How does chemical synapses work

By moving calcium channels, bassoon can contribute to regulating neurotransmitter release, Gundelfinger explains, and in turn synaptic strength. Today microscopy lets scientists like Ege Kavalali, from the University of Texas Southwestern Medical Center in the US, observe synapse proteins move on millisecond scales. By modifying them with green fluorescent protein, his team monitors neurotransmitter release during exocytosis and recycling in endocytosis.

There are competing hypotheses about endocytosis, Kavalali explains. It took over a decade to develop the techniques needed, such as intracellular vesicle impact electrochemical cytometry IVIEC.

IVIEC pierces cell membranes with a 50—nm diameter carbon fibre electrode, while voltages cycle from lower to higher values and back. This oxidises and reduces the chemicals released as the vesicles rupture, and the scientists measure the tiny resulting current changes, which indicate chemical concentrations.

Experiments like this show that most exocytosis events empty vesicles more thoroughly than usually expected in kiss-and-run — but not completely, Ewing says. But how they close is more important for determining how much neurotransmitter they release, he adds. The vesicles have a different membrane composition than the plasma membrane around the cell. Some of that membrane is exchanged. Such membrane composition changes are a molecular memory that might influence plasticity, Ewing speculates.

Membrane composition changes would also help explain how drugs and diet can influence synapse function, he adds. For example, zinc is thought to regulate learning. That activates the release machinery, causing a dangerous neurotransmitter flood.

To do so, it binds to proteins near the synapse, located on the presynaptic terminal. In subsequent years, the scientists found that neurexins are not just there to help out black widow toxins. They bind with neuroligins on post-synaptic terminals, helping align neurons precisely, with a synaptic cleft of around 20nm.

Today, proteomics is finding many other molecules that are potentially significant in brain disorders. 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. Neurotransmitters can either have excitatory or inhibitory effects on the postsynaptic membrane. There are several examples of well known neurotransmitters detailed in Table 1. This depolarization is called an excitatory postsynaptic potential EPSP and makes the postsynaptic neuron more likely to fire an action potential.

Release of neurotransmitter at inhibitory synapses causes inhibitory postsynaptic potentials IPSPs , a hyperpolarization of the presynaptic membrane. For example, when the neurotransmitter GABA gamma-aminobutyric acid is released from a presynaptic neuron, it binds to and opens Cl — channels.

Cl — ions enter the cell and hyperpolarizes the membrane, making the neuron less likely to fire an action potential. This can be accomplished in three ways: the neurotransmitter can diffuse away from the synaptic cleft, it can be degraded by enzymes in the synaptic cleft, or it can be recycled sometimes called reuptake by the presynaptic neuron.

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