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. Despite the amazing advancements in BCI technology, it also 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. Watch this video in which a paralyzed woman use a brain-controlled robotic arm to bring a drink to her mouth, among other images of brain-computer interface technology in action.
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. In fact, 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.
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. These receptors are normally blocked by magnesium ions; however, when the postsynaptic neuron is depolarized by multiple presynaptic inputs in quick succession either from one neuron or multiple neurons , the magnesium ions are forced out allowing Ca ions to pass into the postsynaptic 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. 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, as illustrated in Figure The decrease in AMPA receptors in the membrane makes the postsynaptic neuron less responsive to glutamate released from the presynaptic neuron.
The weakening and pruning of unused synapses allows for unimportant connections to be lost and makes the synapses that have undergone LTP that much stronger by comparison. Neurons have charged membranes because there are different concentrations of ions inside and outside of the cell. Voltage-gated ion channels control the movement of ions into and out of a neuron. When a neuronal membrane is depolarized to at least the threshold of excitation, an action potential is fired.
The action potential is then propagated along a myelinated axon to the axon terminals. In a chemical synapse, the action potential causes release of neurotransmitter molecules into the synaptic cleft. Through binding to postsynaptic receptors, the neurotransmitter can cause excitatory or inhibitory postsynaptic potentials by depolarizing or hyperpolarizing, respectively, the postsynaptic membrane.
In electrical synapses, the action potential is directly communicated to the postsynaptic cell through gap junctions—large channel proteins that connect the pre-and postsynaptic membranes. Synapses are not static structures and can be strengthened and weakened. Two mechanisms of synaptic plasticity are long-term potentiation and long-term depression. Skip to content Chapter The Nervous System. Learning Objectives By the end of this section, you will be able to: Describe the basis of the resting membrane potential Explain the stages of an action potential and how action potentials are propagated Explain the similarities and differences between chemical and electrical synapses Describe long-term potentiation and long-term depression.
Nerve Impulse Transmission within a Neuron. Neuronal Charged Membranes. Concept in Action. Resting Membrane Potential. Table The resting membrane potential is a result of different concentrations inside and outside the cell. Figure Action Potential. The formation of an action potential can be divided into five steps: 1 A stimulus from a sensory cell or another neuron causes the target cell to depolarize toward the threshold potential.
The hyperpolarized membrane is in a refractory period and cannot fire. Myelin and the Propagation of the Action Potential. Synaptic Transmission.
Chemical Synapse. Fusion of a vesicle with the presynaptic membrane causes neurotransmitter to be released into the synaptic cleft , the extracellular space between the presynaptic and postsynaptic membranes, as illustrated in Figure The neurotransmitter diffuses across the synaptic cleft and binds to receptor proteins on the postsynaptic membrane.
Communication at chemical synapses requires release of neurotransmitters. The calcium entry causes synaptic vesicles to fuse with the membrane and release neurotransmitter molecules into the synaptic cleft.
The neurotransmitter diffuses across the synaptic cleft and binds to ligand-gated ion channels in the postsynaptic membrane, resulting in a localized depolarization or hyperpolarization of the postsynaptic neuron. The binding of a specific neurotransmitter causes particular ion channels, in this case ligand-gated channels, on the postsynaptic membrane to open.
Imagine the case of a boat with a small leak below the water line. In order to keep the boat afloat, the small amount of water entering through the leak has to be pumped out, which maintains a lower water level relative to the open sea. Neurons do the same thing, but they pump out positively charged sodium ions. In addition, they pump in positively charged potassium ions potash to the gardeners out there!!
Thus there is a high concentration of sodium ions present outside the neuron, and a high concentration of potassium ions inside. The neuronal membrane also contains specialised proteins called channels , which form pores in the membrane that are selectively permeable to particular ions. Thus sodium channels allow sodium ions through the membrane while potassium channels allow potassium ions through.
OK, so far so good. Now, under resting conditions, the potassium channel is more permeable to potassium ions than the sodium channel is to sodium ions. So there is a slow outward leak of potassium ions that is larger than the inward leak of sodium ions. This means that the membrane has a charge on the inside face that is negative relative to the outside, as more positively charged ions flow out of the neuron than flow in. This difference in the concentrations of ions on either side of the membrane gives rise to the membrane potential and the membrane is said to be polarised.
The resting potential of a neuron is controlled by the difference in total charge between the inside and outside of the cell. For the nervous system to function, neurons must be able to send and receive signals. These signals are possible because each neuron has a charged cellular membrane a voltage difference between the inside and the outside. The charge of this membrane can change in response to neurotransmitter molecules released from other neurons and environmental stimuli.
Any voltage is a difference in electric potential between two points; for example, the separation of positive and negative electric charges on opposite sides of a resistive barrier. 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. 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.
The difference in total charge between the inside and outside of the cell is called the membrane potential. Ion channel configurations : Voltage-gated ion channels are closed at the resting potential and 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. For quiescent cells, the relatively-static membrane potential is known as the resting membrane potential. The resting membrane potential is at equilibrium since it relies on the constant expenditure of energy for its maintenance.
It is dominated by the ionic species in the system that has the greatest conductance across the membrane. For most cells, this is potassium. As potassium is also the ion with the most-negative equilibrium potential, usually the resting potential can be no more negative than the potassium equilibrium potential.
This voltage is called the resting membrane potential and is caused by differences in the concentrations of ions inside and outside the cell. If the membrane were equally permeable to all ions, each type of ion would flow across the membrane and the system would reach equilibrium.
Because ions cannot simply cross the membrane at will, there are different concentrations of several ions inside and outside the cell. 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 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.
More cations leaving the cell than entering it 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 it is established. As more cations are expelled from the cell than are taken in, the inside of the cell remains negatively charged relative to the extracellular fluid.
Signals are transmitted from neuron to neuron via an action potential, when the axon membrane rapidly depolarizes and repolarizes. A neuron can receive input from other neurons via a chemical called a neurotransmitter. If this input is strong enough, the neuron will pass the signal to downstream neurons. Transmission of a signal within a neuron in one direction only, from dendrite to axon terminal is carried out by the opening and closing of voltage-gated ion channels, which cause a brief reversal of the resting membrane potential to create an action potential.
As an action potential travels down the axon, the polarity changes across the membrane. Once the signal reaches the axon terminal, it stimulates other neurons.
Formation of an action potential : The formation of an action potential can be divided into five steps. The hyperpolarized membrane is in a refractory period and cannot fire. At excitatory synapses, positive ions flood the interior of the neuron and depolarize the membrane, decreasing the difference in voltage between the inside and outside of the neuron. Once the threshold potential is reached, the neuron completely depolarizes.
At this point, the sodium channels return to their resting state, ready to open again if the membrane potential again exceeds the threshold potential. For an action potential to communicate information to another neuron, it must travel along the axon and reach the axon terminals where it can initiate neurotransmitter release. Myelin acts as an insulator that prevents current from leaving the axon, increasing the speed of action potential conduction.
Diseases like multiple sclerosis cause degeneration of the myelin, which slows action potential conduction because axon areas are no longer insulated so the current leaks. Action potential travel along a neuronal axon : The action potential is conducted down the axon as the axon membrane depolarizes, then repolarizes.
A node of Ranvier is a natural gap in the myelin sheath along the axon. 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. Nodes of Ranvier : Nodes of Ranvier are gaps in myelin coverage along axons.
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