Year: 2016
Type: article
Abstract: Brain lactate concentration is higher during wakefulness than in sleep. However, it is unknown why arousal is linked to an increase in brain lactate and why lactate declines within minutes of sleep. Here, we show that the glymphatic system is responsible for state-dependent changes in brain lactate concentration. Suppression of glymphatic function via acetazolamide treatment, cisterna magna puncture, aquaporin 4 deletion, or changes in body position reduced the decline in brain lactate normally observed when awake mice transition into sleep or anesthesia. Concurrently, the same manipulations diminished accumulation of lactate in cervical, but not in inguinal lymph nodes when mice were anesthetized. Thus, our study suggests that brain lactate is an excellent biomarker of the sleep-wake cycle and increases further during sleep deprivation, because brain lactate is inversely correlated with glymphatic-lymphatic clearance. This analysis provides fundamental new insight into brain energy metabolism by demonstrating that glucose that is not fully oxidized can be exported as lactate via glymphatic-lymphatic fluid transport.
Language: English
Subfield: Clinical Neurology
Field: Medicine
Domain: Health Sciences
Open Access status: bronze
Awards: The glymphatic system, a new concept in glia biology, Failure of metabolite clearance in a model of multi-lacunar infarcts, ATP as the instigator of inflammatory responses to spinal cord injury, G2299739175, CSF/ISF highways for tau brain clearance, Macroscopic distribution pathways of apoE in CNS, Glymphatic function in a transgenic rat model of Alzheimer's disease, Para-Vascular Basis of Small Vessel Disease
OpenAlex ID: W2480915756