لخّصلي

Introduction

The nervous system coordinates the activities of many other organ systems.The initiation of an action potential is, therefore, an "all-or-none" event; it is generated completely or not at all. Action Potential Gating Mechanisms. The depolarizing and repolarizing phases of the action potential can be explained by relative changes in membrane conductance (permeability) to sodium and potassium. During the rising phase, the nerve cell membrane becomes more permeable to sodium; as a consequence, the membrane potential begins to shift more toward the equilibrium potential for sodium. However, before the membrane potential reaches ENa, sodium permeability begins to decrease and potassium permeability increases. This change in membrane conductance again drives the membrane potential toward EK, accounting for repolarization of the membrane . The action potential can also be viewed in terms of the flow of charged ions through selective ion channels. These voltage-gated channels are closed when the neuron is at rest When the membrane is depolarized, these channels begin to open. The Na_ channel quickly opens its activation gate and allows Na_ ions to flow into the cell. The influx of positively charged Na_ ions causes the membrane to depolarize. In fact, the membrane potential actually reverses, with the inside becoming positive; this is called the overshoot. In the initial stage of the action potential, more Na_ than K_ channels are opened because the K_ channels open more slowly in response to depolarization. This increase in Na_ permeability compared to that of K_ causes the membrane potential to move toward the equilibrium potential for Na_. Propagation and Speed of the Action Potential. After an action potential is generated, it propagates along the axon toward the axon terminal; it is conducted along the axon with no decrement in amplitude. The mode in which action potentials propagate and the speed with which they are conducted along an axon depend on whether the axon is myelinated. The diameter of the axon also influences the speed of action potential conduction: larger-diameter axons have faster action potential conduction velocities than smaller-diameter axons. In unmyelinated axons, voltage-gated Na_ and K_ channels are distributed uniformly along the length of the axonal membrane. An action potential is generated when the axon hillock is depolarized by the passive spread of synaptic potentials along the somatic and dendritic membrane The hillock acts as a "sink" where Na_ions enter the cell.It activates muscles for movement, controls the secretion of hormones from glands, regulates the rate and depth of breathing, and is involved in modulating and regulating a multitude of other physiological processes.we examine the specialized membrane properties of nerve cells that endow them with the ability to produce action potentials, explore the basic mechanisms of synaptic transmission, and discuss aspects of neuronal structure necessary for the maintenance of nerve cell function.This cycle of membrane depolarization, sodium channel activation, sodium ion influx, and membrane depolarization is an example of positive feedback, a regenerative process that results in the explosive activation of many sodium ion channels when the threshold membrane potential is reached.The propagation of action potentials, the release of neurotransmitters,and the activation of receptors constitute the means whereby nerve cells communicate and transmit information to one another and to non neuronal tissues.The membrane of the initial segment contains a high density of voltage-gated sodium and potassium ion channels.When the membrane of the initial segment is depolarized, voltage-gated sodium channels are opened, permitting an influx of sodium ions.To perform these functions, the nervous system relies on neurons, which are designed for the rapid transmission of information from one cell to another by conducting electrical impulses and secreting chemical neurotransmitters.The action potential is a transient change in the membrane potential characterized by a gradual depolarization to threshold, a rapid rising phase, an overshoot, and a repolarization phase.The electrical impulses propagate along the length of nerve fiber processes to their terminals, where they initiate a series of events that cause the release of chemical neurotransmitters.If the depolarization of the initial segment does not reach threshold, then not enough sodium channels are activated to initiate the regenerative process.Electrical signals that depend on the passive properties of the neuronal cell membrane spread electrotonically over short distances.The influx of these positively charged ions further depolarizes the membrane, leading to the opening of other voltagegated sodium channels.PASSIVE MEMBRANE PROPERTIES, THE ACTION POTENTIAL, AND ELECTRICAL SIGNALING BY NEURONS Neurons communicate by a combination of electrical and chemical signaling.Generally, information is integrated and transmitted along the processes of a single neuron electrically and then transmitted to a target cell chemically.The activation of these receptors either excites or inhibits the postsynaptic neuron.The repolarization phase is followed by a brief afterhyperpolarization (undershoot) before the membrane potential again reaches resting level.In most neurons, the axon hillock (initial segment) is the trigger zone that generates the action potential.Released neurotransmitters bind with their receptors on the postsynaptic cell membrane.Action potentials depend on a regenerative wave of channel openings and closings in the membrane.Depolarization of the axon hillock to threshold results in the generation and propagation of an action potential.

Introduction

The nervous system coordinates the activities of many other organ systems. It activates muscles for movement, controls the secretion of hormones from glands, regulates the rate and depth of breathing, and is involved in modulating and regulating a multitude of other physiological processes. To perform these functions, the nervous system relies on neurons, which are designed for the rapid transmission of information from one cell to another by conducting electrical impulses and secreting chemical neurotransmitters.
The electrical impulses propagate along the length of nerve fiber processes to their terminals, where they initiate a series of events that cause the release of chemical neurotransmitters. The release of neurotransmitters occurs at sites of synaptic contact between two nerve cells. Released neurotransmitters bind with their receptors on the postsynaptic cell membrane. The activation of these receptors either excites or inhibits the postsynaptic neuron.
The propagation of action potentials, the release of neurotransmitters,and the activation of receptors constitute the means whereby nerve cells communicate and transmit information to one another and to non neuronal tissues. we examine the specialized membrane properties of nerve cells that endow them with the ability to produce action potentials, explore the basic mechanisms of synaptic transmission, and discuss aspects of neuronal structure necessary for the maintenance of nerve cell function.

PASSIVE MEMBRANE PROPERTIES, THE ACTION POTENTIAL, AND ELECTRICAL SIGNALING BY NEURONS
Neurons communicate by a combination of electrical and chemical signaling. Generally, information is integrated and transmitted along the processes of a single neuron electrically and then transmitted to a target cell chemically. The chemical signal then initiates an electrical change in the target cell. Electrical signals that depend on the passive properties of the neuronal cell membrane spread electrotonically over short distances. These potentials are initiated by local current flow and decay with distance from their site of initiation. Alternatively, an action potential is an electrical signal that propagates over a long distance without a change in amplitude. Action potentials depend on a regenerative wave of channel openings and closings in the membrane.

Characteristics of the Action Potential.
Depolarization of the axon hillock to threshold results in the generation and propagation of an action potential.
The action potential is a transient change in the membrane potential characterized by a gradual depolarization to threshold, a rapid rising
phase, an overshoot, and a repolarization phase.
The repolarization phase is followed by a brief afterhyperpolarization
(undershoot) before the membrane potential again reaches resting level.
The action potential may be recorded by placing a microelectrode inside a nerve cell or its axon. The voltage measured is compared to that detected by a reference electrode placed outside the cell. The difference between the two measurements is a measure of the membrane potential.
This technique is used to monitor the membrane potential at rest, as well as during an action potential.

Initiation of the Action Potential.
In most neurons, the axon hillock (initial segment) is the trigger zone that generates the action potential. The membrane of the initial segment contains a high density of voltage-gated sodium and potassium ion channels. When the membrane of the initial segment is depolarized, voltage-gated sodium channels are opened, permitting an influx of sodium ions. The influx of these positively charged ions further depolarizes the membrane, leading to the opening of other voltagegated sodium channels. This cycle of membrane depolarization, sodium channel activation, sodium ion influx, and membrane depolarization is an example of positive feedback, a regenerative process that results in the explosive activation of many sodium ion channels when the threshold membrane potential is reached. If the depolarization of the initial segment does not reach threshold, then not enough sodium channels are activated to initiate the regenerative process. The initiation of an action potential is, therefore, an “all-or-none” event; it is generated completely or not at all.

Action Potential Gating Mechanisms.
The depolarizing and repolarizing phases of the action potential can be explained by relative changes in membrane conductance (permeability) to sodium and potassium. During the rising phase, the nerve cell membrane becomes more permeable to sodium; as a consequence, the membrane potential begins to shift more toward the equilibrium potential for sodium. However, before the membrane potential reaches ENa, sodium permeability begins to decrease and potassium permeability increases. This change in membrane conductance again drives the membrane potential toward EK, accounting for repolarization of the membrane .
The action potential can also be viewed in terms of the flow of charged ions through selective ion channels. These voltage-gated channels are closed when the neuron is at rest When the membrane is depolarized, these channels begin to open. The Na_ channel quickly opens its
activation gate and allows Na_ ions to flow into the cell. The influx of positively charged Na_ ions causes the membrane to depolarize. In fact, the membrane potential actually reverses, with the inside becoming positive; this is called the overshoot. In the initial stage of the action potential, more Na_ than K_ channels are opened because the K_ channels open more slowly in response to depolarization. This increase in Na_ permeability compared to that of K_ causes the membrane potential to move toward the equilibrium potential for Na_.

Propagation and Speed of the Action Potential.
After an action potential is generated, it propagates along the axon toward the axon terminal; it is conducted along the axon with no decrement in amplitude. The mode in which action potentials propagate and the speed with which they are conducted along an axon depend on whether the axon is myelinated. The diameter of the axon also influences the speed of action potential conduction: larger-diameter axons have faster action potential conduction velocities than smaller-diameter axons.
In unmyelinated axons, voltage-gated Na_ and K_ channels are distributed uniformly along the length of the axonal membrane. An action potential is generated when the axon hillock is depolarized by the passive spread of synaptic potentials along the somatic and dendritic membrane
The hillock acts as a “sink” where Na_ions enter the cell. The “source” of these Na_ ions is the extracellular space along the length of the axon. The entry of Na_ ions into the axon hillock causes the adjacent region of the axon to depolarize as the ions that entered the cell, during the peak of the action potential, flow away from the sink. This local spread of the current depolarizes the adjacent region to threshold and causes an action potential in that region. By sequentially depolarizing adjacent segments of the axon, the action potential propagates or moves along the length of the axon from point to point, like a traveling wave Just as large-diameter tubes allow a greater flow of water than small-diameter tubes because of their decreased resistance, large-diameter axons have less cytoplasmic resistance, thereby permitting a greater flow of ions. This increase
in ion flow in the cytoplasm causes greater lengths of the axon to be depolarized, decreasing the time needed for the action potential to travel along the axon.
Recall that the space constant, _, determines the length along the axon that a voltage change is observed after a local stimulus is applied.
In this case, the local stimulus is the inward sodium current that accompanies the action potential. The larger the space constant, the farther along the membrane a voltage change is observed after a local stimulus is applied.
The space constant increases with axon diameter because the internal axoplasmic resistance, Ra, decreases, allowing the current to spread farther down the inside of the axon before leaking back across the membrane.
When an action potential is generated in one region of the axon, more of the adjacent region that is depolarized by the inward current accompanying the action potential reaches the threshold for action potential generation.
The result is that the speed at which action potentials are conducted, or conduction velocity, increases as a function of increasing axon diameter and concomitant increase in the space constant.
Several factors act to increase significantly the conduction velocity of action potentials in myelinated axons.
Schwann cells in the PNS and oligodendrocytes in the CNS wrap themselves around axons to form myelin, layers of lipid membrane that insulate the axon and prevent the passage of ions through the axonal membrane.

Between the myelinated segments of the axon are the nodes of Ranvier, where action potentials are generated.
The signal that causes these glial cells to myelinate the axons apparently derives from the axon, and its potency is a function of axon size. In general, axons larger than approximately 1 m in diameter are myelinated, and the thickness of the myelin increases as a function of axon diameter.
Since the smallest myelinated axon is bigger than the largest unmyelinated axon, conduction velocity is faster for myelinated axons based on size alone. In addition, the myelin acts to increase the effective resistance of the axonal membrane, Rm, since ions that flow across the axonal membrane must also flow through the tightly wrapped layers of myelin before they reach the extracellular fluid. This increase in Rm increases the space constant. The layers of myelin also decrease the effective capacitance of the axonal membrane because the distance between the extracellular and intracellular conducting fluid compartments is increased. Because the capacitance is decreased, the time constant is decreased, increasing the conduction velocity.
While the effect of myelin on Rm and capacitance are important for increasing conduction velocity, there is an even greater factor at play—an alteration in the mode of conduction. In myelinated axons, voltage-gated Na channels are highly concentrated in the nodes of Ranvier, where the myelin sheath is absent, and are in low density beneath the segments of myelin. When an action potential is initiated at the axon hillock, the influx of Na_ ions causes the adjacent node of Ranvier to depolarize, resulting in an action potential at the node. This, in turn, causes depolarization of the next node of Ranvier and the eventual
initiation of an action potential. Action potentials are successively generated at neighboring nodes of Ranvier; therefore, the action potential in a myelinated axon appears to jump from one node to the next, a process called saltatory conduction This process results in a faster conduction velocity for myelinated than unmyelinated axons. The conduction velocity in mammals ranges from 3 to 120 m/sec for myelinated axons and 0.5 to 2.0 m/sec for unmyelinated axons.