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Synaptic or neuronal activity can trigger transcriptional changes in the nucleus that are important for learning and memory. Tsien, Ma and co-workers here provide a comprehensive review of the complex signalling pathways involved in this excitation–transcription coupling.
A study reports that in the mouse hippocampus, the induction of long-term potentiation is dependent on the structural functions of CaMKII and not its enzymatic activity.
A juvenile hormone-degrading enzyme localized in the insect equivalent of the blood–brain barrier governs which social role, forager or soldier, worker carpenter ants fulfil.
During retinal development in the mouse, angiogenesis was unexpectedly found to depend on temporally restricted dopamine production by retinal ganglion cells, rather than by canonical retinal dopamine neurons.
Increasing levels of glial-derived neurotrophic factor using a gene-therapy approach in a macaque model of alcohol use disorder resulted in a lower tendency to relapse into alcohol consumption after a period of abstinence.
Research has often considered defensive behaviour as entirely mediated by the brain processing threat-related information. In this Review, Tseng et al. elucidate the interconnected network between the brain and body that facilitates defensive responses to threats varying in imminence.
The stress associated with early-life social deprivation in mice results in corticosterone-driven overstimulation of cortical synapse removal by astrocytes and behavioural abnormalities in mature animals.
Stress modulates immune system function and systemic inflammation is linked to stress-related disorders, including depression. Russo and colleagues outline the neural circuits through which the CNS regulates immune cell function in peripheral tissues in response to stress and consider how these responses contribute to stress-related pathophysiology.
Membrane excitability is central to neuronal function, and neurons must be resilient to changes in its underlying parameters. In this Perspective article, Marom and Marder suggest that two complementary mechanisms contribute to the resilience of membrane excitability: rapid ‘kinetic-based’ regulation of ion channel proteins and slower homeostatic control of ion channel membrane densities.
