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Later, synaptic vesicles could also be isolated from other tissues such as the superior cervical ganglion, [40] or the octopus brain. [41] The isolation of highly purified fractions of cholinergic synaptic vesicles from the ray Torpedo electric organ [42] [43] was an important step forward in the study of vesicle biochemistry and function.
However, low levels of EAAT2 are also found in the axon-terminals of hippocampal CA3 pyramidal cells. [14] EAAT2 is responsible for over 90% of glutamate reuptake within the central nervous system (CNS). [7] [12] The EAAT3-4 subtypes are exclusively neuronal, and are expressed in axon terminals, [8] cell bodies, and dendrites.
Vesicular transporters move neurotransmitters into synaptic vesicles, regulating the concentrations of substances within them. [2] Vesicular transporters rely on a proton gradient created by the hydrolysis of adenosine triphosphate (ATP) in order to carry out their work: v-ATPase hydrolyzes ATP, causing protons to be pumped into the synaptic ...
Diagram of a chemical synaptic connection. In the nervous system, a synapse [1] is a structure that allows a neuron (or nerve cell) to pass an electrical or chemical signal to another neuron or a target effector cell. Synapses can be classified as either chemical or electrical, depending on the mechanism of signal transmission between neurons.
Axonal transport, also called axoplasmic transport or axoplasmic flow, is a cellular process responsible for movement of mitochondria, lipids, synaptic vesicles, proteins, and other organelles to and from a neuron's cell body, through the cytoplasm of its axon called the axoplasm. [1]
Alpha-synuclein is a neuronal protein that regulates synaptic vesicle trafficking and subsequent neurotransmitter release. [6] [7] It is abundant in the brain, while smaller amounts are found in the heart, muscle and other tissues. In the brain, alpha-synuclein is found mainly in the axon terminals of presynaptic neurons. [5]
The pre-synaptic axon shows an increase in synaptic volume and area, an increase of synaptic vesicles, clustering of vesicles at the active zone, and polarization of the pre-synaptic membrane. These changes are thought to be mediated by neurotrophin and cell adhesion molecule release from muscle cells, thereby emphasizing the importance of ...
Once the vesicle is released, glutamate is removed from the synaptic cleft by excitatory amino-acid transporters (EAATs). This allows synaptic terminals and glial cells to work together to maintain a proper supply of glutamate, which can also be produced by transamination of 2-oxoglutarate, an intermediate in the citric acid cycle. [1]