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In both human radiation-induced brain injury and a mouse model of this condition, activated microglia release chemokines that attract cytotoxic T cells from the periphery to the lesion site, and this exacerbates neuronal damage in the area.
The representational geometry of neural population activity in the somatosensory cortex of mice allows for high flexibility needed to perform complex tasks and for generalization to novel tasks at the same time.
Primates can quickly detect situations in which their performance deviates from the intended goal by the process of error monitoring. In this Review, Rutishauser and colleagues discuss the neuronal mechanisms that underlie such monitoring in macaques and humans.
In this Journal Club, Janelle Drouin-Ouellet describes the 1989 paper that provided the first evidence for mitochondrial dysfunction in individuals with idiopathic Parkinson disease.
Spectrins are abundant cytoskeletal proteins with multifaceted roles in the nervous system whose dysfunction leads to neurological syndromes. In this review, Lorenzo et al. provide an update on the neurobiology of spectrins and the genetics of neuronal spectrinopathies, together with insights into the pathophysiology of these disorders.
Ion channels in primary sensory neurons are molecular targets for the treatment of chronic pain. In this Perspective, Ovsepian and Waxman assess prospective gene therapies directed towards such targets and discuss their translational potential to enable precision pain medicine.
Recent technological advances have provided insights into the diversity of neuronal subtypes within the midbrain dopamine system. In this Review, Garritsen and colleagues discuss molecular and functional distinctions between subtypes and describe mechanisms underlying their development, wiring and function.
Ketamine-induced dissociated states in mice result from the suppression and activation of cortical pyramidal neuron populations that are active and silent during wakefulness, respectively.
A growing body of epidemiological evidence linking air pollution to multiple brain disorders suggests that these adverse effects are produced by mechanisms that are shared across these disorders. More stringent, targeted regulatory policies may therefore be required to ensure public health protection.
