The Genetics of Slow Tonic Neurovascular Coupling in Mammalian Brain

Individual neurons in the central nervous system have given up their ability to reproduce or to feed themselves, and in exchange for loss of these functions, neurons are able to survive for periods of 100 years or more. Neurons are serviced by oligodendrocytes which protect, and astrocytes which serve as a conduit to provide sustenance obtained from the vascular system, to neurons and oligodendrocytes. For neurons with elongated axons, oligodendrocytes encircle, and in white matter, form lipid-rich myelin sheaths enclosing each axon in order to prevent axon to axon message interactions. Longevity of neurons is required for normal brain function in that it allows neurons to record and store information in the form of “memories” that can then be accessed over their lifetime. To do this, neurons require large amounts of energy, sometimes within seconds (rapid phasic), and at other times over minutes (slow tonic). In this commentary, the genetic mechanisms used by neurons to accomplish slow tonic delivery of energy are described.

Keywords: Brain, Canavan disease, Genes, Genetic engineering, Neurovascular coupling.

Abbreviations Used: Ac, acetate; AcCoA, acetylcoenzyme A; AP, action potential; Asp, aspartate; ASPA, aspartoacylase; CD, Canavan disease; ECF, extracellular fluid; Glc, glucose; Glu, glutamate; Gln, glutamine; GM, gray matter; mGluR3, metabotropic Glu receptor 3; NAA, N-acetylaspartate; NAAG, Nacetylaspartylglutamate; NVC, neurovascular coupling; WM, white matter.