This review examines the cholinergic (Ch) basal forebrain and its role in neurodegeneration. Terminology used to describe Ch cells and the complex region of the basal forebrain are reviewed. Practical autopsy sampling and labeling strategies for Ch cells are discussed and illustrated with the goal of facilitating diagnostic work and autopsy-based studies of this region. The anatomic connectivity of the system is reviewed with an emphasis placed on the dense cholinergic input to the amygdala, the major target of the Ch basal forebrain, as well as the hippocampus. Ch and basal forebrain neuropathology in various neurodegenerative diseases is then briefly discussed, including more recent studies of TDP-43 proteinopathies. Finally, areas for further study that might further the understanding of the Ch system in neurodegeneration are emphasized.

Hippocampal remapping, in which place cells form distinct activity maps across different environments, is a well-established phenomenon with a range of theoretical interpretations. Some theories propose that remapping helps to minimize interference between competing spatial memories, whereas others link it to shifts in an underlying latent state representation. However, how these interpretations of remapping relate to one another, and what types of activity changes they are compatible with, remains unclear. To unify and elucidate the mechanisms behind remapping, we here adopt a neural coding and population geometry perspective. Assuming that hippocampal population activity can be understood through a linearly-decodable latent space, we show that there are three possible mechanisms to induce remapping: (i) a true change in the mapping between neural and latent space, (ii) modulation of activity due to non-spatial mixed selectivity of place cells, or (iii) neural variability in the null space of the latent space that reflects a redundant code. We simulate and visualize examples of these remapping types in a network model, and relate the resultant remapping behavior to various models and experimental findings in the literature. Overall, our work serves as a unifying framework with which to visualize, understand, and compare the wide array of theories and experimental observations about remapping, and may serve as a testbed for understanding neural response variability under various experimental conditions.

Social learning enables a subject to make decisions by observing the actions of another. How neural circuits acquire relevant information during observation to guide subsequent behavior is unknown. Utilizing an observational spatial working memory task, we show that neurons in the rat anterior cingulate cortex (ACC) associated with spatial trajectories during self-running in a maze are reactivated when observing another rat running the same maze. The observation-induced ACC activities are reduced in error trials and are correlated with activities of hippocampal place cells representing the same trajectories. The ACC activities during observation also predict subsequent hippocampal place cell activities during sharp-wave ripples and spatial contents of hippocampal replay prior to self-running. The results support that ACC neurons involved in decisions during self-running are reactivated during observation and interact with hippocampal replay to guide subsequent spatial navigation.

Sleep entails profound changes in the brain and body, marked by altered states of consciousness and reduced somatic and autonomic motor activity. Regarding "how" sleep is regulated, whole-brain screening revealed large sleep-control networks spanning the forebrain, midbrain, and hindbrain. We unify diverse experimental evidence under a "motor theory," in which the sleep-control mechanism is integral to somatic and autonomic motor circuits. Regarding the "why" question, sleep deprivation impairs cognition, emotion, metabolism, and immunity. We propose catecholamine (dopamine, noradrenaline, and adrenaline) inactivation as the fundamental biological process underlying sleep's numerous benefits. Beyond brain arousal and motor activity, catecholamines regulate metabolism and immunity; their sleep-dependent suppression yields wide-ranging advantages, promoting repair and rejuvenation. Furthermore, catecholaminergic neurons are metabolically vulnerable; their need for rest and recovery may drive homeostatic sleep pressure. Together, the motor theory offers a unifying framework for sleep control, while the catecholamine hypothesis posits a core mechanism mediating sleep's multifaceted benefits.