LTP is a process by which synaptic connections between neurons become stronger with frequent activation. LTP is thought to be a way in which the brain changes in response to experience, and thus may be a mechanism underlying learning and memory.
There are a number of ways in which LTP can occur. The best-known mechanism involves a glutamate receptor known as the NMDA and AMPA receptor. In the postsynaptic neuron, both NMDA and AMPA receptors are together and activated by the binding of the neurotransmitter glutamate. AMPA receptor is permeable to the sodium ions, and NMDA is permeable to both sodium and calcium ions. In NMDA-receptor dependent LTP, glutamate release first activates a subtype of glutamate receptor known as the AMPA receptor. NMDA receptors are found nearby these AMPA receptors, but are not activated by low levels of glutamate release because the ion channel of an NMDA receptor is blocked by a magnesium ion. If frequent action potentials cause greater stimulation of AMPA receptors, however, this will cause the postsynaptic neuron to depolarize, which eventually causes the voltage-dependent magnesium blockage of the NMDA receptor to be removed, allowing calcium ions to flow in through the NMDA receptor. This influx of calcium initiates cellular mechanisms that cause more AMPA receptors to be inserted into the neuron’s membrane. The new AMPA receptors are also more responsive to glutamate, and allow more positively charged ions to enter the cell when activated. Now, the postsynaptic cell is more sensitive to glutamate because it has more receptors to respond to it. Additionally, there are thought to be signals that travel back across the synapse to stimulate greater levels of glutamate release.
Thus, as said before LTP makes the synapses stronger and more likely to be activated in the future.