Final answer:
Protein kinases such as CaMKII are activated by the influx of calcium through NMDA receptors, leading to a cascade of events that result in gene expression and the development of new synapses, crucial for synaptic plasticity and long-term potentiation (LTP).
Step-by-step explanation:
The development of new synapses and synaptic plasticity involves complex protein signaling pathways in neurons. One of the key players in this process is calcium (Ca2+), which enters the neuron through NMDA receptors during synaptic activity. The influx of Ca2+ activates a series of protein kinases, such as CaMKII and PKA, which in turn initiate a signaling cascade. This cascade can lead to the phosphorylation of AMPA receptors, increasing their conduction efficiency, and can also trigger gene transcription involved in the neuronal changes underpinning synaptic plasticity.
Essentially, proteins like CaMKII act as gene regulators for developing new synapses by responding to the postsynaptic calcium spikes caused by neurotransmitter release and synaptic activity. This process leads to long-term potentiation (LTP), a cellular mechanism for learning and memory. Therefore, it is the coordinated action of intracellular Ca2+ levels, protein kinases, and gene expression that controls the development of new synapses, crucial for neural plasticity and cognitive functions.