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.

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.

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.

Work related to place tuning, spatial navigation, orientation and direction. Mainly includes articles on connectivity in the hippocampus, retrosplenial cortex, and related areas.

Basal Ganglia Advances is a collection highlighting research on the structure, function, and disorders of the basal ganglia. It features studies spanning neuroscience, clinical insights, and computational models, serving as a hub for advances in movement, cognition, and behavior.

Recent advances in the field of Voltage Imaging, with a special focus on new constructs and novel implementations.

The precise structural and functional characteristics of input circuits targeting histaminergic neurons remain poorly understood. Here, using a rabies virus retrograde tracing system combined with fluorescence micro-optical sectioning tomography, we construct a 3D monosynaptic long-range input atlas of male mouse histaminergic neurons. We identify that the hypothalamus, thalamus, pallidum, and hippocampus constitute major input sources, exhibiting diverse spatial distribution patterns and neuronal type ratios. Notably, a specific layer distribution pattern and co-projection structures of upstream cortical neurons are well reconstructed at single-cell resolution. As histaminergic system is classically involved in sleep-wake regulation, we demonstrate that the lateral septum (predominantly supplying inhibitory inputs) and the paraventricular nucleus of the thalamus (predominantly supplying excitatory inputs) establish monosynaptic connections, exhibiting distinct functional dynamics and regulatory roles in rapid-eye-movement sleep. Collectively, our study provides a precise long-range input map of mouse histaminergic neurons at mesoscopic scale, laying a solid foundation for future systematic study of histaminergic neural circuits.

Nonpharmaceutical approaches based on gamma entrainment using sensory stimuli (GENUS) have shown promise in reducing Alzheimer's disease pathology in mouse models. While human studies remain limited, GENUS has been shown to alleviate aspects of neurodegeneration in patients with Alzheimer's disease. In this study, we analyze intracranial EEG data from 490 contacts across eleven patients with refractory epilepsy in response to three visual stimulation conditions. We find that 40 Hz visual stimulation successfully entrains neural activity beyond early visual areas, including the hippocampus and other cortical regions such as the temporal and frontal lobes. Additionally, we show that synchronization increases between the hippocampus and other cortical areas in response to the 40 Hz visual stimulation. Furthermore, combining stimulation with a simple visual oddball task alters the direction of information flow from frontal regions to the hippocampus and enhances both the strength and spatial extent of neural entrainment. These findings highlight the potential influence of cognitive engagement during sensory gamma stimulation and provide additional insights into the neurophysiological effects of 40 Hz visual stimulation.

Dysfunction of the basal ganglia is implicated in a wide range of neurological and psychiatric disorders. Our understanding of the operation of the basal ganglia is largely derived on data from studies conducted on mice, which are frequently used as model organisms for various clinical conditions. The striatum, the largest compartment of the basal ganglia, consists of 90-95% striatal projection neurons (SPNs). It is therefore crucial to establish if human and mouse SPNs have distinct or similar properties, as this has implications for the relevance of mouse models for understanding the human striatum. To address this, we compared the general organization of the somato-dendritic tree of SPNs, the dimensions of the dendrites, the density and size of spines (spine surface area), and ion channel subtypes in human and mouse SPNs. Our findings reveal that human SPNs are significantly larger, but otherwise the organisation of the dendritic tree (dendrogram) with an average of approximately 5 primary dendrites, is similar in both species. Additionally in both humans and mice, over 90% of the spines are located on the terminal branches of each dendrite. Human spines are somewhat larger (4.3 versus 3.1 μm2) and the terminal dendrites have a uniform diameter in both humans and mice, although somewhat broader in the latter (1.0 versus 0.6 μm). The composition of ion channels is also largely conserved. These data have been used to simulate human SPNs building on our previous detailed simulation of mouse SPNs. We conclude that the human SPNs essentially appear as enlarged versions of the mouse SPNs. This similarity suggests that both species process information in a comparable manner, supporting the relevance of mouse models for studying the human striatum.