BIO 301 Human physiology Neurons and the Nervous System | ![]() |
Loshuman nervous systemconsists of billions ofnerve cells (or neurons)more supporting (neuroglial) cells. Neurons can respond to stimuli (such as touch, sound, light, etc.), conduct impulses, and communicate with each other (and with other types of cells, such as muscle cells).
Nervous system
The nucleus of a neuron is located in the cell body. Extending out from the cell body are processes called dendrites and axons. These processes vary in number and relative length, but they always serve to conduct impulses (with dendrites conducting impulses toward the cell body and axons conducting impulses away from the cell body).
http://en.wikipedia.org/wiki/Image:Complete_neuron_cell_diagram_en.svg
Neurons can respond to stimuli and conduct impulses because a membrane potential is established across the cell membrane. In other words, there is an uneven distribution of ions (charged atoms) on the two sides of a nerve cell's membrane. This can be illustrated with a voltmeter:
With one electrode placed inside a neuron and the other outside, the voltmeter 'measures' the difference in the distribution of ions inside versus outside. And in this example, the voltmeter reads -70 mV (mV = millivolts). In other words, the inside of the neuron is slightly negative relative to the outside. This difference is known as the resting membrane potential. How is this potential established?
![]() | The membranes of all nerve cells have a potential difference between them, with the inside of the cell negative to the outside (a). In neurons, stimuli can change this potential difference by opening sodium channels in the membrane. For example, neurotransmitters interact specifically with sodium channels (or gates). Sodium ions then flow into the cell, reducing the voltage across the membrane. Once the potential difference reaches a voltage threshold, the reduced voltage causes hundreds of sodium gates in that region of the membrane to briefly open. Sodium ions flood the cell, completely depolarizing the membrane (b). This opens more voltage-gated ion channels in the adjacent membrane, and thus a wave of depolarization travels through the cell: the action potential. As the action potential approaches its peak, the sodium gates close and the potassium gates open, allowing ions to flow out of the cell to restore normal membrane potential (c) (Gutkin and Ermentrout 2006). |
Establishment of the resting membrane potential
Membranes are polarized, that is, they have a RESTING MEMBRANE POTENTIAL. This means that there is an uneven distribution of ions (atoms with a positive or negative charge) on the two sides of the nerve cell membrane. This POTENTIAL usually measures around 70 millivolts (with the INSIDE of the membrane negative relative to the outside). Thus, RESTING MEMBRANE POTENTIAL is expressed as -70 mV, with the minus meaning that the inside is negative with respect to (or compared to) the outside. It is called a REST potential because it occurs when a membrane is not being stimulated or conducting impulses (that is, it is at rest).
Source:http://www.millersv.edu/~bio375/CELL/membrane/membrane.htm
neuron resting potential
What factors contribute to this membrane potential?
Two ions are responsible: sodium (Na+) and potassium (K+). An uneven distribution of these two ions occurs on both sides of a nerve cell's membrane because transporters actively transport these two ions: sodium from the inside to the outside and potassium from the outside to the inside. AS A RESULT of this active transport mechanism (commonly known asSODIUM-POTASSIUM PUMP), there is a higher concentration of sodium outside than inside and a higher concentration of potassium inside than outside (Animation: How the sodium-potassium pump works).
The sodium-potassium pump
Used with permission fromGary Kaiser
sodium-potassium pump
The nerve cell membrane also contains special passageways for these two ions which are commonly known as GATES orCHANNELS. Thus, there are SODIUM GATES and POTASSIUM GATES. These gates represent the only way these ions can diffuse across a nerve cell's membrane. IN A RESTING NERVE CELL MEMBRANE, all of the sodium gates are closed and some of the potassium gates are open. AS A RESULT, sodium cannot diffuse across the membrane and remains largely outside the membrane. HOWEVER, some potassium ions can diffuse.
IN GENERAL, therefore, there are a lot of positively charged potassium ions inside the membrane and a lot of positively charged sodium ions PLUS a few potassium ions on the outside. THIS MEANS THAT THERE ARE MORE POSITIVE CHARGES OUTSIDE THAN INSIDE. In other words, there is an uneven distribution of ions or a resting membrane potential. This potential will be maintained until the membrane is disturbed or stimulated. So if it's a strong enough stimulus, an action potential will occur.
potassium channel
Voltage detection in a sodium ion channel. Voltage sensors on sodium channels are charged 'shovels'
that move through the interior of the fluid membrane. Strain sensors (two of which are shown here) are mechanically connected to
the 'gate' of the channel. Each voltage sensor has four positive charges (amino acids) (slightly modified from Sigworth 2003).
In a cross-sectional view of the voltage-gated potassium channel,
two of the four blades move up and down, opening and closing the
central pore through which potassium ions exit the cell, restoring the
normal negative polarity inside the cell, positive external polarity.
An action potential is a very rapid change in membrane potential that occurs when the membrane of a nerve cell is stimulated. Specifically, the membrane potential goes from the resting potential (typically -70 mV) to some positive value (typically around +30 mV) in a very short period of time (just a few milliseconds).
What causes this potential change to occur? Thethe stimulus causes the sodium gates (or channels) to openand because there is more sodium on the outside than on the inside of the membrane, sodium diffuses rapidly into the nerve cell. All that positively charged sodium causes the membrane potential to become positive (the inside of the membrane is now positive with respect to the outside). Sodium channels open only briefly and then close again.
The potassium channels then open, and since there is more potassium inside the membrane than outside, the positively charged potassium ions diffuse out. As these positive ions leave, the inside of the membrane again becomes negative with respect to the outside (Animation:Voltage controlled channels) .
Source:http://faculty.washington.edu/chudler/ap.html
Threshold stimulus and potential
- Action potentials only occur when the membrane is stimulated (depolarized) enough for sodium channels to open fully. The minimum stimulus needed to elicit an action potential is calledthreshold stimulus.
- The threshold stimulus causes the membrane potential to become less negative (because a stimulus, however small, causes some sodium channels to open and allows some positively charged sodium ions to diffuse through).
- If the membrane potential reachespotencial umbral(usually 5 - 15 mV less negative than the resting potential), all voltage-gated sodium channels open. Sodium ions rapidly diffuse inward and depolarization occurs.
all or nothing law- action potentials are produced to the maximum or not produced at all. In other words, there is no partial or weak action potential. Either the potential threshold is reached and an action potential is produced, or it is not reached and no action potential is produced.
Refractory periods:
ABSOLUTE -
- During an action potential, a second stimulus will not produce a second action potential (no matter how strong that stimulus is).
- corresponds to the period that sodium channels are open (usually just a millisecond or less)
Source:http://members.aol.com/Bio50/LecNotes/lecnot11.html
RELATIVE -
- Another action potential can be produced, but only if the stimulus is greater than the threshold stimulus.
- corresponds to the period in which the potassium channels are open (several milliseconds)
- the nerve cell membrane becomes progressively more "responsive" (easier to stimulate) as the relative refractory period progresses. Thus, it takes a very strong stimulus to cause an action potential at the beginning of the relative refractory period, but only a slightly above-threshold stimulus to cause an action potential near the end of the relative refractory period.
The absolute refractory period places a limit on the rate at which a neuron can conduct impulses, and the relative refractory period allows variation in the rate at which a neuron conducts impulses. This variation is important because it is one of the ways our nervous system recognizes differences in stimulus intensity, for example, dim light = retinal cells conduct fewer impulses per second versus stronger light = retinal cells. the retina conducts more impulses per second.
How does the relative refractory period allow for variation in the velocity of impulse conduction? Suppose that the relative refractory period of a neuron has a duration of 20 milliseconds and, furthermore, that the stimulus threshold for that neuron (determined, for example, in a laboratory experiment with that neuron) is 0.5 volts. If this neuron is continuously stimulated at a level of 0.5 volts, then an action potential (and impulse) will be generated every 20 milliseconds (because once an action potential has been generated with a threshold stimulus [and ignoring the period absolute refractory period], another action potential cannot occur until the relative refractory period ends). Therefore, in this example, the pacing rate (and impulse conduction) would be 50 per second (1 second = 1000 ms; 1000 ms divided by 20 ms = 50).
If we increase the stimulus (for example, from 0.5 volts to 1 volt), what happens to the rate at which action potentials (and impulses) are produced? Since 1 volt is a stimulus above threshold, it means that once an action potential is generated, another one will occur.in less than 20msor, in other words, before the end of the relative refractory period. So, in our example, increasing the stimulus will increase the impulse conduction rate above 50 per second. Without more information, it is not possible to calculate the exact rate. However, just understand that increasing the intensity of the stimulus will result in an increase in the conduction velocity of the impulse.
refractory periods
impulse conduction-an impulseit is simply the movement of action potentials along a nerve cell. Action potentials are localized (affect only a small area of the nerve cell membrane). Thus, when one occurs, only a small area of the membrane depolarizes (or "reverses" the potential). As a result, for a fraction of a second, areas of the membrane adjacent to each other have opposite charges (the depolarized membrane is negative on the outside and positive on the inside, while adjacent areas remain positive on the outside and negative on the inside). An electrical circuit (or 'mini-circuit') develops between these areas of opposite charge (or, in other words, the flow of electrons between these areas). This 'mini-circuit' stimulates the adjacent area and therefore an action potential is produced. This process is repeated and action potentials travel across the nerve cell membrane. This "movement" of action potentials is called an impulse.
Driving speed:
- impulses normally travel along neurons at a speed between 1 and 120 meters per second
- driving speed is influenced bythe presence or absence of myelin
- Myelinated neurons (ormyelinated neurons) conduct impulses much faster than those without myelin.
The myelin sheath (blue) surrounding axons (yellow) is produced by glial cells (Schwann cells in the PNS, oligodendrocytes in the CNS). These cells produce large membranous tracts that wrap the axons in successive layers that are then compacted by exclusion from the cytoplasm (black) to form the myelin sheath. The thickness of the myelin sheath (the number of turns around the axon) is proportional to the diameter of the axon.
METROYelinization, the process by which glial cells wrap neuron axons in myelin sheaths, ensures rapid conduction of electrical impulses in the nervous system. The formation of myelin sheaths is one of the most spectacular examples of cell-cell interaction and coordination in nature. Myelin sheaths are made up of vast membranous extensions of glial cells: Schwann cells in the peripheral nervous system (PNS) and oligodendrocytes in the central nervous system (CNS). The axon is wrapped several times (like a jelly roll) by these sheet-like extensions of membrane to form the final myelin sheath, or internode. Internodes can be up to 1 mm long and are separated from their neighbors by a small gap (node of Ranvier) of 1 micrometer. The concentration of voltage-gated sodium channels in the axon membrane in the node and the high electrical resistance of the multilayer myelin sheath ensure that action potentials jump from node to node (a process termed "saltatory conduction") (ffrench-Constant 2004 ).
Schwann cells (or oligodendrocytes) are located at regular intervals along the process (axons and, for some neurons, dendrites), so a section of a myelinated axon would look like this:
Among the myelinated areas are unmyelinated areas called nodes of Ranvier. Because fat (myelin) acts as an insulator, the myelin-coated membrane will not conduct an impulse. So, in a myelinated neuron,Action potentials occur only along nodes.and therefore impulses 'jump' over the myelinated areas, going from node to node in a process calledsaltatory conduction(with the word saltatoria meaning 'to jump'):
Whyimpulse 'polish' on areas of myelin, an impulse travels much faster through a myelinated neuron than through an unmyelinated neuron.
Impulse conduction and Schwann cells
types of neurons -The three main types of neurons are:
![]() multipolar neuron | ![]() unipolar neuron | ![]() bipolar neuron |
multipolar neuronsThey are so named because they have many (multiple) processes extending from the cell body: many dendrites plus a single leaxon. Functionally, these neurons are either motor (they conduct impulses that will cause an activity such as muscle contraction) or association (they conduct impulses and allow 'communication' between neurons within the central nervous system).
unipolar neuronsthey have a single cell body process. However, this single, very short process splits into longer processes (adendrite plus an axon). Unipolar neurons are sensory neurons that conduct impulses to the central nervous system.
bipolar neuronsThey have two processes: an axon and a redendrite. These neurons are also sensory. For example, biopolar neurons can be found in the retina of the eye.
neuroglial or glial cells-general functions include:
1 - forming myelin sheaths
2 - protects neurons (via phagocytosis)
3 - regulate the internal environment of neurons
no central nervous system
synapse=point of transmission of impulses between neurons; Impulses are transmitted from presynaptic neurons to postsynaptic neurons.
synapsethey usually occur between the axon of a presynaptic neuron and a dendrite, or cell body, of a postsynaptic neuron. At a synapse, the end of the axon is "swollen" and is called the terminal medulla or synaptic knob. Within the end bulb are many synaptic vesicles (containingchemical neurotransmitters) and mitochondria (which supply ATP to produce more neurotransmitters). Between the terminal cord and the dendrite (or cell body) of the postsynaptic neuron, there is a space commonly known as the synaptic cleft. Therefore, the presynaptic and postsynaptic membranes do not come into contact. This means that the impulse cannot be transmitted directly. Instead, the impulse is transmitted by releasing chemicals called chemical transmitters (or neurotransmitters).
http://www.nia.nih.gov/NR/rdonlyres/4E12F6CF-2436-47DB-8CC5-607E82B2B8E4/2372/neurons_big1.jpg
Micrograph of a synapse (Schikorski and Stevens 2001).
synaptic transmission
postsynaptic membrane receptors
Structural features of a typical nerve cell (i.e. neuron) and synapse. This drawing shows the main components of a typical neuron, including the cell body with the nucleus; the dendrites that receive signals from other neurons; and the axon that transmits nerve signals to other neurons at a specialized structure called a synapse. When the nerve signal reaches the synapse, it causes the release of chemical messengers (ie neurotransmitters) from the storage vesicles. Neurotransmitters travel through a tiny space between cells and then interact with protein molecules (ie, receptors) located in the membrane surrounding the neuron receiving the signal. This interaction causes biochemical reactions that result in the generation or prevention of a new nerve signal, depending on the type of neuron, neurotransmitter, and receptor involved.Goodlett e Horn 2001).
synapse
When an impulse arrives at the end bulb, the final medulla membrane becomes more permeable to calcium. Calcium diffuses into the terminal medulla and activates enzymes that cause synaptic vesicles to move into the synaptic cleft. Some vesicles fuse with the membrane and release their neurotransmitter (a good example of exocytosis). Neurotransmitter molecules diffuse across the cleft and dock at receptor sites on the postsynaptic membrane. When these sites are filled, sodium channels open, allowing internal diffusion of sodium ions. This, of course, causes the membrane potential to become less negative (or, in other words, closer to the threshold potential). If enough neurotransmitters are released and enough sodium channels open, the membrane potential will reach threshold. In this case, an action potential is produced and propagates along the membrane of the postsynaptic neuron (ie, the impulse will be transmitted). Of course, if not enough neurotransmitter is released, the impulse will not be transmitted.
impulse transmission- The nerve impulse (action potential) travels down the presynaptic axon to the synapse, where it activates voltage-gated calcium channels that lead to calcium influx, triggering the simultaneous release of neurotransmitter molecules from many synaptic vesicles in the synapse. fuse the membranes of the vesicles to that of the nerve terminal. Neurotransmitter molecules diffuse across the synaptic cleft, binding briefly to receptors on the postsynaptic neuron to activate them, triggering physiological responses that can be excitatory or inhibitory, depending on the receptor. Neurotransmitter molecules are rapidly pumped back into the presynaptic nerve terminal via transporters, destroyed by enzymes near the receptors (eg, degradation of acetylcholine by cholinesterase), or diffused into the surrounding area.
This describes what happens when an "excitatory" neurotransmitter is released at a synapse. However, not all neurotransmitters are "excitatory".
Types of neurotransmitters:
- 1- Exciters: neurotransmitters that make the membrane potential less negative (by increasing the permeability of the membrane to sodium) and therefore tend to "excite" or stimulate the postsynaptic membrane.
2 - Inhibitors: neurotransmitters that make the membrane potential more negative (by increasing the permeability of the membrane to potassium) and therefore tend to "inhibit" (or make less likely) the transmission of an impulse. An example of an inhibitory neurotransmitter is gamma aminobutyric acid (GABA; shown below). Medically, GABA has been used to treat both epilepsy and hypertension. Another example of an inhibitory neurotransmitter is beta-endorphin, which causes a decrease in the perception of pain by the CNS.
Neurotransmitters (acetylcholine is described from about 2:55)
Used with permission fromJuan W. Kimball
- 1 - Temporary addition - transmission of an impulse by rapid stimulation of one or more presynaptic neurons
2 - Spatial addition - transmission of an impulse by simultaneous or almost simultaneous stimulation of two or more presynaptic neurons
Used with permission fromJuan W. Kimball
Addition
Related and useful links:
The physical factors behind the action potential
Explore the brain and spinal cord
cited literature
ffrench-Constant, C., H. Colognato e R. J. M. Franklin. 2004.Neuroscience: Myelin Mysteries Unraveled. Science 304:688-689.
Goodlet, C.R. and K.H. Horn. 2001. Mechanisms of alcohol-induced damage in the developing nervous system. Alcohol Research and Health 25:175–184.
Gutkin, B. e G. B. Ermentrout. 2006.Neuroscience: Very gnarly spikes in the cortex?Nature 440: 999-1000.
Schikorski, T. e C. F. Stevens. 2001.Morphological correlates of functionally defined synaptic vesicle populations. Nature Neuroscience 4: 391-395.
Sigworth, F. J. 2003. Structural Biology: Transistors of Life. Nature 423:21-22.
Zhou, M., Joao H. Morais-Cabral, Sabine Mann, and Roderick MacKinnon. 2001. Potassium channel receptor site for gate inactivation and quaternary amine inhibitors. Nature 411:657-661.
Back to BIO 301 Syllabus
LectureNotes 3 - Muscle
LectureNotes 4 - Blood and Bodily Defenses I
LectureNotes 4b - Blood and Bodily Defenses II
LectureNotes 5 - Cardiovascular system
LectureNotes 6 - Respiratory system