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Regulation of the timing of sleep based on circadian rhythms and regulation of the need for sleep based on sleep debt have been considered separate mechanisms. Johanna Meijer and colleagues now show in rats that sleep state influences neuronal activity in the suprachiasmatic nucleus, the main circadian pacemaker, suggesting that these processes are functionally linked. See pages 1005 and 1122.
A homeostatic control mechanism that monitors and reacts to the need for sleep has been thought to function independently of the brain's circadian clock in previous studies. Now simultaneous recordings of sleep stages and electrical activity in the suprachiasmatic nucleus in behaving animals reveal feedback from sleep centers to the circadian pacemaker.
How is synaptic facilitation mediated? New work suggests that a calcium-sensing molecule, neuronal calcium sensor-1 (NCS-1) transduces a residual calcium signal into an enhancement of transmitter release at excitatory synapses in the hippocampus.
HIV-associated neurodegeneration likely involves release of signals from activated glial cells. A new study reveals that matrix metalloproteinase from HIV-1-infected macrophages or microglia cleaves the chemokine SDF-1 to generate a potent neurotoxin.
Corticotropin releasing factor (CRF) is a critical integrator of the central stress response. A new study now provides conclusive evidence that CRF-mediated forebrain activation underlies the behavioral response, such as anxiety, to stress.