Depolarization stimulates the release of the neuro-transmitter from the terminal end of the neuron.
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.
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Calcium (Ca2+) channels open on the synaptic end bulb in response to depolarization (from the action potential), inducing exocytosis of synaptosomes containing neurotransmitter, resulting in neurotransmitter being released into the synaptic cleft...further propagating the signal to the next neuron or set of neurons.
The effect of a neurotransmitter is determined by the type of receptors it binds to on the postsynaptic neuron. If the neurotransmitter activates ion channels that allow positive ions to flow into the neuron, it typically has an excitatory effect, leading to depolarization. Conversely, if it opens channels for negative ions or closes channels for positive ions, it results in hyperpolarization and an inhibitory effect. Thus, the same neurotransmitter can have different effects depending on the receptor type and the ions involved.
Depolarization at the motor end plate upon arrival of action potentials triggers the release of neurotransmitter acetylcholine into the synaptic cleft. This acetylcholine then binds to receptors on the muscle cell membrane, initiating muscle contraction by depolarizing the muscle cell membrane and allowing the action potential to propagate along the muscle fiber.
The combining of the neurotransmitter with the muscle membrane receptors causes the membrane to become permeable to sodium ions and depolarization of the membrane. This depolarization triggers an action potential that leads to muscle contraction.
Glutamate is the primary excitatory neurotransmitter in the central nervous system. It enhances the transmission of signals between neurons by promoting the depolarization of postsynaptic 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.
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Calcium (Ca2+) channels open on the synaptic end bulb in response to depolarization (from the action potential), inducing exocytosis of synaptosomes containing neurotransmitter, resulting in neurotransmitter being released into the synaptic cleft...further propagating the signal to the next neuron or set of neurons.
EPSP stands for excitatory postsynaptic potential. It is a temporary depolarization of postsynaptic membrane potential caused by the flow of positively charged ions into the neuron, usually due to the binding of neurotransmitters to their receptors. EPSPs can help to trigger an action potential in the neuron.
The effect of a neurotransmitter is determined by the type of receptors it binds to on the postsynaptic neuron. If the neurotransmitter activates ion channels that allow positive ions to flow into the neuron, it typically has an excitatory effect, leading to depolarization. Conversely, if it opens channels for negative ions or closes channels for positive ions, it results in hyperpolarization and an inhibitory effect. Thus, the same neurotransmitter can have different effects depending on the receptor type and the ions involved.
The first step toward generating a skeletal muscle contraction is the release of acetylcholine (ACh) at the neuromuscular junction. This neurotransmitter binds to receptors on the muscle fiber's membrane, leading to the depolarization of the muscle cell and the initiation of an action potential. This depolarization triggers the release of calcium ions from the sarcoplasmic reticulum, ultimately leading to muscle contraction.
Depolarization in a hair cell is triggered by mechanical stimulation, such as sound waves or movement, while depolarization in a typical neuron is triggered by chemical signals.
Depolarization at the motor end plate upon arrival of action potentials triggers the release of neurotransmitter acetylcholine into the synaptic cleft. This acetylcholine then binds to receptors on the muscle cell membrane, initiating muscle contraction by depolarizing the muscle cell membrane and allowing the action potential to propagate along the muscle fiber.
When a neurotransmitter binds to its receptor on the motor endplate, it triggers the opening of ion channels in the postsynaptic membrane. This allows for the influx of ions, typically leading to depolarization of the muscle cell membrane and initiation of a muscle action potential. Subsequently, this leads to contraction of the muscle fiber.
A neurotransmitter is a chemical or peptide in synapses, usually between neurons, a neuron and muscle or a neuron and other organ. The neurotransmitter transmits information to and from and within the brain. When a neurotransmitter is released from the presynaptic cell in response to depolarization of the cell by an action potential, it diffuses across the synaptic cleft and binds a receptor or ligand-gated ion channel on the postsynaptic cell. Binding on the postsynaptic cell alters the resting potential of the postsynaptic cell in either an inhibitory or excitatory manner, making the cell less susceptible or more susceptible (respectively) to an action potential. Examples include, but are not limited to, acetylcholine, GABA, noradrenaline, serotonin and dopamine.