When the positive potential becomes greater than the threshold potential, it causes the opening of sodium channels. The sodium ions rush into the neuron and cause the shift in membrane potential from negative to positive. Depolarization of a small portion of neuron generates a strong nerve impulse. The nerve impulse travels along the entire length of neuron up to the synaptic terminal. Once the nerve impulse reaches the synaptic terminal, it causes release of neurotransmitters.
These neurotransmitters diffuse across the synaptic cleft. They act as a chemical stimulus for the post-synaptic neuron. These neurotransmitters, in turn, cause the depolarization of postsynaptic neurons. Vascular endothelial cells line the inner surface of blood vessels. These cells have structural capability to withstand the cardiovascular forces. They also play an important role in maintaining the functionality of the cardiovascular system.
These cells use the process of depolarization to alter their structural strength. When the endothelial cells are in a depolarized state, they have marked decreased structural strength and rigidity. In depolarized state , endothelial cells also cause a marked decrease in vascular tone of blood vessels. Depolarization of cardiac myocytes causes contraction of the cells and thus heart contraction occurs. Depolarization first begins in the SA node, which is also called the cardiac pacemaker. SA node has automaticity.
The resting membrane potential of SA node is less negative than that of other cardiac cells. This causes opening of sodium channels. Sodium ions continue to diffuse into the cells of SA node. The calcium ions then rush in, causing depolarization. Beginning in the SA node, the depolarization spreads to atria and through AV node an AV bundle to Purkinje fibers causing depolarization and contraction of ventricles.
The excitation of skeletal muscle by motor neurons causes the opening of voltage-gated sodium channels. The opening of sodium channels causes depolarization of the skeletal muscle. The action potential from the motor neuron also travels through the T-tubules.
Thus, contraction of skeletal muscle occurs. This entire process is also termed as excitation-contraction coupling. There are certain drugs that can block the process of depolarization.
They cause persistent opening of the ion channels. The positively charged ions continue to diffuse into the cells. As a result, the cells are unable to recover from the initial period of depolarization. Depolarization occurs when the nerve cell reverses these charges; to change them back to an at-rest state, the neuron sends another electrical signal. The entire process occurs when the cell allows specific ions to flow into and out of the cell. Polarization is the existence of opposite electrical charges on either side of a cell membrane.
In brain cells, the inside is negatively charged and the outside is positively charged. At least three elements are needed to make this possible. First, the cell needs molecules such as salts and acids, which have electrical charges on them. Second, the cell needs a membrane that will not let electrically charged molecules freely pass through it. Such a membrane serves to separate charges. Third, the cells need to have protein pumps in the membrane that can move electrically charged molecules to one side, storing one type of molecule on this side and another type on the other side.
A cell becomes polarized by moving and storing different types of electrically-charged molecules on different sides of its membrane. An electrically charged molecule is called an ion. Neurons pump sodium ions out of themselves, while bringing potassium ions in. Long-term potentiation and depression : Calcium entry through postsynaptic NMDA receptors can initiate two different forms of synaptic plasticity: long-term potentiation LTP and long-term depression LTD.
LTP arises when a single synapse is repeatedly stimulated. 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. 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. Short-term synaptic plasticity acts on a timescale of tens of milliseconds to a few minutes. Short-term synaptic enhancement results from more synaptic terminals releasing transmitters in response to presynaptic action potentials. Synapses will strengthen for a short time because of either an increase in size of the readily- releasable pool of packaged transmitter or an increase in the amount of packaged transmitter released in response to each action potential.
Depletion of these readily-releasable vesicles causes synaptic fatigue. Short-term synaptic depression can also arise from post-synaptic processes and from feedback activation of presynaptic receptors. Long-term potentiation LTP is a persistent strengthening of a synaptic connection, which can last for minutes or hours. These receptors are normally blocked by magnesium ions. Activated AMPA receptors allow positive ions to enter the cell.
Therefore, 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 so that the postsynaptic neuron is more likely to fire in response to presynaptic neurotransmitter release.
Some drugs co-opt the LTP pathway; this synaptic strengthening can lead to addiction. 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. With the decrease in AMPA receptors in the membrane, the postsynaptic neuron is less responsive to the glutamate released from the presynaptic neuron.
The weakening and pruning of unused synapses trims unimportant connections, leaving only the salient connections strengthened by long-term potentiation. Privacy Policy. Skip to main content. The Nervous System. Search for:. How Neurons Communicate. Nerve Impulse Transmission within a Neuron: Resting Potential The resting potential of a neuron is controlled by the difference in total charge between the inside and outside of the cell.
Learning Objectives Explain the formation of the resting potential in neurons. Key Takeaways Key Points When the neuronal membrane is at rest, the resting potential is negative due to the accumulation of more sodium ions outside the cell than potassium ions inside the cell.
Potassium ions diffuse out of the cell at a much faster rate than sodium ions diffuse into the cell because neurons have many more potassium leakage channels than sodium leakage channels. Sodium-potassium pumps move two potassium ions inside the cell as three sodium ions are pumped out to maintain the negatively-charged membrane inside the cell; this helps maintain the resting potential.
Key Terms ion channel : a protein complex or single protein that penetrates a cell membrane and catalyzes the passage of specific ions through that membrane membrane potential : the difference in electrical potential across the enclosing membrane of a cell resting potential : the nearly latent membrane potential of inactive cells. Nerve Impulse Transmission within a Neuron: Action Potential Signals are transmitted from neuron to neuron via an action potential, when the axon membrane rapidly depolarizes and repolarizes.
Learning Objectives Explain the formation of the action potential in neurons. Key Takeaways Key Points Action potentials are formed when a stimulus causes the cell membrane to depolarize past the threshold of excitation, causing all sodium ion channels to open. When the potassium ion channels are opened and sodium ion channels are closed, the cell membrane becomes hyperpolarized as potassium ions leave the cell; the cell cannot fire during this refractory period.
The action potential travels down the axon as the membrane of the axon depolarizes and repolarizes. Myelin insulates the axon to prevent leakage of the current as it travels down the axon. Nodes of Ranvier are gaps in the myelin along the axons; they contain sodium and potassium ion channels, allowing the action potential to travel quickly down the axon by jumping from one node to the next. Key Terms action potential : a short term change in the electrical potential that travels along a cell depolarization : a decrease in the difference in voltage between the inside and outside of the neuron hyperpolarize : to increase the polarity of something, especially the polarity across a biological membrane node of Ranvier : a small constriction in the myelin sheath of axons saltatory conduction : the process of regenerating the action potential at each node of Ranvier.
Synaptic Transmission Synaptic transmission is a chemical event which is involved in the transmission of the impulse via release, diffusion, receptor binding of neurotransmitter molecules and unidirectional communication between neurons.
Learning Objectives Describe the process of synaptic transmission. Key Takeaways Key Points In a chemical synapse, the pre and post synaptic membranes are separated by a synaptic cleft, a fluid filled space. The neurotransmitter termination can occur in three ways — reuptake, enzymatic degradation in the cleft and diffusion.
Signal Summation Signal summation occurs when impulses add together to reach the threshold of excitation to fire a neuron. Learning Objectives Describe signal summation. Key Takeaways Key Points Simultaneous impulses may add together from different places on the neuron to reach the threshold of excitation during spatial summation.
When individual impulses cannot reach the threshold of excitation on their own, they can can add up at the same location on the neuron over a short time; this is known as temporal summation.
The action potential of a neuron is fired only when the net change of excitatory and inhibitory impulses is non-zero.
0コメント