The brain's memory function involves patterns of neural population spiking activity, shaped by experience and recurring over time. These neural population patterns are typically studied with respect to the three stages of acquisition, retention, and retrieval. Despite intensive investigation, the relationship between the features of population activity and the properties, computations, and codes for memory remains elusive. In this perspective, we synthesize recent advances in the study of memory from the viewpoint of brain network physiology, aiming for a comprehensive mapping between the properties and computations of memory and the features of population-activity codes. We propose that brain memory circuits implement trade-offs between conflicting demands on population codes. We anticipate that an important challenge for both discovery and translational neuroscience of memory is to study these trade-offs, delineating a safe zone in the population-activity space where neuronal circuits operate efficiently.
The mechanisms linking hypertension to cognitive decline remain unclear. Schaeffer et al. show that angiotensin II damages endothelium, oligodendrocyte precursors, and interneurons via AT1 signaling, independent of blood pressure. Targeting this pathway may protect the brain beyond pressure control alone.1.
Zhou et al.1 identify a C5aR1+ microglial subtype that amplifies neuroinflammation after traumatic brain injury and intracerebral hemorrhage. The mechanism reveals microglial-astrocyte-neutrophil crosstalk driving cerebral edema, highlighting C5aR1 as a therapeutic target and raising new questions about complement-glial interactions.
In this issue of Neuron, Zheng et al.1 show how separate neural ensembles in the paraventricular thalamus respond to and gate fat and sugar consumption. Moreover, they revealed the role of histamine receptor 3 in gating fat-specific neural response and consumption.
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