When a neurotransmitter binds to a receptor on the postsynaptic side of the synapse, it changes the postsynaptic cell's excitability: it makes the postsynaptic cell either more or less likely to fire an action potential. If the number of excitatory postsynaptic events is large enough, they will add to cause an action potential in the postsynaptic cell and a continuation of the "message. Many psychoactive drugs and neurotoxins can change the properties of neurotransmitter release, neurotransmitter reuptake and the availability of receptor binding sites.
Sherrington, in It was probably Charles S. Sherrington who coined the term synapse. The word "synapse" is derived from the Greek words "syn" and "haptein" that mean "together" and "to clasp," respectively.
They are who you are. See some synapses "Up Close and Personal". Play the Interactive Word Search Game on the neuron and neurotransmitters. Betarbet, R.
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Lee, C. Mitochondrial clustering at the vertebrate neuromuscular junction during presynaptic differentiation. Lee, Y. Cell 15, — Li, H. Bcl-xL induces Drp1-dependent synapse formation in cultured hippocampal neurons. Lnenicka, G. Although mitochondria have an established role in the post-tetanic potentiation of synaptic strength, little is known about their impact on other forms of short-term synaptic plasticity. Lastly, while we know that mitochondria influence neurotransmitter release and synaptic plasticity in large nerve terminals very little is known about their influence in small terminals, typical of the mammalian CNS.
These are glaring gaps in our knowledge, particularly as synaptic plasticity allows for changes in synaptic strength, a phenomenon underlying learning and memory. More troubling perhaps, is that mitochondrial dysfunction is found at the epicenter of many neurodegenerative conditions for which the pathogenesis and progression are poorly understood. The central hypothesis is that mitochondria influence neurotransmitter release through multiple mechanisms, and the architecture of the nerve terminal and its firing history determines which mechanism is influential.
We bring a combined electrophysiological, imaging and genetic approach to address this hypothesis at Drosophila nerve terminals in vivo, and we introduce a novel peripheral synapse with a single release-site as a model for central synapses with the same architecture. An understanding of how mitochondrial function influences synaptic transmission under non-pathological conditions will provide the foundation required to understand the role of mitochondria in pathological conditions.
Mitochondria are organelles within all cells of the human body that generate most of our energy. They concentrate within nerve endings where they power communication between nerves, a fundamental activity of the brain.
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