GABA-related Synaptic Plasticity in Neuropathic Hypersensitivity
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Abstract
It was believed that the role of synapse was simply to send information between the neural network and the other nerve cell or the neuronal cell and the muscle cell. In addition, it was thought that these compounds that were made during the development were relatively strong, as did the solder joining of two electronic components. The thrilling development in neurobiology over the last 40 years has made it possible for most synapses to be extremely plastic. They can change their strength by their own actions or activities in another way. Synaptic structures such as active region, postsynaptic density (PSD) and dendritic spine are strongly correlated with their dimensions and correlate with synaptic intensity. Synaptic plasticity controls the communication between two neurons. The power of communication between two synapses can be compared to the state of the conversation. Neuropathic pain can be classified as peripheral or central to its genesis and is divided into episodic and persistent symptoms. Episodic neuropathic pain occurs during complete remission of the symptoms, while continuous neuropathic pain is a condition for continuous acute pain. Gamma-Aminobutyric acid (GABA) is the inhibitory neurotransmitter in the central nervous system (CNS), which has been identified functioning as an essential modulator of synaptic plasticity in the CNS development and degeneration. We hereby reviewed the role of GABA in synaptic plasticity in the context of neuropathic hypersensitivity.
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GABA, Synaptic Plasticity, Nerve Injury, Neuropathic Pain, Mechanisms
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