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Synaptic Transmission
From Tori Hickey. Due 1/23/17

Basic Information
Synaptic transmission is defined as “the process by which signaling molecules, called neurotransmitters, are released by a presynaptic neuron and bind to/activate the receptors of a different, postsynaptic neuron” (Wikipedia, 2017). This process allows for communication between neurons. An action potential (electrical event in response to a stimuli) will take place in the initial (unmyelinated) segment of the axon. It will propagate down the axon and cause a release of a neurotransmitter at the axon terminals. These neurotransmitters will then carry across the gap junction or synapse and bind to their respective receptors on the dendrites of a different neuron. This way the neurons can carry information across the body. Some common neurotransmitters found in the body include dopamine, norepinephrine, epinephrine, histamine, serotonin, etc, each one having an important role in the normal functions of everyday life.

Action Potentials and Minis
Action potentials are electrical events that play a central role in cell-to-cell communication. These events are elicited by voltage-gated ion channels in the plasma membrane. Sodium and calcium channels open when the membrane potential increases to a specific threshold (approximately -70mV in humans). Once they open, sodium and calcium ions flow into the cell producing a rise in membrane potential. This influx causes the membrane potential polarity to reverse causing the ion channels to inactivate. Potassium channels are then opened, allowing the potassium inside the cell to flow outwardly, returning the membrane potential to its original resting state. This shift allows for an action potential to occur. The action potential will travel down the neuron to the terminal buttons where it causes a release of neurotransmitters. Once the action potential is fired, the cell enters a refractory period where it remains inactive, allowing ample time for the action potential to travel down the neuron.

Action potentials require a stimulus to be elicited, but there are smaller spontaneous events that also take place across a synapse. Without any stimulation, small vesicles on the presynaptic neuron fuse with the membrane constantly. When these vesicles fuse, it releases a neurotransmitter all the same, which will then bind to the receptors on a postsynaptic neuron giving a much smaller electrical event. These events are called miniature end plate potentials (MEPPs, or minis) and is the smallest amount of signal that one neuron can send to another. The normal evoked endplate potential (EPP) is the threshold required to fire an action potential. As of currently, it is still not quite clear of the reason that these minis take place. There is ongoing research as to why these spontaneous events take place, and what function they have in synaptic transmission. Future research plans on focusing on a ketogenic diet, this includes the disruption of glutamatergic synaptic transmission and inhibition of glycolysis which is thought to decrease the electric excitability of neurons. Decreasing the excitability of neurons could possibly allow researchers to develop a treatment for epilepsy (Lutas and Yellen, 2013).

Bernard Katz
Sir Bernard Katz was a German biophysicist who won the Nobel Prize in physiology and medicine in 1970. Katz's research focused on the fundamental properties of synapses. His work influenced the study of organophosphates and organochlorines. These were used to study nerve agents and pesticides post-war (Sakmann, 2007).

Bernard Katz hypothesized that MEPPs were caused by the spontaneous and random release of  ACh. Katz claimed that the EPP is due to the summation effects of many vesicles fusing, therefore MEPPs, occurring at the same time. Katz and his colleagues experimented with this mechanism by lowering the extracellular concentration of calcium to reduce the EPPs so they could focus on the MEPPs. Using his results, he proposed the Quantal Hypothesis of Synaptic Transmission, stating that, “An action potential in the presynaptic cell produces an influx of Ca2+which promotes the exocytosis of synaptic vesicles from the presynaptic terminal. There is a statistical variability in the amount of vesicles that can be released. When the extracellular calcium concentration is low, sometimes there is not enough calcium to release any vesicles. At other times, there is enough calcium to cause the release of one vesicle and other times two vesicles, or three vesicles, and so forth. Each peak is therefore an integral multiple of the next, indicating that these vesicles are released in a quantized fashion.” (Byrne, 2015)