RESUMEN
Conscious perception is greatly diminished during sleep, but the underlying circuit mechanism is poorly understood. We show that cortical ignition-a brain process shown to be associated with conscious awareness in humans and non-human primates-is strongly suppressed during non-rapid-eye-movement (NREM) sleep in mice due to reduced cholinergic modulation and rapid inhibition of cortical responses. Brain-wide functional ultrasound imaging and cell-type-specific calcium imaging combined with optogenetics showed that activity propagation from visual to frontal cortex is markedly reduced during NREM sleep due to strong inhibition of frontal pyramidal neurons. Chemogenetic activation and inactivation of basal forebrain cholinergic neurons powerfully increased and decreased visual-to-frontal activity propagation, respectively. Furthermore, although multiple subtypes of dendrite-targeting GABAergic interneurons in the frontal cortex are more active during wakefulness, soma-targeting parvalbumin-expressing interneurons are more active during sleep. Chemogenetic manipulation of parvalbumin interneurons showed that sleep/wake-dependent cortical ignition is strongly modulated by perisomatic inhibition of pyramidal neurons.
Asunto(s)
Electroencefalografía , Parvalbúminas , Sueño , Animales , Ratones , Neuronas Colinérgicas/fisiología , Lóbulo Frontal/metabolismo , Parvalbúminas/metabolismo , Sueño/fisiología , Vigilia/fisiologíaRESUMEN
Phosphorus (P) and sulfur (S) are usually involved simultaneously in the immobilization of heavy metals in sewage sludge during pyrolysis, and thus their speciation in sewage sludge-derived biochar (SSB) profoundly affects the recycling of the nutrients and the environmental risks of sewage sludge. Here, we investigated the speciation evolution of P and S in SSB induced by ageing processes in soil using X-ray absorption near edge structure spectroscopy. Results showed that Ca-bound compounds like hydroxyapatite dominated the P forms, while over 60% of S existed as reduced inorganic sulfides in the SSB. The stable Ca-associated P species in SSB tended to be transformed gradually into relatively soluble species during ageing in soil. The speciation composition of S in SSB remained almost unaffected when aged in pot soils, whereas about 33.6% of reduced sulfides were transformed into oxidized species after 1-year ageing in field soils. SSB significantly increased the proportion of sulfides and the contents of available P and S in the amended soil but showed relatively weak effects on the speciation distribution of P in the soil because of their similar compositions. These findings provide insights into biogeochemistry of nutrients and behaviors of heavy metals in SSB after its application to the soil environments.
Asunto(s)
Metales Pesados , Contaminantes del Suelo , Carbón Orgánico/química , Fósforo , Aguas del Alcantarillado/química , Suelo/química , Contaminantes del Suelo/análisis , Sulfuros , AzufreRESUMEN
A crucial step in understanding the sleep-control mechanism is to identify sleep neurons. Through systematic anatomical screening followed by functional testing, we identified two sleep-promoting neuronal populations along a thalamo-amygdala pathway, both expressing neurotensin (NTS). Rabies-mediated monosynaptic retrograde tracing identified the central nucleus of amygdala (CeA) as a major source of GABAergic inputs to multiple wake-promoting populations; gene profiling revealed NTS as a prominent marker for these CeA neurons. Optogenetic activation and inactivation of NTS-expressing CeA neurons promoted and suppressed non-REM (NREM) sleep, respectively, and optrode recording showed they are sleep active. Further tracing showed that CeA GABAergic NTS neurons are innervated by glutamatergic NTS neurons in a posterior thalamic region, which also promote NREM sleep. CRISPR/Cas9-mediated NTS knockdown in either the thalamic or CeA neurons greatly reduced their sleep-promoting effect. These results reveal a novel thalamo-amygdala circuit for sleep generation in which NTS signaling is essential for both the upstream glutamatergic and downstream GABAergic neurons.