Ted Abel

Jun 12, 2024 | nature.com | Utku Kaya |Ted Abel |Kourosh Maboudi |Nathaniel Kinsky |Bapun Giri |Kamran Diba

Memories benefit from sleep1, and the reactivation and replay of waking experiences during hippocampal sharp-wave ripples (SWRs) are considered to be crucial for this process2. However, little is known about how these patterns are impacted by sleep loss. Here we recorded CA1 neuronal activity over 12 h in rats across maze exploration, sleep and sleep deprivation, followed by recovery sleep. We found that SWRs showed sustained or higher rates during sleep deprivation but with lower power and higher frequency ripples. Pyramidal cells exhibited sustained firing during sleep deprivation and reduced firing during sleep, yet their firing rates were comparable during SWRs regardless of sleep state. Despite the robust firing and abundance of SWRs during sleep deprivation, we found that the reactivation and replay of neuronal firing patterns was diminished during these periods and, in some cases, completely abolished compared to ad libitum sleep. Reactivation partially rebounded after recovery sleep but failed to reach the levels found in natural sleep. These results delineate the adverse consequences of sleep loss on hippocampal function at the network level and reveal a dissociation between the many SWRs elicited during sleep deprivation and the few reactivations and replays that occur during these events. A study of neuronal activity in rats finds that sleep loss adversely affects hippocampal function and memory by dissociating hippocampal sharp-wave ripples from memory replay and reactivation events.

May 7, 2024 | biorxiv.org | Satya Murthy Tadinada |Utsav Mukherjee |Emily Walsh |Ted Abel

AbstractcAMP signaling is critical for memory consolidation and certain of forms long-term potentiation (LTP). Phosphodiesterases (PDEs), enzymes that degrade the second messenger cAMP and cGMP, are highly conserved during evolution and represent a unique set of drug targets, given the involvement of these enzymes in several pathophysiological states including brain disorders.

Mar 27, 2024 | nature.com | Ted Abel

NEWS AND VIEWS 27 March 2024 A population of neurons that engages mechanisms of the innate immune system during memory formation has been uncovered in mice. Surprisingly, inflammatory signalling might pave the way for long-term memory. How do memories last? Spanish surrealist Salvador Dalí pondered this question in his famous work The Persistence of Memory.

Nov 4, 2023 | nature.com | Yann Vanrobaeys |Zeru Peterson |Snehajyoti Chatterjee |Li-Chun Lin |Thomas Nickl-Jockschat |Ted Abel | +2 more

Sleep deprivation has far-reaching consequences on the brain and behavior, impacting memory, attention, and metabolism. Previous research has focused on gene expression changes in individual brain regions, such as the hippocampus or cortex. Therefore, it is unclear how uniformly or heterogeneously sleep loss affects the brain. Here, we use spatial transcriptomics to define the impact of a brief period of sleep deprivation across the brain in male mice. We find that sleep deprivation induced pronounced differences in gene expression across the brain, with the greatest changes in the hippocampus, neocortex, hypothalamus, and thalamus. Both the differentially expressed genes and the direction of regulation differed markedly across regions. Importantly, we developed bioinformatic tools to register tissue sections and gene expression data into a common anatomical space, allowing a brain-wide comparison of gene expression patterns between samples. Our results suggest that distinct molecular mechanisms acting in discrete brain regions underlie the biological effects of sleep deprivation. Sleep deprivation impacts molecular changes across brain regions. Here, the authors utilize a spatial. transcriptomics approach to elucidate acute sleep deprivation-induced gene expression signature. across regions and subregions of the brain.

Aug 28, 2023 | biologicalpsychiatryjournal.com | Maya Evans |Ted Abel |Thomas Nickl-Jockschat

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