Spreading depression (SD) is a transient wave of near-complete neuronal and glial depolarization associated with massive transmembrane ionic and water shifts. It is evolutionarily conserved in the central nervous systems of a wide variety of species from locust to human. The depolarization spreads slowly at a rate of only millimeters per minute by way of grey matter contiguity, irrespective of functional or vascular divisions, and lasts up to a minute in otherwise normal tissue. As such, SD is a radically different breed of electrophysiological activity compared with everyday neural activity, such as action potentials and synaptic transmission. Seventy years after its discovery by Leao, the mechanisms of SD and its profound metabolic and hemodynamic effects are still debated. What we did learn of consequence, however, is that SD plays a central role in the pathophysiology of a number of diseases including migraine, ischemic stroke, intracranial hemorrhage, and traumatic brain injury. An intriguing overlap among them is that they are all neurovascular disorders. Therefore, the interplay between neurons and vascular elements is critical for our understanding of the impact of this homeostatic breakdown in patients. The challenges of translating experimental data into human pathophysiology notwithstanding, this review provides a detailed account of bidirectional interactions between brain parenchyma and the cerebral vasculature during SD and puts this in the context of neurovascular diseases.

https://www.physiology.org/doi/pdf/10.1152/physrev.00027.2014

Spreading Depression, Spreading Depolarizations, and the Cerebral Vasculature

Is facial muscular movement capable of alterning emotional state? Facial feedback theories answer this question in the affirmative but do not specify the intervening process. Cognitive appraisal theories do not address this question at all. The vascular theory of emotional efference (VTEE) holds that facial muscular movement, by its action on the cavernous sinus, may restrict venous flow and thereby influence cooling of the arterial blood supply to the brain

/pdf/feeling-and-facial-efference-implications-of-the-vascular-3l0n6xym3s.pdf

Feeling and facial efference: implications of the vascular theory of emotion.

The neurobiological mechanisms of both sleep and circadian regulation have been unraveled partly in the last decades. A network of brain structures, rather than a single locus, is involved in arousal state regulation, whereas the suprachiasmatic nucleus (SCN) has been recognized as a key structure for the regulation of circadian rhythms. Although most models of sleep regulation include a circadian component, the actual mechanism by which the circadian timing system promotes—in addition to homeostatic pressure—transitions between sleep and wakefulness remains to be elucidated. Little more can be stated presently than a probable involvement of neuronal projections and neurohumoral factors originating in the SCN. This paper reviews the relation among body temperature, arousal state, and the circadian timing system and proposes that the circadian temperature rhythm provides an additional signaling pathway for the circadian modulation of sleep and wakefulness. A review of the literature shows that increased brain temperature is associated with a type of neuronal activation typical of sleep in some structures (hypothalamus, basal forebrain), but typical of wakefulness in others (midbrain reticular formation, thalamus). Not only local temperature, but also skin temperature are related to the activation type in these structures. Warming of the skin is associated with an activation type typical of sleep in the midbrain reticular formation, hypothalamus, and cerebral cortex (CC). The decreasing part of the circadian rhythm in core temperature is mainly determined by heat loss from the skin of the extremities, which is associated with strongly increased skin temperature. As such, alterations in core and skin

More than a marker: interaction between the circadian regulation of temperature and sleep, age-related changes, and treatment possibilities

http://www.buzsakilab.com/content/PDFs/Grosmark2012.pdf

REM Sleep Reorganizes Hippocampal Excitability

A comparative study of the role of the cerebral arterial blood in the regulation of brain temperature in five mammals

1. In chronically-prepared sheep, intracranial temperatures were measured in the cavernous sinus among the vessels of the carotid rete and at the circle of Willis extravascularly, and in the preoptic area and in other brain stem regions. Extracranial temperatures were measured intravascularly in the carotid or internal maxillary arteries and on the nasal mucosa and the skin of the ear.

2. At 20° C ambient temperature, shifts in temperature of the hypothalamus and of other brain sites paralleled temperature shifts in the cerebral arterial blood which was cooler than central arterial blood. During periods of arousal and of paradoxical sleep, vasoconstriction of the nasal mucosa and the ear skin occurred and temperatures at the cerebral arteries and in the brain rose without a comparable rise in central arterial blood temperature.

3. Anaesthetic doses of barbiturate abolished the temperature oscillations in the cerebral arterial blood and the brain. When air was blown rapidly over the nasal mucosa in anaesthetized animals, temperatures dropped precipitously in the cavernous sinus, at the cerebral arteries, and in the brain, while central arterial temperature fell only slightly. Injections of latex into the facial venous system demonstrated a venous pathway from the nasal mucosa to the cavernous sinus.

4. When sheep were exposed to 45-50° C ambient temperature, respiratory rate increased 5-10 times and the temperature gradient between central and cerebral arterial blood widened.

5. It is concluded that venous blood returning from the nasal mucosa and the skin of the head to the cavernous sinus cools the central arterial blood in the carotid rete. This is an important factor in the maintenance of hypothalamic temperature in the wool-covered, long-nosed, panting sheep and undoubtedly affects hypothalamic thermoreceptors and temperature regulation in artiodactyls.

https://physoc.onlinelibrary.wiley.com/doi/pdf/10.1113/jphysiol.1968.sp008626

The influence of the nasal mucosa and the carotid rete upon hypothalamic temperature in sheep

The plexus of arteries which make up the carotid rete in the cat seems to be able to modify the temperature of central arterial blood as it enters the cranial cavity.

Carotid Rete and Brain Temperature of Cat

The rise in brain temperature in the rabbit during paradoxical sleep originates in a temperature rise of the cerebral arterial blood. Heat loss from the ear is a major factor in the regulation of arterial blood temperature in the rabbit, and the primary thermal event in paradoxical sleep is a vasoconstriction of the skin of the ear which results in a rise in arterial blood and brain temperatures. These thermal correlates of paradoxical sleep are not present in a cold environment when the ear skin is already maximally vasoconstricted. The persistence of peripheral vasoconstriction during paradoxical sleep in a hot environment suggests a disturbance in autonomic thermoregulatory control.

http://science.sciencemag.org/content/sci/157/3796/1586.full.pdf

Mary Ann Baker

Papers

A comparative study of the role of the cerebral arterial blood in the regulation of brain temperature in five mammals

The influence of the nasal mucosa and the carotid rete upon hypothalamic temperature in sheep

Carotid Rete and Brain Temperature of Cat

Autonomic basis for the rise in brain temperature during paradoxical sleep.

Intracranial heat exchange and regulation of brain temperature in sheep.