Post-synaptic potentials can travel up to a few millimeters along the dendrites of a neuron before they die out. The strength and duration of the signal can be influenced by various factors such as the size and shape of the neuron, the properties of the synaptic connection, and the presence of neurotransmitters.
A synaptic potential exists at the INPUT of a neuron (dendrite), and an action potential occurs at the OUTPUT of a neuron (axon). (from OldGuy)(from Ilantoren:) A synaptic potential is the result of many excitatory post synaptic potentials (epsp) each one caused by the synaptic vesicles released by the pre-synaptic terminus. If there are enough of these epsp then the responses will summate and depolarize the post-synaptic membrane at the axon hillock enough to fire an action potential.
The cause of excitatory post-synaptic potentials is the influx of sodium ions into the postsynaptic neuron. This influx of positive charge depolarizes the neuron, making it more likely to generate an action potential.
Protein molecules on the post-synaptic cell membrane form receptor sites that bind with neurotransmitters released from the pre-synaptic neuron. This binding triggers downstream signaling pathways within the post-synaptic cell, leading to various cellular responses.
Acetylcholine (ACh) does not remain on the post-synaptic membrane because it is rapidly broken down by the enzyme acetylcholinesterase. This enzymatic degradation occurs in the synaptic cleft, preventing prolonged stimulation of the post-synaptic receptors. Additionally, the reuptake of choline into the pre-synaptic neuron helps recycle components for future neurotransmitter synthesis. This process ensures that synaptic transmission is brief and precisely regulated.
The cause of synaptic delay is attributed mainly to the time needed for the synaptic vesicles to release neurotransmitter into the synaptic cleft. While it can be considered a combination of binding to the presynaptic membrane (which is relatively a transient process) and subsequent exocytosis of the neurotransmitter, the main factor is release. Additionally, it does take a very short period of time for the neurotransmitter to diffuse across the synaptic cleft and bind to to its receptors on the post-synaptic membrane.
Local graded potentials are small changes in membrane potential that occur in response to neurotransmitter binding to ligand-gated ion channels on the post-synaptic neuron. These potentials can summate and affect the likelihood that an action potential will be generated in the neuron. They are also referred to as synaptic potentials.
A synaptic potential exists at the INPUT of a neuron (dendrite), and an action potential occurs at the OUTPUT of a neuron (axon). (from OldGuy)(from Ilantoren:) A synaptic potential is the result of many excitatory post synaptic potentials (epsp) each one caused by the synaptic vesicles released by the pre-synaptic terminus. If there are enough of these epsp then the responses will summate and depolarize the post-synaptic membrane at the axon hillock enough to fire an action potential.
The process by which inhibitory and excitatory post-synaptic potentials summate and control the rate of firing of a neuron.
Synapses occur between two neurons. Electrical activitiy in the pre-synaptic neuron influences the post-synaptic neuron. There are two types of synapses in the body: Electrical and chemical. Electrical synapses occur in pre and post synaptic neurons that are joined via gap junctions. Currents from action potentials flow across the junction through channels called connexons. This current will depolarize the membrane of the post synaptic neuron to threshold, which will continue the action potential in the cell. Electrical synapses are fast and bidirectional. However, they are mainly found in cardiac and smooth muscles, and not in the mammalian nervous system.Chemical synapses use neurotransmitters. Depolarization occurs in the pre-synaptic neuron and calcium ions rush in. The calcium ions activate neurotransmitter release into the synaptic cleft. The neurotransmitters reach the post-synaptic neuron and cause action potentials to develop.Note: this can go into much more detail
The cause of excitatory post-synaptic potentials is the influx of sodium ions into the postsynaptic neuron. This influx of positive charge depolarizes the neuron, making it more likely to generate an action potential.
The small space separating pre and post-synaptic neurons is called the synaptic cleft. This cleft allows for the transmission of chemical signals, known as neurotransmitters, from the pre-synaptic neuron to the post-synaptic neuron to occur. The neurotransmitters are released by the pre-synaptic neuron and bind to receptors on the post-synaptic neuron to transmit the signal.
Yes
Calcium ions enter the presynaptic neuron resulting in the release of neurotransmitter from the per-synaptic membrane. The neurotransmitter diffuses across the synaptic cleft, fusing with the receptors of the post-synaptic membrane. This changes the sodium channels to open and sodium ions will to flow into the post-synaptic neuron, depolarizing the post-synaptic membrane. This initiates an action potential. After the post-synaptic neuron has been affected, the neurotransmitter is removed by a type of enzyme called cholinesterase. The inactivated neurotransmitter then returns to the pre-synaptic neuron.
Chemically Gated Channels.
Protein molecules on the post-synaptic cell membrane form receptor sites that bind with neurotransmitters released from the pre-synaptic neuron. This binding triggers downstream signaling pathways within the post-synaptic cell, leading to various cellular responses.
Acetylcholine (ACh) does not remain on the post-synaptic membrane because it is rapidly broken down by the enzyme acetylcholinesterase. This enzymatic degradation occurs in the synaptic cleft, preventing prolonged stimulation of the post-synaptic receptors. Additionally, the reuptake of choline into the pre-synaptic neuron helps recycle components for future neurotransmitter synthesis. This process ensures that synaptic transmission is brief and precisely regulated.
The synapse between pre synaptic and post synaptic neuron. Here the acetylcholine is released. It is destroyed by the enzyme acetylcholinesterase in milliseconds, once the impulse is passed to the post synaptic neuron