Cortical GABA Levels in Primary Insomnia

Morgan, Peter T.; Pace‐Schott, Edward F.; Mason, Graeme F.; Forselius, Erica; Fasula, Madonna; Valentine, Gerald; Sanacora, Gerard

doi:10.5665/sleep.1880

Cited by 88 publications

(70 citation statements)

References 55 publications

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“…Despite contradictory evidence, 52 results have largely been interpreted within the context of the hyperarousal hypothesis. For example, increased 45 and decreased 46 GABA in the occipital cortex of patients with insomnia have been reported to be consistent with the hyperarousal model of insomnia. However, sleep regulatory molecules interact with each other in complex ways (described in more detail later), and many of their eff ects are dependent on the milieu of the brain state; that is, they are state-dependent.…”

Section: Molecular Mechanisms Of Sleep and Insomniamentioning

confidence: 63%

The Pathophysiology of Insomnia

Levenson

Kay

Buysse

2015

Chest

290

147

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Insomnia disorder is characterized by chronic dissatisfaction with sleep quantity or quality that is associated with diffi culty falling asleep, frequent nighttime awakenings with diffi culty returning to sleep, and/or awakening earlier in the morning than desired. Although progress has been made in our understanding of the nature, etiology, and pathophysiology of insomnia, there is still no universally accepted model. Greater understanding of the pathophysiology of insomnia may provide important information regarding how, and under what conditions, the disorder develops and is maintained as well as potential targets for prevention and treatment.The aims of this report are (1) to summarize current knowledge on the pathophysiology of insomnia and (2) to present a model of the pathophysiology of insomnia that considers evidence from various domains of research. Working within several models of insomnia, evidence for the pathophysiology of the disorder is presented across levels of analysis, from genetic to molecular and cellular mechanisms, neural circuitry, physiologic mechanisms, sleep behavior, and self-report. We discuss the role of hyperarousal as an overarching theme that guides our conceptualization of insomnia. Finally, we propose a model of the pathophysiology of insomnia that integrates the various types of evidence presented.

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Section: Molecular Mechanisms Of Sleep and Insomniamentioning

confidence: 63%

The Pathophysiology of Insomnia

Levenson

Kay

Buysse

2015

Chest

290

147

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“…For purposes of screening and acclimation to the scanner environment before undergoing the acetate infusion, we offered to perform a 1 H MRS scan on subjects before the infusion day. Five out of seven heavy drinkers and six out of seven light drinkers included in the study underwent 1 H MRS. 1 H MRS. 1 H MRS studies were performed with a 4T magnet (Oxford Magnetic Technology) and a Bruker spectrometer (Bruker Instruments), as described previously (63). The head of the subject was comfortably secured to a platform with the region of interest apposed to an 8-cm distributed capacitance surface coil tuned to 170 MHz.…”

Section: Methodsmentioning

confidence: 99%

Increased brain uptake and oxidation of acetate in heavy drinkers

Jiang

Gulanski²,

Feyter³

et al. 2013

J. Clin. Invest.

Self Cite

119

114

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When a person consumes ethanol, the body quickly begins to convert it to acetic acid, which circulates in the blood and can serve as a source of energy for the brain and other organs. This study used 13 C magnetic resonance spectroscopy to test whether chronic heavy drinking is associated with greater brain uptake and oxidation of acetic acid, providing a potential metabolic reward or adenosinergic effect as a consequence of drinking. Seven heavy drinkers, who regularly consumed at least 8 drinks per week and at least 4 drinks per day at least once per week, and 7 light drinkers, who consumed fewer than 2 drinks per week were recruited. The subjects were administered [2-13 C]acetate for 2 hours and scanned throughout that time with magnetic resonance spectroscopy of the brain to observe natural 13 C abundance of N-acetylaspartate (NAA) and the appearance of 13 C-labeled glutamate, glutamine, and acetate. Heavy drinkers had approximately 2-fold more brain acetate relative to blood and twice as much labeled glutamate and glutamine. The results show that acetate transport and oxidation are faster in heavy drinkers compared with that in light drinkers. Our finding suggests that a new therapeutic approach to supply acetate during alcohol detoxification may be beneficial.

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“…В последующих работах [4] у больных инсомнией было выявлено 12% повышение уровня ГАМК в височных отделах при общем ее снижении в головном мозге, что может являться компенсаторной реакцией.…”

Section: предрасполагающие факторыunclassified