Receptors, phosphoinositol hydrolysis and plasticity of nerve cells

Excitatory amino acid neurotransmission has been shown to be necessary but may not be sufficient, for the production of LTP and other prolonged changes in synaptic transmission. Excitatory neurotransmission may produce depolarization-induced increases in intracellular calcium that cause PI hydrolysis and synergistically potentiate receptor-G protein induced PI hydrolysis. This synergistic potentiation of phosphoinositide hydrolysis, and increased [Ca]i due to positive cross stimulation, may lead to depolarization block, a persistent increase in protein kinase activation, altered morphology, oncogene activity and other plasticity changes important in memory.