients and structural support for neurons in the PNS.

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23
Q

What do microglia do?

A

Microglia scavenge and degrade dead cells and protect the brain from invading microorganisms.

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24
Q

What do oligodendrocytes do?

A

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.

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25
Q

What do Schwann cells do?

A

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.

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26
Q

What do radial glia do?

A

Radial glia serve as scaffolds for developing neurons as they migrate to their end destinations.

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27
Q

What do ependymal cells do?

A

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.

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28
Q

What allows neurons to transmit signals?

A

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.

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29
Q

How do charged molecules and ions cross membranes?

A

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.

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30
Q

What are voltage-gated ion channels?

A

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.

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31
Q

What is membrane potential?

A

The difference in total charge between the inside and outside of a cell.

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32
Q

When are voltage-gated ion channels inactivated?

A

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.

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33
Q

What is the resting membrane potential?

A

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.

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34
Q

How is the resting membrane potential established and maintained?

A

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.

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35
Q

How does a membrane potential change?

A

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.

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36
Q

What is an action potential?

A

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.

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37
Q

What happens when a neuron becomes depolarized?

A

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.

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38
Q

What happens when a neuron becomes hyperpolarized?

A

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.

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39
Q

How does an action potential spread down an axon?

A

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.

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40
Q

How is the speed of conduction of an action potential determined?

A

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.

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41
Q

What does myelin do?

A

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.

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42
Q

What do nodes of Ranvier do?

A

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.

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43
Q

What do synapses do?

A

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.

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44
Q

How are neurotransmitters released in a chemical synapse?

A

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.

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45
Q

How do neurotransmitters transmit a signal in a chemical synapse?

A

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.

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46
Q

How are signals transmitted in chemical synapses?

A
  1. Action potential arrives at axon terminal.
  2. Voltage-gated Ca2+ channels open and Ca2+ enters the axon terminal.
  3. Ca2+ entry causes neurotransmitter-containing synaptic vesicles to release their contents by exocytosis.
  4. Neurotransmitter diffuses across the synaptic cleft and binds to ligand-gated ion channels on the postsynaptic membrane.
  5. Binding of neurotransmitter opens ligand-gated ion channels, resulting in graded potentials.
  6. Reuptake by the presynaptic neuron, enzymatic degradation, and diffusion reduce neurotransmitter levels, terminating the signal.
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47
Q

What happens when a neurotransmitter binds a ligand-gated ion channel?

A

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.

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48
Q

What is an example of excitatory postsynaptic potential (EPSP)?

A

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.

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49
Q

What is an example of an inhibitory postsynaptic potential (IPSP)?

A

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.

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50
Q

How are the conditions for signal transmission in a chemical synapse reset?

A

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.

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51
Q

What is an example of a drug that inhibits neurotransmitter degradation in chemical synapses?

A

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.

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52
Q

What are some examples of different chemical neurotransmitters?

A

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.

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53
Q

How do electrical synapses transmit signals?

A

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.

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54
Q

What are some differences between chemical and electrical synapses?

A

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.

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55
Q

What is signal summation?

A

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.

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56
Q

What happens to individuals who suffer from ALS?

A

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.

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57
Q

How are machines used to treat ALS?

A

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.

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58
Q

What is a brain-computer interface (BCI)?

A

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.

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59
Q

What are some different forms of BCI?

A

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.

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60
Q

How can BCI be used to treat patients with ALS?

A

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.

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61
Q

What are some limitations of BCI technology?

A

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.

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62
Q

What is synaptic plasticity?

A

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.

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63
Q

How does long-term potentiation (LTP) work?

A

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.

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64
Q

How does long-term depression (LTD) work?

A

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. 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 allow for unimportant connections to be lost and makes the synapses that have undergone LTP that much stronger by comparison.

65
Q

What type of cascade occurs in LTP?

A

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.

66
Q

What type of cascade occurs in LTD?

A

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.

67
Q

What are meninges?

A

The CNS is made up of the brain and spinal cord and is covered with three layers of protective coverings called meninges (from the Greek word for membrane).

68
Q

What is the dura mater?

A

The outermost meninge is the dura mater (Latin for “hard mother”). As the Latin suggests, the primary function for this thick layer is to protect the brain and spinal cord. The dura mater also contains vein-like structures that carry blood from the brain back to the heart.

69
Q

What is the arachnoid mater?

A

The middle meninge is the web-like arachnoid mater.

70
Q

What is the pia mater?

A

The innermost meninge is the pia mater (Latin for “soft mother”), which directly contacts and covers the brain and spinal cord like plastic wrap.

71
Q

What is cerebrospinal fluid (CSF)?

A

The space between the arachnoid and pia maters is filled with cerebrospinal fluid (CSF). CSF is produced by a tissue called choroid plexus in fluid-filled compartments in the CNS called ventricles. The brain floats in CSF, which acts as a cushion and shock absorber and makers the brain neutrally buoyant. CSF also functions to circulate chemical substances throughout the brain and into the spinal cord.

72
Q

What is a hydrocephalus?

A

The entire brain contains only about 8.5 tablespoons of CSF, but CSF is constantly produced in the ventricles. This creates a problem when a ventricle is blocked—the CSF builds up and creates swelling and the brain is pushed against the skull. This swelling condition is called hydrocephalus (“water head”) and can cause seizures, cognitive problems, and even death if a shunt is not inserted to remove the fluid and pressure.

73
Q

What are the parts of the brain?

A

The brain is the part of the central nervous system that is contained in the cranial cavity of the skull. It includes the cerebral cortex, limbic system, basal ganglia, thalamus, hypothalamus, and cerebellum.

74
Q

What are the ways a brain can be sectioned?

A

There are three different ways that a brain can be sectioned in order to view internal structures: a sagittal section cuts the brain left to right, a coronal section cuts the brain front to back, and a horizontal section cuts the brain top to bottom.

75
Q

What is the cerebral cortex?

A

The outermost part of the brain is a thick piece of nervous system tissue called the cerebral cortex, which is folded into hills called gyri (singular: gyrus) and valleys called sulci (singular: sulcus). The cortex is made up of two hemispheres—right and left—which are separated by a large sulcus. A thick fiber bundle called the corpus callosum (Latin: “tough body”) connects the two hemispheres and allows information to be passed from one side to the other.

76
Q

What do the different hemispheres of the cerebral cortex do?

A

Although there are some brain functions that are localized more to one hemisphere than the other, the functions of the two hemispheres are largely redundant. In fact, sometimes (very rarely) an entire hemisphere is removed to treat severe epilepsy. While patients do suffer some deficits following the surgery, they can have surprisingly few problems, especially when the surgery is performed on children who have very immature nervous systems.

77
Q

What is split-brain?

A

In some surgeries to treat severe epilepsy, the corpus callosum is cut instead of removing an entire hemisphere. This causes a condition called split-brain, which gives insights into unique functions of the two hemispheres. For example, when an object is presented to patients’ left visual field, they may be unable to verbally name the object (and may claim not to have seen the object at all). This is because the visual input from the left visual field crosses and enters the right hemisphere and cannot then signal to the speech center, which generally is found in the left side of the brain. If a split-brain patient is asked to pick up a specific object out of a group of objects with the left hand, the patient will be able to do so but will still be unable to vocally identify it.

78
Q

How do scientists determine which areas of the brain are involved in which functions?

A

Each cortical hemisphere contains regions called lobes that are involved in different functions. Scientists use various techniques to determine what brain areas are involved in different functions: they examine patients who have had injuries or diseases that affect specific areas and see how those areas are related to functional deficits. They also conduct animal studies where they stimulate brain areas and see if there are any behavioral changes. They use a technique called transmagnetic stimulation (TMS) to temporarily deactivate specific parts of the cortex using strong magnets placed outside the head; and they use functional magnetic resonance imaging (fMRI) to look at changes in oxygenated blood flow in particular brain regions that correlate with specific behavioral tasks. These techniques, and others, have given great insight into the functions of different brain regions but have also showed that any given brain area can be involved in more than one behavior or process, and any given behavior or process generally involves neurons in multiple brain areas.

79
Q

What are the lobes of the hemispheres of the cerebral cortex?

A

Each hemisphere of the mammalian cerebral cortex can be broken down into four functionally and spatially defined lobes: frontal, parietal, temporal, and occipital.

80
Q

What does the frontal lobe do?

A

The frontal lobe is located at the front of the brain, over the eyes. This lobe contains the olfactory bulb, which processes smells, The frontal lobe also contains the motor cortex, which is important for planning and implementing movement. Areas within the motor cortex map to different muscle groups, and there is some organization to this map. For example, the neurons that control movement of the fingers are next to the neurons that control movement of the hand. Neurons in the frontal lobe also control cognitive functions like maintaining attention, speech, and decision-making. Studies of humans who have damaged their frontal lobes show that parts of this area are involved in personality, socialization, and assessing risk.

81
Q

What does the parietal lobe do?

A

The parietal lobe is located at the top of the brain. Neurons in the parietal lobe are involved in speech and also reading. Two of the parietal lobe’s main functions are processing somatosensation—touch sensations like pressure, pain, heat, cold—and processing proprioception—the sense of how parts of the body are oriented in space. The parietal lobe contains a somatosensory map of the body similar to the motor cortex.

82
Q

What does the occipital lobe do?

A

The occipital lobe is located at the back of the brain. It is primarily involved in vision—seeing, recognizing, and identifying the visual world.

83
Q

What does the temporal lobe do?

A

The temporal lobe is located at the base of the brain by the ears and is primarily involved in processing and interpreting sounds. It also contains the hippocampus (Greek for “seahorse”)—a structure that processes memory formation.

84
Q

How was the role of the hippocampus determined?

A

The role of the hippocampus in memory was partially determined by studying one famous epileptic patient, HM, who had both sides of his hippocampus removed in an attempt to cure his epilepsy. His seizures went away, but he could no longer form new memories (although he could remember some facts from before his surgery and could learn new motor tasks).

85
Q

How is brain size correlated with intelligence?

A

Compared to other vertebrates, mammals have exceptionally large brains for their body size. An entire alligator’s brain, for example, would fill about one and a half teaspoons. This increase in brain to body size ratio is especially pronounced in apes, whales, and dolphins. While this increase in overall brain size doubtlessly played a role in the evolution of complex behaviors unique to mammals, it does not tell the whole story. Scientists have found a relationship between the relatively high surface area of the cortex and the intelligence and complex social behaviors exhibited by some animals. This increased surface area is due, in part, to increased folding of the cortical sheet (more sulci and gyri). For example, a rat cortex is very smooth with very few sulci and gyri. Cat and sheep cortices have more sulci and gyri. Chimps, humans, and dolphins have even more.

86
Q

What does the basal ganglia do?

A

Interconnected brain areas called the basal ganglia (or basal nuclei) play important roles in movement control and posture, and also regulate motivation.

87
Q

What are some conditions caused by damage to the basal ganglia?

A

Damage to the basal ganglia, as in Parkinson’s disease, leads to motor impairments like a shuffling gait when walking. There is another case where, when a wasp sting led to bilateral basal ganglia damage in a 25-year-old businessman, he began to spend all his days in bed, and showed no interest in anything or anybody. But when he was externally stimulated—as when someone asked to play a card game with him—he was able to function normally. Interestingly, he and other similar patients do not report feeling bored or frustrated by their state.

88
Q

What does the thalamus do?

A

The thalamus (Greek for “inner chamber”) acts as a gateway to and from the cortex. It receives sensory and motor inputs from the body and also receives feedback from the cortex. This feedback mechanism can modulate conscious awareness of sensory and motor inputs depending on the attention and arousal state of the animal. The thalamus helps regulate consciousness, arousal, and sleep states.

89
Q

What is a condition that is caused by damage to the thalamus?

A

A rare genetic disorder called fatal familial insomnia causes the degeneration of thalamic neurons and glia. This disorder prevents affected patients from being able to sleep, among other symptoms, and is eventually fatal.

90
Q

What does the hypothalamus do?

A

Below the thalamus is the hypothalamus. The hypothalamus controls the endocrine system by sending signals to the pituitary gland, a pea-sized endocrine gland that releases several different hormones that affect other glands as well as other cells. This relationship means that the hypothalamus regulates important behaviors that are controlled by these hormones. The hypothalamus is the body’s thermostat—it makes sure key functions like food and water intake, energy expenditure, and body temperature are kept at appropriate levels. Neurons within the hypothalamus also regulate circadian rhythms, sometimes called sleep cycles.

91
Q

What does the limbic system do?

A

The limbic system is a connected set of structures that regulates emotion, as well as behaviors related to fear and motivation. It plays a role in memory formation and includes parts of the thalamus and hypothalamus as well as the hippocampus. One important structure within the limbic system is a temporal lobe structure called the amygdala (Greek for “almond”). The two amygdala are important both for the sensation of fear and for recognizing fearful faces. The cingulate gyrus helps regulate emotions and pain.

92
Q

What does the cerebellum do?

A

The cerebellum (Latin for “little brain”) sits at the base of the brain on top of the brainstem. The cerebellum controls balance and aids in coordinating movement and learning new motor tasks.

93
Q

What does the brainstem do?

A

The brainstem connects the rest of the brain with the spinal cord. It consists of the midbrain, medulla oblongata, and the pons. Motor and sensory neurons extend through the brainstem allowing for the relay of signals between the brain and spinal cord. Ascending neural pathways cross in this section of the brain allowing the left hemisphere of the cerebrum to control the right side of the body and vice versa. The brainstem coordinates motor control signals sent from the brain to the body. The brainstem controls several important functions of the body including alertness, arousal, breathing, blood pressure, digestion, heart rate, swallowing, walking, and sensory and motor information integration.

94
Q

What is the spinal cord?

A

Connecting to the brainstem and extending down the body through the spinal column is the spinal cord. The spinal cord is a thick bundle of nerve tissue that carries information about the body to the brain and from the brain to the body. The spinal cord is contained within the bones of the vertebrate column but is able to communicate signals to and from the body through its connections with spinal nerves (part of the PNS).

95
Q

What is white matter and gray matter?

A

A cross-section of the spinal cord looks like a white oval containing a gray butterfly-shape. Myelinated axons make up the “white matter” and neuron and glial cell bodies make up the “gray matter”. Gray matter is also composed of interneurons, which connect two neurons each located in different parts of the body.

96
Q

Which parts of the spinal cord transmit which kinds of information?

A

Axons and cell bodies in the dorsal spinal cord convey mostly sensory information from the body to the brain. Axons and cell bodies in the ventral spinal cord primarily transmit signals controlling movement from the brain to the body.

97
Q

How does the spinal cord control motor reflexes?

A

The spinal cord also controls motor reflexes. These reflexes are quick, unconscious movements—like automatically removing a hand from a hot object. Reflexes are so fast because they involve local synaptic connections. For example, the knee reflex that a doctor tests during a routine physical is controlled by a single synapse between a sensory neuron and a motor neuron. While a reflex may only require the involvement of one or two synapses, synapses with interneurons in the spinal column transmit information to the brain to convey what happened.

98
Q

What is the impact of spinal cord injuries?

A

In the United States, there are around 10,000 spinal cord injuries each year. Because the spinal cord is the information superhighway connecting the brain with the body, damage to the spinal cord can lead to paralysis. The extent of the paralysis depends on the location of the injury along the spinal cord and whether the spinal cord was completely severed. For example, if the spinal cord is damaged at the level of the neck, it can cause paralysis from the neck down, whereas damage to the spinal column further down may limit paralysis to the legs.

99
Q

How are spinal cord injuries treated?

A

Spinal cord injuries are notoriously difficult to treat because spinal nerves do not regenerate, although ongoing research suggests that stem cell transplants may be able to act as a bridge to reconnect severed nerves. Researchers are also looking at ways to prevent the inflammation that worsens nerve damage after injury. One such treatment is to pump the body with cold saline to induce hypothermia. This cooling can prevent swelling and other processes that are thought to worsen spinal cord injuries.

100
Q

What is an analogy for the peripheral nervous system (PNS)?

A

The PNS is the connection between the central nervous system and the rest of the body. The CNS is like the power plant of the nervous system. It creates the signals that control the functions of the body. The PNS is like the wires that go to individual houses. Without those “wires”, the signals produced by the CNS could not control the body (and the CNS would not be able to receive sensory information from the body either).

101
Q

What are the systems of the PNS?

A

The PNS can be broken down into the autonomic nervous system, which controls bodily functions without conscious control, and the sensory-somatic nervous system, which transmits sensory information from the skin, muscles, and sensory organs to the CNS and sends motor commands from the CNS to the muscles.

102
Q

What does the autonomic nervous system do?

A

The autonomic nervous system serves as the relay between the CNS and the internal organs. It controls the lungs, the heart, smooth muscle, and exocrine and endocrine glands. The autonomic nervous system controls these organs largely without conscious control; it can continuously monitor the conditions of these different systems and implement changes as needed. Signaling to the target tissue usually involves two synapses: a preganglionic neuron (originating in the CNS) synapses to a neuron in a ganglion that, in turn, synapses on the target organ. There are two divisions of the autonomic nervous system that often have opposing effects: the sympathetic nervous system and the parasympathetic nervous system.

103
Q

What does the sympathetic nervous system do?

A

The sympathetic nervous system is responsible for the “fight or flight” response that occurs when an animal encounters a dangerous situation. Examples of functions controlled by the sympathetic nervous system include an accelerated heart rate and inhibited digestion. These functions help prepare an organism’s body for the physical strain required to escape a potentially dangerous situation or to fend off a predator.

104
Q

How does the sympathetic nervous system work?

A

Most preganglionic neurons in the sympathetic nervous system originate in the spinal cord. The axons of these neurons release acetylcholine on postganglionic neurons within sympathetic ganglia (the sympathetic ganglia form a chain that extends alongside the spinal cord). The acetylcholine activates the postganglionic neurons. Postganglionic neurons then release norepinephrine onto target organs. The effects of the sympathetic nervous system are quite pervasive. This is both because one preganglionic neuron synapses on multiple postganglionic neurons, amplifying the effect of the original synapse, and because the adrenal gland also releases norepinephrine (and the closely related hormone epinephrine) into the blood stream.

105
Q

What are the physiological effects of the sympathetic nervous system?

A

The physiological effects of this norepinephrine release include dilating the trachea and bronchi (making it easier for the animal to breathe), increasing heart rate, and moving blood from the skin to the heart, muscles, and brain (so the animal can think and run). The strength and speed of the sympathetic response helps an organism avoid danger, and scientists have found evidence that it may also increase LTP—allowing the animal to remember the dangerous situation and avoid it in the future.

106
Q

What does the parasympathetic nervous system do?

A

The parasympathetic nervous system allows an animal to “rest and digest”.

107
Q

How does the parasympathetic nervous system work?

A

Parasympathetic preganglionic neurons have cell bodies located in the brainstem and in the sacral (toward the bottom) spinal cord. The axons of the preganglionic neurons release acetylcholine on the postganglionic neurons, which are generally located very near the target organs. Most postganglionic neurons release acetylcholine onto target organs, although some release nitric oxide.

108
Q

What are the physiological effects of the parasympathetic nervous system?

A

The parasympathetic nervous system reset organ function after the sympathetic nervous system is activated (the common adrenaline dump one feels after a “fight-or-flight” event). Effects of acetylcholine release on target organs include slowing of heart rate, lowered blood pressure, and stimulation of digestion.

109
Q

What does the sensory-somatic nervous system do?

A

The sensory-somatic nervous system is made up of cranial and spinal nerves and contains both sensory and motor neurons. Sensory neurons transmit sensory information from the skin, skeletal muscle, and sensory organs to the CNS. Motor neurons transmit messages about desired movement from the CNS to the muscles to make them contract. Without its sensory-somatic nervous system, an animal would be unable to process any information about its environment and could not control motor movements.

110
Q

What are the synapses of the sensory-somatic nervous system?

A

Unlike the autonomic nervous system, which has two synapses between the CNS and the target organ, sensory and motor neurons have only one synapse—one ending of the neuron is at the organ and the other directly contacts a CNS neuron. Acetylcholine is the main neurotransmitter released at these synapses.

111
Q

What do cranial nerves do?

A

Humans have 12 cranial nerves, nerves that emerge from or enter the skull (cranium), as opposed to the spinal nerves, which emerge from the vertebral column. Each cranial nerve is accorded a name. Some cranial nerves transmit only sensory information. For example, the olfactory nerve transmits information about smells from the nose to the brainstem. Other cranial nerves transmit almost solely motor information. For example, the oculomotor nerve controls the opening and closing of the eyelid and some eye movements. Other cranial nerves contain a mix of sensory and motor fibers. For example, the glossopharyngeal nerve has a role in both taste (sensory) and swallowing (motor).

112
Q

What do spinal nerves do?

A

Spinal nerves transmit sensory and motor information between the spinal cord and the rest of the body. Each of the 31 spinal nerves (in humans) contains both sensory and motor axons. The sensory neuron cell bodies are grouped in structures called dorsal root ganglia. Each sensory neuron has one projection—with a sensory receptor ending in skin, muscle, or sensory organs—and another that synapses with a neuron in the dorsal spinal cord. Motor neurons have cell bodies in the ventral gray matter of the spinal cord that project to muscle through the ventral root. These neurons are usually stimulated by interneurons within the spinal cord but are sometimes directly stimulated by sensory neurons.

113
Q

What are some neurodegenerative disorders?

A

Neurodegenerative disorders are illnesses characterized by a loss of nervous system functioning that are usually caused by neuronal death. These diseases generally worsen over time as more and more neurons die. The symptoms of a particular neurodegenerative disease are related to where in the nervous system the death of neurons occurs. Spinocerebellar ataxia, for example, leads to neuronal death in the cerebellum. The death of these neurons causes problems in balance and walking. Neurodegenerative disorders include Huntington’s disease, amyotrophic lateral sclerosis, Alzheimer’s disease and other types of dementia disorders, and Parkinson’s disease.

114
Q

How prevalent is Alzheimer’s disease?

A

Alzheimer’s disease is the most common cause of dementia in the elderly. In 2012, an estimated 5.4 million Americans suffered from Alzheimer’s disease, and payments for their care are estimated at $200 billion. Roughly one in every eight people age 65 or older has the disease. Due to the aging of the baby-boomer generation, there are projected to be as many as 13 million Alzheimer’s patients in the United States in the year 2050.

115
Q

What are some symptoms of Alzheimer’s disease?

A

Symptoms of Alzheimer’s disease include disruptive memory loss, confusion about time or place, difficulty planning or executing tasks, poor judgment, and personality changes. Problems smelling certain scents can also be indicative of Alzheimer’s disease and may serve as an early warning sign. Many of these symptoms are also common in people who are aging normally, so it is the severity and longevity of the symptoms that determine whether a person is suffering from Alzheimer’s.

116
Q

How was Alzheimer’s disease discovered?

A

Alzheimer’s disease was named for Alois Alzheimer, a German psychiatrist who published a report in 1911 about a woman who showed severe dementia symptoms. Along with his colleagues, he examined the woman’s brain following her death and reported the presence of abnormal clumps.

117
Q

What is the effect of Alzheimer’s disease on the brain?

A

Abnormal clumps can be detected in the brain, which are called amyloid plaques, along with tangled brain fibers called neurofibrillary tangles. Amyloid plaques, neurofibrillary tangles, and an overall shrinking of brain volume are commonly seen in the brains of Alzheimer’s patients. Loss of neurons in the hippocampus is especially severe in advanced Alzheimer’s patients.

118
Q

What causes Alzheimer’s disease?

A

One form of the disease is usually caused by mutations in one of three known genes. This rare form of early onset Alzheimer’s disease affects fewer than five percent of patients with the disease and causes dementia beginning between the ages of 30 and 60. The more prevalent, late-onset form of the disease likely also has a genetic component. One particular gene, apolipoprotein E (APOE) has a variant (E4) that increases a carrier’s likelihood of getting the disease. Many other genes have been identified that might be involved in the pathology.

119
Q

How is Alzheimer’s disease treated?

A

Unfortunately there is no cure for Alzheimer’s disease. Current treatments focus on managing the symptoms of the disease. Because decrease in the activity of cholinergic neurons (neurons that use the neurotransmitter acetylcholine) is common in Alzheimer’s disease, several drugs used to treat the disease work by increasing acetylcholine neurotransmission, often by inhibiting the enzyme that breaks down acetylcholine in the synaptic cleft. Other clinical interventions focus on behavioral therapies like psychotherapy, sensory therapy, and cognitive exercises.

120
Q

How can Alzheimer’s disease be prevented?

A

Since Alzheimer’s disease appears to hijack the normal aging process, research into prevention is prevalent. Smoking, obesity, and cardiovascular problems may be risk factors for the disease, so treatments for those may also help to prevent Alzheimer’s disease. Some studies have shown that people who remain intellectually active by playing games, reading, playing musical instruments, and being socially active in later life have a reduced risk of developing the disease.

121
Q

Who discovered Parkinson’s disease?

A

Parkinson’s disease was first characterized by James Parkinson in 1817.

122
Q

How prevalent is Parkinson’s disease?

A

Each year, 50K-60K people in the United States are diagnosed with the disease.

123
Q

What is the effect of Parkinson’s disease on the brain?

A

Parkinson’s disease causes the loss of dopamine neurons in the substantia nigra, a midbrain structure that regulates movement.

124
Q

What are some symptoms of Parkinson’s disease?

A

Loss of the dopamine neurons causes many symptoms including tremor (shaking of fingers or a limb), slowed movement, speech changes, balance and posture problems, and rigid muscles. The combination of these symptoms often causes a characteristic slow hunched shuffling walk. Patients with Parkinson’s disease can also exhibit psychological symptoms, such as dementia or emotional problems.

125
Q

What causes Parkinson’s disease?

A

Although some patients have a form of the disease known to be caused by a single mutation, for most patients the exact causes of Parkinson’s disease remain unknown: the disease likely results from a combination of genetic and environmental factors (similar to Alzheimer’s disease). Post-mortem analysis of brains from Parkinson’s patients shows the presence of Lewy bodies—abnormal protein clumps—in dopaminergic neurons. The prevalence of these Lewy bodies often correlates with the severity of the disease.

126
Q

How is Parkinson’s disease treated?

A

There is no cure for Parkinson’s disease, and treatment is focused on easing symptoms. One of the most commonly prescribed drugs for Parkinson’s is L-DOPA, which is a chemical that is converted into dopamine by neurons in the brain. This conversion increases the overall level of dopamine neurotransmission and can help compensate for the loss of dopaminergic neurons in the substantia nigra. Other drugs work by inhibiting the enzyme that breaks down dopamine.

127
Q

What are some neurodevelopmental disorders?

A

Neurodevelopmental disorders occur when the development of the nervous system is disturbed. There are several different classes of neurodevelopmental disorders. Some, like Down Syndrome, cause intellectual deficits. Others specifically affect communication, learning, or the motor system. Some disorders like autism spectrum disorder and attention deficit/hyperactivity disorder have complex systems.

128
Q

How prevalent is ASD?

A

Autism spectrum disorder (ASD) is a neurodevelopmental disorder. Its severity differs from person to person. Estimates for the prevalence of the disorder have changed rapidly in the past few decades. Current estimates suggest that one in 88 children will develop the disorder. ASD is four times more prevalent in males than females.

129
Q

What are some symptoms of ASD?

A

A characteristic symptom of ASD is impaired social skills. Children with autism may have difficulty making and maintaining eye contact and reading social cues. They also may have problems feeling empathy for others. Other symptoms of ASD including repetitive motor behaviors (such as rocking back and forth), preoccupation with specific subjects, strict adherence to certain rituals, and unusual language use. Up to 30% of patients with ASD develop epilepsy, and patients with some forms of the disorder (like Fragile X) also have intellectual disability. Because it is a spectrum disorder, other ASD patients are very functional and have good-to-excellent language skills. Many of these patients do not feel that they suffer from a disorder and instead think that their brains just process information differently.

130
Q

What causes ASD?

A

Except for some well-characterized, clearly genetic forms of autism (like Fragile X and Rett’s Syndrome), the causes of ASD are largely unknown. Variants of several genes correlate with the presence of ASD, but for any given patient, many different mutations in different genes may be required for the disease to develop. At a general level, ASD is thought to be a disease of “incorrect” wiring. Accordingly, brains of some ASD patients lack the same level of synaptic pruning that occurs in non-affected people. In the 1990s, a research paper linked autism to a common vaccine given to children. This paper was retracted when it was discovered that the author falsified data, and follow-up studies have showed no connection between vaccines and autism.

131
Q

How is ASD treated?

A

Treatment for autism usually combines behavioral therapies and interventions, along with medications to treat other disorders common to people with autism (depression, anxiety, obsessive compulsive disorder). Although early interventions can help mitigate the effects of the disease, there is currently no cure for ASD.

132
Q

How prevalent is ADHD?

A

Approximately three to five percent of children and adults are affected by attention deficit/hyperactivity disorder (ADHD). Like ASD, ADHD is more prevalent in males than females.

133
Q

What are some symptoms of ADHD?

A

Symptoms of the disorder include inattention (lack of focus), executive functioning difficulties, impulsivity, and hyperactivity beyond what is characteristic of the normal developmental stage. Some patients do not have the hyperactive component of symptoms and are diagnosed with a subtype of ADHD: attention deficit disorder (ADD). Many people with ADHD also show comorbidity, in that they develop secondary disorders in addition to ADHD. Examples include depression or obsessive compulsive disorder (OCD).

134
Q

What causes ADHD?

A

The cause of ADHD is unknown, although research points to a delay and dysfunction in the development of the prefrontal cortex and disturbances in neurotransmission. According to studies of twins, the disorder has a strong genetic component. There are several candidate genes that may contribute to the disorder, but no definitive links have been discovered. Environmental factors, including exposure to certain pesticides, may also contribute to the development of ADHD in some patients.

135
Q

How is ADHD treated?

A

Treatment for ADHD often involves behavioral therapies and the prescription of stimulant medications, which paradoxically cause a calming effect in these patients.

136
Q

What are neurologists?

A

Neurologists are physicians who specialize in disorders of the nervous system. They diagnose and treat disorders such as epilepsy, stroke, dementia, nervous system injuries, Parkinson’s disease, sleep disorders, and multiple sclerosis. Neurologists are medical doctors who have attended college, medical school, and completed three to four years of neurology residency.

137
Q

How do neurologists use physical exams to diagnose patients?

A

When examining a new patient, a neurologist takes a full medical history and performs a complete physical exam. The physical exam contains specific tasks that are used to determine what areas of the brain, spinal cord, or peripheral nervous system may be damaged. For example, to check whether the hypoglossal nerve is functioning correctly, the neurologist will ask the patient to move his or her tongue in different ways. If the patient does not have full control over tongue movements, then the hypoglossal nerve may be damaged or there may be a lesion in the brainstem where the cell bodies of these neurons resides (or there could be damage to the tongue muscle itself).

138
Q

What other tools do neurologists use to diagnose patients?

A

If the patient has had a seizure, for example, the neurologist can use electroencephalography (EEG), which involves taping electrodes to the scalp to record brain activity, to try to determine which brain regions are involved in the seizure. In suspected stroke patients, a neurologist can use a computerized tomography (CT) scan, which is a type of X-ray, to look for bleeding in the brain or a possible brain tumor. To treat patients with neurological problems, neurologists can prescribe medications or refer the patient to a neurosurgeon for surgery.

139
Q

What are mental illnesses?

A

Mental illnesses are nervous system disorders that result in problems with thinking, mood, or relating with other people. These disorders are severe enough to affect a person’s quality of life and often make it difficult for people to perform the routine tasks of daily living.

140
Q

How prevalent are mental illnesses?

A

Debilitating mental disorders plague approximately 12.5M Americans (about 1 in 17 people) at an annual cost of more than $300B.

141
Q

What are some mental illnesses?

A

There are several types of mental disorders including schizophrenia, major depression, bipolar disorder, anxiety disorders and phobias, post-traumatic stress disorders, and obsessive-compulsive disorders (OCD), among others.

142
Q

How are mental disorders characterized and catalogued?

A

The American Psychiatric Association publishes the Diagnostic and Statistical Manual of Mental Disorders (or DSM), which describes the symptoms required for a patient to be diagnosed with a particular mental disorder. Each newly released version of the DSM contains different symptoms and classifications as scientists learn more about these disorders, their causes, and how they relate to each other.

143
Q

What are some symptoms of schizophrenia?

A

Schizophrenia is a serious and often debilitating mental illness affecting one percent of people in the United States. Symptoms of the disease include the inability to differentiate between reality and imagination, inappropriate and unregulated emotional responses, difficulty thinking, and problems with social situations. People with schizophrenia can suffer from hallucinations and hear voices; they may also suffer from delusions. People also have so-called “negative” symptoms like a flattened emotional state, loss of pleasure, and loss of basic drives.

144
Q

What causes schizophrenia?

A

Many schizophrenic patients are diagnosed in their late adolescence or early 20s. The development of schizophrenia is thought to involve malfunctioning dopaminergic neurons and may also involve problems with glutamate signaling.

145
Q

How is schizophrenia treated?

A

Treatment for schizophrenia usually requires antipsychotic medications that work by blocking dopamine receptors and decreasing dopamine neurotransmission in the brain. This decrease in dopamine can cause Parkinson’s disease-like symptoms in some patients. While some classes of antipsychotics can be quite effective at treating the disease, they are not a cure, and most patients must remain medicated for the rest of their lives.

146
Q

How prevalent is major depression?

A

Major depression affects approximately 6.7% of the adults in the United States each year and is one of the most common mental disorders.

147
Q

What are some symptoms of major depression?

A

To be diagnosed with major depressive disorder, a person must have experienced a severely depressed mood lasting longer than two weeks along with other symptoms including a loss of enjoyment in activities that were previously enjoyed, changes in appetite and sleep schedules, difficulty concentrating, feelings of worthlessness, and suicidal thoughts.

148
Q

What causes major depression?

A

The exact causes of major depression are unknown and likely include both genetic and environmental risk factors. Some research supports the “classic monoamine hypothesis”, which suggests that depression is caused by a decrease in norepinephrine and serotonin neurotransmission. One argument against this hypothesis is the fact that some antidepressant medications cause an increase in norepinephrine and serotonin release within a few hours of beginning treatment—but clinical results of these medications are not seen until weeks later. This has led to alternative hypotheses: for example, dopamine may also be decreased in depressed patients, or it may actually be an increase in norepinephrine and serotonin that causes the disease, and antidepressants force a feedback loop that decreases this release.

149
Q

How is major depression treated?

A

Treatments for depression include psychotherapy, electroconvulsive therapy, deep-brain stimulation, and prescription medications. There are several classes of antidepressant medications that work through different mechanisms. For example, monoamine oxidase inhibitors (MAO inhibitors) block the enzyme that degrades many neurotransmitters (including dopamine, serotonin, norepinephrine), resulting in increased neurotransmitter in the synaptic cleft. Selective serotonin reuptake inhibitors (SSRIs) block the reuptake of serotonin into the presynaptic neuron. This blockage results in an increase in serotonin in the synaptic cleft. Other types of drugs such as norepinephrine-dopamine reuptake inhibitors and norepinephrine-serotonin inhibitors are also used to treat depression.

150
Q

What are some other types of neurological disorders?

A

There are several neurological disorders that cannot be easily categorized as mental illnesses, neurodevelopmental disorders or neurodegenerative disorders. These include chronic pain conditions, cancers of the nervous system, epilepsy disorders, and stroke.

151
Q

How prevalent is epilepsy?

A

Estimates suggest that up to 3% of people in the United States will be diagnosed with epilepsy in their lifetime.

152
Q

What are the symptoms of epilepsy?

A

While there are several different types of epilepsy, all are characterized by recurrent seizures.

153
Q

What causes epilepsy?

A

Epilepsy itself can be a symptom of a brain injury, disease, or other illness. For example, people who have intellectual disability or ASD can experience seizures, presumably because the developmental wiring malfunctions that caused their disorders also put them at risk for epilepsy. For many patients, however, the cause of their epilepsy is never identified and is likely to be a combination of genetic and environmental factors.

154
Q

How is epilepsy treated?

A

Often, seizures can be controlled with anticonvulsant medications. However, for very severe cases, patients may undergo brain surgery to remove the brain area where seizures originate.

155
Q

What causes a stroke?

A

A stroke results when blood fails to reach a portion of the brain for a long enough time to cause damage. Without the oxygen supplied by blood flow, neurons in this brain region die. Stroke is often caused by blood clots and can also be caused by the bursting of a weak blood vessel.

156
Q

What are the symptoms of a stroke?

A

The neuronal death during a stroke can cause many different symptoms—depending on the brain area affected—including headache, muscle weakness or paralysis, speech disturbances, sensory problems, memory loss, and confusion.

157
Q

How prevalent are strokes?

A

Strokes are extremely common and are the third most common cause of death in the United States. On average one person experiences a stroke every 40 seconds in the United States. Approximately 75% of strokes occur in people older than 65.

158
Q

What are some risk factors for strokes?

A

Risk factors for stroke include high blood pressure, diabetes, high cholesterol, and a family history of stroke. Smoking doubles the risk of stroke.

159
Q

How are strokes treated?

A

Because a stroke is a medical emergency, patients with symptoms of a stroke should immediately go to the emergency room, where they can receive drugs that will dissolve any clot that may have formed. These drugs will not work if the stroke was caused by a burst blood vessel or if the stroke occurred more than three hours before arriving at the hospital. Treatment following a stroke can include blood pressure medication (to prevent future strokes) and (sometimes intense) physical therapy.