Short review on the role of intracellular calcium in synaptic plasticity

Calcium (Ca) is ubiquitous second messenger in every living organism. Ca is inevitable, as the neurone functions in information reception, integration, processing, interpretation and subsequent activation of the peripheral nervous system to produce effect in the target organ. Normal intracellular calcium concentration ([Ca2+]i) ranges between 70 nM -150 nM [1]. The above mentioned functions connote plasticity. Synaptic plasticity is activity dependent alteration in synaptic strength, which mediates memory storage mechanism [2-4]. Donald Hebb (1949) postulated that excitatory synapses that link two cells could be strengthened if both cells were simultaneously activated [5]. This can be divided into long and short term plasticity. The long term plasticity is subdivided into long term potentiation (LTP) and depression (LTD). The short term plasticity is also subdivided into short term potentiation (STP) and depression (STD). I took a look at the various forms of synaptic plasticity and later on x-rayed the role of Ca in long-term, short-term plasticity and also the influence of neuronal Ca stores on calcium dynamic. Ca serves as a trigger for neurotransmitter release, sustains long term plasticity, which encodes long term memory and learning. The residual Ca mediates short term plasticity which likewise encodes short term memory. Thus calcium is essential in all forms of synaptic plasticity

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