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Let's picture a presynaptic neuron, a synaptic cleft, and a postsynaptic neuron.
An action potential reaches the terminal of a presynaptic neurone and triggers an opening of Ca ions enters into the depolarized terminal. This influx of Ca ions causes the presynaptic vesicles to fuse with the presynaptic membrane. This releases the neurotransmitters into the synaptic cleft.
The neurotransmitters diffuse through the synaptic cleft and bind to specific postsynaptic membrane receptors. This binding changes the receptors into a ion channel that allows cations like Na to enter into the postsynaptic neuron. As Na enters the postsynaptic membrane, it begins to depolarize and an action potential is generated.
What else can I help you with?
Are neurotransmitters that depress the resting potential called excitatory?
No, neurotransmitters that depress the resting potential are called inhibitory neurotransmitters. Excitatory neurotransmitters have the opposite effect, causing depolarization and increasing the likelihood of an action potential.
Which electrolyte flows into the cell to initiate depolarization?
potassium The answer of potassium is dead wrong. Sodium is the electrolyte that flows into the cell to initiate depolarization. Potassium flows into the cell during repolarization.
What allow the nerve impulses that initiate muscle contraction to travel along the sarcolmena?
Nerve impulses initiate muscle contraction by traveling along the sarcolemma through a process called depolarization. When a nerve impulse reaches the neuromuscular junction, it releases neurotransmitters that bind to receptors on the sarcolemma, leading to a change in membrane potential. This depolarization creates an action potential that propagates along the sarcolemma and into the T-tubules, allowing the signal to reach the muscle fibers and trigger contraction. Additionally, the presence of voltage-gated sodium channels facilitates the rapid transmission of these impulses.
Opening of these channels leads to what of the motor endplate?
Opening of these channels leads to depolarization of the motor endplate, which triggers the release of neurotransmitters (such as acetylcholine) from synaptic vesicles. This initiates the muscle contraction process by activating the muscle fibers.
Binding of the neurotransmitters with muscle membrane receptors causes the membrane to become permeable to sodium resulting in the influx of sodium ions an what of the membrane?
depolarization
How do neurotransmitters initiate action potentials?
Neurotransmitters can help bring another neuron to the point where it initiates an action potential by binding to postsynaptic receptor sites. If the receptors are the type that allow positively charged ions to flux through the cell membrane, and if this happens on a large enough scale (i.e., multiple sites are hit at once), then the probability of an action potential occurring becomes very high.
What causes Local depolarization that leads to generate action potential?
Local depolarization is caused by the opening of voltage-gated sodium channels in response to the binding of neurotransmitters or other stimuli. This influx of sodium ions results in membrane depolarization, reaching the threshold potential needed to generate an action potential.
Is depolarization in the heart passed cell to cell in the same way they are the neuromuscular junction?
No, depolarization in the heart is not passed cell to cell in the same way as at the neuromuscular junction. In the heart, gap junctions allow for direct electrical coupling between adjacent cardiac muscle cells, allowing the depolarization signal to quickly spread from cell to cell. In the neuromuscular junction, depolarization is transmitted by the release of neurotransmitters across the synaptic cleft from a neuron to a muscle cell.
What neurotransmitter usually depolarizes post synaptic neurons?
The neurotransmitter that typically depolarizes postsynaptic neurons is glutamate. Glutamate binds to its receptors, such as AMPA and NMDA receptors, resulting in an influx of sodium ions (Na+) into the postsynaptic neuron. This depolarization can lead to the generation of an action potential if the depolarization reaches the threshold. Other neurotransmitters, like acetylcholine, can also cause depolarization in specific contexts.
Neurotransmitters attach to what molecules in the cell membrane?
Neurotransmitters attach to specific proteins called receptors on the cell membrane. These receptors are typically ligand-gated ion channels or G protein-coupled receptors that initiate cellular responses when neurotransmitters bind to them.
Where EPSP is produced?
Excitatory postsynaptic potentials (EPSPs) are produced at the postsynaptic membrane of neurons, specifically in response to the binding of neurotransmitters to receptors on that membrane. These neurotransmitters are released from the presynaptic neuron during synaptic transmission. The binding of the neurotransmitters typically leads to the opening of ion channels, allowing positively charged ions (such as sodium) to flow into the postsynaptic cell, resulting in depolarization and the generation of an EPSP.
How are nerve impulses prevented from traveling the wrong way on axon?
On the axon hillock, there is a concentration of sodium channels whose role are to initiate the depolarization and signal transmission allong the axon. Once the all or none threshold is reached, depolarization occurs in a cascade unidirectional along the length of the axon, with potassium channels open just following the sodium-channel mediated depolarization, such that there is no back-propagation of the signal.
