Blood flow in the brain is regulated by neurons and astrocytes. Knowledge of how these cells control blood flow is crucial for understanding how neural computation is powered, for interpreting functional imaging scans of brains, and for developing treatments for neurological disorders. It is now recognized that neurotransmitter-mediated signalling has a key role in regulating cerebral blood flow, that much of this control is mediated by astrocytes, that oxygen modulates blood flow regulation, and that blood flow may be controlled by capillaries as well as by arterioles. These conceptual shifts in our understanding of cerebral blood flow control have important implications for the development of new therapeutic approaches.

/pdf/glial-and-neuronal-control-of-brain-blood-flow-mtem2xge3x.pdf

Glial and neuronal control of brain blood flow.

Spreading depression (SD) and the related hypoxic SD-like depolarization (HSD) are characterized by rapid and nearly complete depolarization of a sizable population of brain cells with massive redi...

https://www.physiology.org/doi/pdf/10.1152/physrev.2001.81.3.1065

Mechanisms of Spreading Depression and Hypoxic Spreading Depression-Like Depolarization

The characteristic form and development of sensory disturbances during migraine auras suggests that the underlying mechanism is a disturbance of the cerebral cortex, probably the cortical spreading depression (CSD) of Leao. The demonstration of unique changes of brain blood flow during attacks of migraine with aura, which have been replicated in animal experiments during CSD, constitutes another important line of support for the 'spreading depression' theory, which may be a key to an understanding of the migraine attack. Cortical spreading depression is a short-lasting depolarization wave that moves across the cortex at a rate of 3-5 mm/min. A brief phase of excitation heralds the reaction which is immediately followed by prolonged nerve cell depression synchronously with a dramatic failure of brain ion homeostasis, efflux of excitatory amino acids from nerve cells and enhanced energy metabolism. Recent experimental work has shown that CSD in the neocortex of a variety of species including man is dependent on activation of a single receptor, the N-methyl-D-aspartate receptor, one of the three subtypes of glutamate receptors. The combined experimental and clinical studies point to fruitful areas in which to look for migraine treatments of the future and provide a framework within which important aspects of the migraine attack can be modelled.

Pathophysiology of the migraine aura. The spreading depression theory.

Spreading depression: a review of the clinical relevance.

We examined the effect of blockade of N-methyl-d-aspartate (NMDA) and non-NMDA subtype glutamate receptors on anoxic depolarization (AD) and cortical spreading depression (CSD). [K+]e and the direc...

https://journals.sagepub.com/doi/pdf/10.1038/jcbfm.1992.32

The Effect of Glutamate Receptor Blockade on Anoxic Depolarization and Cortical Spreading Depression

GRAFSTE~N (1956) proposed that the propagation of spreading depression is due to the release of potassium by excited cortical neural elements. The released K would depolarize adjacent elements and this depolarization would result in their excitation, and additional release of K. This concept accounts for the slow propagation of spreading depression (2-4mm/min). In support of this mechanism a release of 42K during spreading depression was demonstrated from the cortical surface in animals in which the cortex had been loaded with the tracer (BRINLEY, KANDEL and MARSHALL, 1960; KRIVANEK and BURES, 1960). Some of the features of spreading depression, like the slow potential change (LEAo, 1947), the impedance increase ( L E ~ o and FERREIRA, 1953; FREYGANG and LANDAU, 1955; VAN HARREVELD and OCHS, 1957), and the transport of water and chloride into apical dendrites (VAN HARREVELD, 1958; VAN HARREVELD and SCHADB, 1959), can be explained by the assumption that a permeability increase of the neuronal membrane for Na, and perhaps also for K and C1, occurs. Such a membrane change would result in depolarization of the apical dendrites and account for the slow potential change and the transport of extracellular NaCl and water into cellular elements by Donnan forces (VAN HARREVELD and OCHS, 1957; VAN HARREVELD, 1962). Since the current used to measure tissue impedance is mainly carried by extracellular electrolytes (VAN HARREVELD and OCHS, 1956) this would result in an impedance rise of the tissue. Asphyxiation of the cortex, after a latency of 2-3 min, causes a similar slow potential change ( L E ~ o , 1947) and a more pronounced impedance change ( L E ~ o and FERREIRA, 1953; VAN HARREVELD and OCHS, 1956) and water and electrolyte transport (VAN HARREVELD, 1957; VAN HARREVELD and SCHADB, 1959) than are observed during spreading depression. A similar explanation fits these asphyxia1 symptoms. An increase in membrane permeability for Na is not the primary result of an increase in Kconcentration of the medium outsidea nervous structure. Such changes are produced, however, in nerve cells by certain amino acids, such as glutamic acid which is present in high concentration in the cortical tissue (CURTIS, PHILLIS and WATKINS, 1960). This observation suggests an alternate mechanism for the propagation of spreading depression in which glutamic acid instead of K is released by the excited neural elements. Such a release would not only depolarize and stimulate adjacent nervous elements as in the mechanism of propagation proposed by GRAFSTEIN (1956), but

Amino acid release from the cerebral cortex during spreading depression and asphyxiation.

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Amino acid release from the cerebral cortex during spreading depression and asphyxiation.