绿领巾之歌怎么跳?:大脑电！人在什么时候大脑里有电？？

大脑异常放电是大脑神经元突发性异常放电，导致短暂的大脑功能障碍的一种慢性疾病。而癫痫(epileptic seizure)是指脑神经元异常和过度超同步化放电所造成的临床现象。其特征是突然和一发作过性症状，由于异常放电的神经元在大脑中的部位不同，而有多种多样的表现。可以是运动感觉神经或自主神经的伴有或不伴有意识或警觉程度的变化。
而癫痫（羊癫疯）发作是指脑神经元异常和过度超同步化放电所造成的临床现象。其特征是忽然和一过性症状，由于异常放电的神经元在大脑中的部位不同而又多种多样的表现，可以是运动﹑感觉﹑精神或自主神经的，伴有或不伴有意识和警觉程度的变化。对临床上确实无症状而仅在脑电图(EEG)上出现异常放电者，不称之为癫痫（羊癫疯）发作。因为癫痫（羊癫疯）是脑的疾患，身体其他部位的神经元(如三叉神经元或脊髓前角神经元)异常和过度放电不属于癫痫（羊癫疯）发作

听“探索频道”说过
人在思考问题的时候
所产生的电能，可以把一盏十瓦的电灯给点亮

十瓦很高吗？
那我可能就是记错了
反正不是十瓦就是五瓦
探索频道说过的。
然后就是那句“今天，你又有何新发现？”

任何时候，人的神经系统的信息传递就是通过电来传递的，神经纤维就象一条条电线。

任何时候，只是强弱不同

你说的那个叫动作电位，这里有图文并茂的英文介绍：

Action potential
From Wikipedia, the free encyclopedia.
http://en.wikipedia.org/wiki/Action_potential

A. A schematic view of an idealized action potential illustrates its various phases as the action potential passes a point on a cell membrane. B. Actual recordings of action potentials are often distorted compared to the shematic view because of variations in electrophysiological techniques used to make the recording.
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A. A schematic view of an idealized action potential illustrates its various phases as the action potential passes a point on a cell membrane. B. Actual recordings of action potentials are often distorted compared to the shematic view because of variations in electrophysiological techniques used to make the recording.

An action potential is a wave of electrical discharge that travels along the membrane of a cell. Action potentials are used by the body to communicate fast internal messages between its tissues making them an essential feature of animal life at the microscopic level. They can be created by many types of body cells, but are used most extensively by the nervous system to send messages between nerve cells and from nerve cells to other body tissues such as muscles and glands.

Many plants also exhibit action potentials that travel the length of their phloem to coordinate activity. The principal difference between plant and animal action potentials is that plants mainly use potassium and calcium currents while animals typically use potassium and sodium.

Action potentials are an essential carrier of the neural code. Their properties may constrain the sizes of evolving anatomies and enable centralized control and coordination of organs and tissues.
Contents
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* 1 Overview
* 2 Underlying mechanism
o 2.1 Resting membrane potential
o 2.2 Action potential phases
* 3 Threshold and initiation
* 4 Circuit model
* 5 Propagation
o 5.1 Speed of propagation
o 5.2 Saltatory conduction
+ 5.2.1 Detailed mechanism
+ 5.2.2 Resilience to injury
+ 5.2.3 Role in disease
* 6 Refractory period
* 7 Why an action potential?
* 8 See also
* 9 References
o 9.1 General sources
o 9.2 Primary sources
* 10 External links

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Overview

An electrical voltage, or potential, always exists between the inside and outside of a cell. The voltage of an inactive cell stays at a negative value (inside relative to outside the cell) and varies within a small range. When the membrane potential of an excitable cell is depolarized beyond a threshold, the cell will undergo (or "fire") an action potential (see Threshold and initiation).

At its most basic, an action potential is a very rapid swing in the polarity of the membrane potential from negative to positive and back, the entire cycle lasting a few milliseconds. Each turn of the cycle minimally involves a rising phase, a falling phase, and finally an undershoot (see Action potential phases). In specialized muscle cells of the heart, such as the pacemaker cells, a plateau phase of intermediate voltage may precede the falling phase.

Action potentials are measured with the recording techniques of electrophysiology (and more recently with neurochips containing EOSFETs). An oscilloscope recording the membrane potential from a single point on an axon shows each stage of the action potential enacted—rising phase, falling phase, and undershoot—as the wave passes. Together, these phases trace an arc that resembles a distorted sine wave. Its amplitude depends on whether the action potential wave has reached that point or passed it and how long ago.

The action potential does not dwell in one location of the cell's membrane, but travels along the membrane (see Propagation). It can travel along an axon for long distances, for example to carry signals from the brain to the tip of the spinal cord. In large animals, such as giraffes and whales, the distance traveled can be many meters.

The speed and simplicity of action potentials vary significantly between cells, in particular between cells of different types. However, the amplitudes of the voltage swings tend to be roughly the same between cells. Within any one excitable cell, consecutive action potentials typically are indistinguishable.
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Underlying mechanism
The hydrophobic cell membrane prevents charged molecules from easily diffusing through it, permitting a potential difference to exist across the membrane.
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The hydrophobic cell membrane prevents charged molecules from easily diffusing through it, permitting a potential difference to exist across the membrane.
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Resting membrane potential

The membrane voltage changes that take place during an action potential result from changes in the permeability of the membrane to specific ions (particularly sodium and potassium), the internal and external concentrations of which cells maintain in an imbalance. This imbalance makes possible not only action potentials but also the resting cell potential arises through the work of pumps (eg, the sodium-potassium exchanger) as well as ion channels (eg, the potassium leak channel). While the cell is at its resting potential the electric forces between the sodium and potassium of the neuron is counterbalanced by the "diffusive forces," creating a state of equilibrium.
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Action potential phases

The changes in membrane permeability and the onset and cessation of ionic currents during an action potential reflect the opening and closing of ion channels which provide portals through the membrane for ions. Residing in and spanning the membrane, some of these proteins sense and respond to changes in membrane potential (see [1] for an illustration).

In a simplified model of the action potential, the resting potential of a patch of membrane is maintained by a potassium leak channel. The rising phase of the action potential occurs when the sodium channel opens causing the sodium permeability to greatly exceed the potassium permeability. The membrane potential is driven toward ENa (see Goldman equation). In other cells, such as cardiac pacemaker cells, the rising phase is governed by the concentration of calcium rather than sodium.

After a short delay, the voltage-dependent (delayed-rectifier) potassium channel opens and the voltage-gated sodium channel inactivates. As a consequence, the membrane potential is driven back toward the resting potential, resulting in the action potential's falling phase.

As more potassium channels are open than sodium channels (at this point the potassium leak channel and voltage-dependent potassium channel are open and the sodium channel is closed), the potassium permeability is now larger than it was before the action potential was generated (at rest only the potassium leak channel is open). As a result, the membrane potential approaches EK more closely than it did at rest, causing the action potential to undershoot (see Action Potential Form and Nomenclature). The delayed-rectifier potassium channel, being voltage-dependent, is closed by the hyperpolarized voltage, and the cell returns to its resting potential.

The rising and falling phases of an action potential are often mistakenly called depolarization and hyperpolarization, respectively. Technically, depolarization is any change in membrane potential that results in a voltage closer to zero. Similarly, hyperpolarization is any change in which membrane potential grows away from zero. During the rising phase, the membrane potential first approaches zero, then becomes more positive; thus the rising phase comprises both depolarization and repolarization. Likewise, the falling phase is composed of both depolarization and hyperpolarization. While it is technically incorrect to equate the rising and falling phases with depolarization and hyperpolarization, this usage is common among professors, physicians, and neuroscience textbooks.
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Threshold and initiation
A plot of current (ion flux) against voltage (transmembrane potential) illustrates the action potential threshold (red arrow) of an idealized cell.
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A plot of current (ion flux) against voltage (transmembrane potential) illustrates the action potential threshold (red arrow) of an idealized cell.

Action potentials are triggered when an initial depolarization reaches threshold. This threshold potential varies, but generally is about 15 millivolts above the cell's resting membrane potential, occuring when the inward sodium current exceeds the outward potassium current. The net influx of positive charges carried by sodium ions depolarizes the membrane potential, leading to the further opening of voltage-gated sodium channels. These channels support greater inward current causing further depolarization, creating a positive-feedback cycle that drives the membrane potential to a very depolarized level.

The action potential threshold can be shifted by changing the balance between sodium and potassium currents. For example, if sodium channels are partly inactivated as a population, then a given level of depolarization will open fewer sodium channels and a greater threshold of depolarization will be necessary to initiate an action potential. This is the basis for the refractory period (see Refractory period).

Action potentials are largely dictated by the interplay between sodium and potassium ions (though there are minor contributions from other ions such as calcium and chloride), and as such are often modeled using hypothetical cells containing only two transmembrane ion channels (a voltage-gated sodium channel and a non-voltage-gated potassium channel). The origin of the action potential threshold may be studied using so-called I/V curves (right) that plot currents through ion channels against the cell's membrane potential. Four significant points in the I/V curve are indicated by arrows in the figure:

1. The green arrow indicates the resting potential of the cell and also the value of the equilibrium potential for potassium (Ek). Since the K+ channel is the only one open at these negative voltages, the cell will rest at Ek. Note that a stable resting potential will be present at any voltage where the summed I/V (green line) crosses the zero current (x-axis) point with a positive slope, such as at the green arrow. Consider why: any perturbation of the membrane potential in the negative direction will result in inward current that will depolarize the cell back toward the crossing point, while, any perturbation of the membrane potential in the positive direction will result in an outward current that will hyperpolarize the cell back toward the crossing point. Thus, any perturbation of the membrane potential around a positive slope crossing will tend to return the voltage to that crossing value.
2. The yellow arrow indicates the equilibrium potential for Na+ (ENa). In this two-ion system, ENa is the natural limit of membrane potential beyond which a cell cannot pass. Current values illustrated in this graph that exceed ENa are measured by artificially pushing the cell's voltage past its natural limit. Note however, that ENa could only be reached if the potassium current were absent.
3. The blue arrow indicates the maximum voltage that the peak of the action potential can approach. This is the actual natural maximum membrane potential that this cell can reach. It cannot reach ENa because of the counteracting influence of the potassium current.
4. The red arrow indicates the action potential threshold. This is the point where Isum becomes net-inward. Note that this is a zero-current crossing, but with a negative slope. Any such "negative slope crossing" of the zero current level in an I/V plot is an unstable point. At any voltage negative to this crossing, the current is outward and so a cell will tend to return to its resting potential. At any voltage positive of this crossing, the current is inward and will tend to depolarize the cell. This depolarization leads to more inward current, thus the sodium current become regenerative. Note that the point at which the green line reaches its most negative value is the point where all sodium channels are open. Depolarizations beyond that point thus decrease the sodium current as the driving force decreases as the membrane potential approaches ENa.

The action potential threshold is commonly confused with the "threshold" of sodium channel opening. This is incorrect because sodium channels have no threshold. Instead, they open in response to depolarization in a stochastic manner. Depolarization does not so much open the channel as it increases the probability of the channel being open. Even at hyperpolarized potentials, a sodium channel will open very occasionally. In addition, the threshold of an action potential is not the voltage at which sodium current becomes significant; it is the point where it exceeds the potassium current.

Biologically in neurons, depolarization typically originates in the dendrites at synapses. In principle, however, an action potential may be initiated anywhere along a nerve fiber. In his discovery of "animal electricity," Luigi Galvani made a leg of a dead frog kick as in life by touching a sciatic nerve with his scalpel, to which he had inadvertently transferred a negative, static-electric charge, thus initiating an action potential.
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Circuit model
A. A basic RC circuit superimposed on an image of a membrane bilayer shows the relationship between the two. B. More elaborate circuits can be used to model membranes containing ion channels, such as this one containing at channels for sodium (blue) and potassium (green).
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A. A basic RC circuit superimposed on an image of a membrane bilayer shows the relationship between the two. B. More elaborate circuits can be used to model membranes containing ion channels, such as this one containing at channels for sodium (blue) and potassium (green).

Cell membranes that contain ion channels can be modeled as RC circuits to better understand the propagation of action potentials in biological membranes. In such a circuit, the resistor represents the membrane's ion channels, while the capacitor models the insulating lipid membrane. Variable resistors are used for voltage-gated ion channels since their resistance changes with voltage. A fixed resistor represents the potassium leak channels that maintain the membrane's resting potential. The sodium and potassium gradients across the membrane are modeled as voltage sources (batteries).
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Propagation
Propagating action potentials can be modeled by joining several RC circuits, each one representing a patch of membrane.
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Propagating action potentials can be modeled by joining several RC circuits, each one representing a patch of membrane.

In unmyelinated axons, action potentials propagate as an interaction between passively spreading membrane depolarization and voltage-gated sodium channels. When a single patch of cell membrane is depolarized sufficiently to open its voltage-taged sodium channels, sodium ions enter the cell by facilitated diffusion. Once inside, positively-charged sodium ions "nudge" adjacent ions down the axon by electrostatic repulsion (analogous to the principal behind Newton's cradle) and attract negative ions away from the adjacent membrane. As a result, a wave of positivity moves down the axon without any individual ion moving very far. Once the adjacent path of membrane is depolarized sufficiently, the voltage-gated sodium channels in the adjacent patch open, regenerating the cycle. The process repeats itself down the length of the axon, with an action potential being regenerated at each segment of membrane.
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Speed of propagation

Action potentials propagate faster in axons of larger diameter, other things being equal. The primary reason is that axial resistance of the axon lumen is lower with larger diameters, owing to an increase in the ratio of cross-sectional area to membrane surface area. Since membrane surface area is the chief factor impeding action potential propagation in an unmyelinated axon, increasing this ratio is a particularly effective means of increasing conduction speed.

An extreme example of an animal using axon diameter as a means of speeding action potential conduction is found in the Atlantic squid. The squid giant axon controls the muscle contraction associated with the squid's predator escape response. This axon can be upwards of 1 mm in diameter, and is presumably an adaptation to allow very fast activation of the escape response behavior. The velocity of nerve impulses in these fibers is among the fastest in nature.
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Saltatory conduction

In myelinated axons, saltatory conduction is the process by which an action potential appears to jump along the length of an axon, being regenerated only at uninsulated segments (the nodes of Ranvier). Saltatory conduction increases nerve conduction velocity without having to dramatically increase axon diameter.

It has played an important role in the evolution of larger and more complex organisms whose nervous systems must rapidly transmit action potentials across greater distances. Without saltatory conduction, conduction velocity would require large increases in axon diameter, resulting in organisms with nervous systems too large to fit into their bodies.
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Detailed mechanism

The main impediment to conduction speed in unmyelinated axons is membrane capacitance. The capacity of a capacitor can be decreased by decreasing the cross-sectional area of its plates, or by increasing the distance between plates. The nervous system uses myelin as its main strategy to decrease membrane capacitance. Myelin is an insulating sheath wrapped around axons by Schwann cells and oligodendrocytes, neuroglia that flatten their cytoplasm to form large sheets made up mostly of plasma membrane. These sheets wrap around the axon, moving the conducting plates (the intra- and extracellular fluid) farther apart to decrease membrane capacitance.

The resulting insulation allows the rapid (essentially instantaneous) conduction of ions through a myelinated segment of axon, but prevents the regeneration of action potentials through those segments. Action potentials are only regenerated at the unmyelinated nodes of Ranvier spaced intermittently between myelinated portions. An abundance of voltage-gated sodium channels on these bare segments (up to four orders of magnitude greater than their density in unmyelinated axons [2]) allows action potentials to be efficiently regenerated at the nodes of Ranvier.

As a result of myelination, the insulated portion of the axon behaves like a passive wire: it conducts action potentials rapidly because its membrane capacitance is low, and minimizes the degradation of action potentials because its membrane resistance is high. When this passively propagated signal reaches a node of Ranvier, it initiates an action potential, which subsequently travels passively to the next node where the cycle repeats.
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Resilience to injury

The length of myelinated segments of axon is important to saltatory conduction. They should be as long as possible to maximize the length of fast passive conduction, but not so long that the decay of the passive signal is too great to reach threshold at the next node of Ranvier. In reality, myelinated segments are long enough for the passively propagated signal to travel for at least two nodes while retaining enough amplitude to fire an action potential at the second or third node. Thus, the safety factor of saltatory conduction is high, allowing transmission to bypass nodes in case of injury.
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Role in disease

只要大脑还活着!就有脑电!一直到死透!才拉闸停电!