ABSTRACT
The number of methods by which glutamatergic neurotransmission may be hypothetically modulated is incalculable. Such control is maintained by the content of the genome and regulation of its expression at the DNA, RNA, and protein levels. It is affected by presynaptic glutamate release with one or more cotransmitters. The synaptic neurons are regulated by a multitude of extraneuronal factors, including the glial cells, gap junctions, stimulatory or inhibitory inputs and their rates, pH, and a vast network of other cells inside and outside the central nervous system that secrete transmitter substances. The intracellular machinery of synaptic cells may vary among individuals on a genetic, allelic, or proteonomic basis. Because we do not have the capability to regulate neural networks at present, I shall restrict subsequent observations to the single synapse. We are also limited in being able to alter transcription and translation, and so I shall discuss molecular genetics and pharmacogenomics fairly superficially.
