The contribution of methyl groups to electron spin decoherence of nitroxides in glassy matrices.

Long electron spin coherence lifetimes are crucial for high sensitivity and resolution in many pulse electron paramagnetic resonance (EPR) experiments aimed at measuring hyperfine and dipolar couplings, as well as in potential quantum sensing applications of molecular spin qubits. In immobilized systems, methyl groups contribute significantly to electron spin decoherence as a result of methyl torsional quantum tunneling. We examine the electron spin decoherence dynamics of the nitroxide radical 2,2,6,6-tetramethylpiperidin-1-oxyl (TEMPO) in both a methyl-free solvent and a methyl-containing solvent at cryogenic temperature.

The effects of P2Y12 loss on microglial gene expression, dynamics, and injury response in the cerebellum and cerebral cortex.

Despite the emerging consensus that microglia are critical to physiological and pathological brain function, it is unclear how microglial roles and their underlying mechanisms differ between brain regions. Microglia throughout the brain express common markers, such as the purinergic receptor P2Y12, that delineate them from peripheral macrophages. P2Y12 is a critical sensor of injury but also contributes to the sensing of neuronal activity and remodeling of synapses, with microglial loss of P2Y12 resulting in behavioral deficits.

Dopaminergic signaling regulates microglial surveillance and adolescent plasticity in the frontal cortex.

Adolescence is a sensitive period for frontal cortical development and cognitive maturation. The dopaminergic (DA) mesofrontal circuit is particularly malleable in response to changes in adolescent experience and DA activity. However, the cellular mechanisms engaged in this plasticity remain unexplored.

Adolescent neurostimulation of dopamine circuit reverses genetic deficits in frontal cortex function.

Dopamine system dysfunction is implicated in adolescent-onset neuropsychiatric disorders. Although psychosis symptoms can be alleviated by antipsychotics, cognitive symptoms remain unresponsive and novel paradigms investigating the circuit substrates underlying cognitive deficits are critically needed. The frontal cortex and its dopaminergic input from the midbrain are implicated in cognitive functions and undergo maturational changes during adolescence.

Adolescent neurostimulation of dopamine circuit reverses genetic deficits in frontal cortex function.

Dopamine system dysfunction is commonly implicated in adolescent-onset neuropsychiatric disorders. Although psychosis symptoms can be alleviated by antipsychotics, cognitive symptoms remain unresponsive to such pharmacological treatments and novel research paradigms investigating the circuit substrates underlying cognitive deficits are critically needed. The frontal cortex and its dopaminergic input from the midbrain are implicated in cognitive functions and undergo maturational changes during adolescence.