Articles in 2015

Chronic pain and anxiety may be mechanistically linked by a presynaptic form of long-term potentiation that occurs at synapses in the anterior cingluate cortex.

A new study shows that boosting mTORC1 activity in the striatum can ameliorate disease phenotypes in a mouse model of Huntington disease.

Activation of nuclear factor-κB in astrocytes leads to the release of complement factor 3, which impairs neuronal function, and this mechanism may contribute to Alzheimer disease.

The cerebellar cortex drives smooth goal-directed movement as well as a range of other functions. Apps and colleagues describe studies that have revealed variations in the cytoarchitecture, molecular composition, physiological properties and vulnerability to cell death of different cerebellar cortical regions, and discuss the idea that these underlie different forms of information processing.

Although we understand much about mechanisms of spatial navigation in the mammalian brain in the context of laboratory investigations, our knowledge of the neural bases of 'real-world' navigation is more limited. Ulanovsky and colleagues here describe how we can approach this problem through experimental research and theoretical models of large-scale navigation in bats and rats.

Various neurodegenerative diseases are characterized by aggregates of pathological proteins, and increasing evidence suggests these disease-associated proteins may 'spread' via neuronal connections. Trojanowski and colleagues describe the molecular mechanisms of such spreading, and present the findings from neuropathological and imaging studies in humans that support this process.

Chemokine receptors and opioid receptors in nociceptive pathways interact in ways that can alter opioid function. In this Progress article, Réaux-Le Goazigo and colleagues discuss how crosstalk between chemokine and opioid receptors offers a new framework for the development of novel analgesic therapies to alleviate pain.

The neuregulin 1 receptor ERBB4 tunes synapse strength in the thalamic reticular nucleus as part of a circuit that regulates selective attention.