Volume 25 Issue 8, August 2024

The maladaptive reward learning associated with morphine administration is shown here to be mediated by changes in dopamine-release dynamics in reward circuitry resulting from increased myelination specifically in the ventral tegmental area.

A new modelling method developed in male Drosophila melanogaster maps how populations of neurons transform visual stimuli into courtship behaviours without recording neural activity.

Acid-sensing ion channel 3 in nociceptors exacerbates inflammation in psoriasis by inducing the release of calcitonin gene-related peptide from these neurons.

In this Journal Club, Adrien Peyrache highlights a 1998 paper that showed memory formation as a dynamic process involving multiple brain areas.

Sabine Krabbe describes a 1993 study of classical conditioning in the honeybee that provided early insights into the mechanisms of predictive learning.

Central nervous system (CNS) neurons and glial cells are generated by both direct and indirect neurogenesis. In this Review, Thor outlines the landscape of indirect neurogenesis during CNS development in key species, including humans, and describes the main genetic mechanisms that contribute to its region-specific, neural progenitor cell-specific and temporal control.

At early developmental stages, spontaneous activity in the mammalian cortex is characterized by the occurrence of highly synchronous network events. Portera-Cailliau and colleagues describe these activity patterns, their underlying mechanisms and function, and their transition to the desynchronized activity observed in adult individuals.

Recent advances in the development of gene therapy tools provide hope that these approaches might modulate the altered gene expression that characterizes many CNS disorders. Gao et al. provide an overview of current gene therapy strategies, highlighting the interdependence of therapeutic modality, delivery vehicle and administration route for translational success.

There are a number of models that have attempted to explain why people with Parkinson disease move slowly. In this Perspective, Williams identifies the inconsistencies in these models and suggests that these may be addressed by a different model that considers disordered information transmission as fundamental to slow movement development.