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#hippocampus

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"We now leave #navigation to our #phones. The result: more of us are getting hopelessly lost." #JohnHarris
theguardian.com/commentisfree/
"#GPS has cut us off from a basic human skill. It’s no wonder #mountain #rescuers are being called out so often. [...] Between 2019 and 2024, the total number of #rescues had increased by 24%, and there was a marked jump among the 18 to 24 age group, among whom callouts almost doubled. [...] across #Britain, there is evidently a mounting problem about the gap between people’s urge to experience wild and open spaces, and their ability to cope when they actually get there. [...] research suggesting that “people with greater lifetime GPS experience have worse #spatialmemory during self-guided navigation”. [...] retested 3 years after the initial research, when they found that “greater GPS use since initial testing was associated with a steeper decline in hippocampal-dependent spatial memory”. The #hippocampus is the part of the brain that deals with navigation: among London taxi drivers, the need to memorise so many geographical details was found to cause it to increase in size. But here were findings that suggested the opposite: reliance on automated #directions reducing people’s capacity to navigate for themselves." #cartography
Thx #SophieBerrebi

The Guardian · We now leave navigation to our phones. The result: more of us are getting hopelessly lostBy John Harris

From the lab of Helene Schmidt:

"Large-scale 3D EM connectomics dataset of mouse hippocampal area CA1", Corteze et al. 2025
biorxiv.org/content/10.1101/20

Spectacular.

bioRxiv · Large-scale 3D EM connectomics dataset of mouse hippocampal area CA1The hippocampal formation is thought to be crucial for memory and learning, with subarea cornu ammonis 1 (CA1) considered to play a major role in spatial and episodic memory formation, and for evaluating the match between retrieved memories and current sensory information. While enormous progress has been made in classifying CA1 neurons based on molecular, morphological, and functional properties, and in identifying their role in behavioral tasks, a clear understanding of the underlying circuits is still missing. Here, we present the first large-scale three dimensional (3D) electron microscopy dataset of mouse CA1 at nanometer-scale resolution. The dataset is available online and can be readily used for circuit reconstructions, as demonstrated for inputs to CA1 superficial layers. Example volume segmentations show that automated reconstruction detection is feasible. Using these data, we find evidence against the long-held assumption of a homogeneous pyramidal cell population. Furthermore we find substantial possibly long-range axonal innervation of stratum-lacunosum interneurons, suggested previously to originate in L2 of MEC. These first analyses illustrate the usability of this dataset for finally clarifying the connectomic properties of mouse CA1, a key structure in mammalian brains. ### Competing Interest Statement The authors have declared no competing interest.

I keep going back to this question about #TemporalCreditAssignment and #HippocampalReplay:
As an "agent" you want to learn the value of places and which places are likely to lead to reward;

-1) if a place leads to higher than expected reward, you'll want to propagate back the reward info from the reward throughout the places that led to the reward. If replay does that you should see an increase of replay at a new reward site and the replay sequences should start at the reward and reflect what you just did to reach it. Right?

-2) if a place leads to lower than expected reward, you'll also want to propagate that lowered value, pretty much in the same way, so if replay does that you should see a similar replay rate and content for increased OR decreased reward sites. Right?

-3) if a place has had unchanged reward for a while and you're just in exploitation mode (just going there again and again because you know that's the best place to go to in the environment) then you shouldn't need to update anything and replay rate should be quite low at that unchanged reward side. Right?

That's not at all what replay is doing IRL, so does that mean replay is not used for temporal credit assignment? Or did I (very likely) miss something?

"In mice, here we reveal a non-pyramidal excitatory neuron type — the “ovoid” neuron — that is spatially adjacent to subiculum pyramidal cells but differs in gene expression, electrophysiology, morphology, and connectivity. Functionally, novel object encounters drive sustained ovoid neuron activity, whereas familiar objects fail to drive activity even months after single-trial learning."

nature.com/articles/s41467-025

NatureAtypical hippocampal excitatory neurons express and govern object memory - Nature CommunicationsPyramidal cells are classically thought to comprise the excitatory output of the subiculum. Here, the authors show the existence of “ovoid cells”, excitatory subiculum neurons with specialized gene expression, morphology, projections, and function.

@johnwidloski and I are co-organizing a symposium on #HippocampalReplay at the #EBBS25 in Bordeaux!

Our goal: From the state of the art in awake replay models & existing data, determine the next big questions and most informative future experiments to finally figure out what is awake replay for!

Our speakers:

  • John Widloski
  • Lisa Genzel
  • Jacob Bakermans
  • Elisa Massi

Meeting dates: 28 June to 1 July 2025 (our symposium is on the last day

Programme: ebbs2025.azuleon.org/programme

The abstract submission deadline for posters (and early bird registration) is on 31 March 2025 - I hope to see you there!

ebbs2025.azuleon.orgEBBS 2025 :: ProgrammeThe website of the 51st EBBS Meeting :: EBBS 2025

Hippocampal subfield volume alterations and associations with severity measures in long COVID and ME/CFS: A 7T MRI study 13.01.25

#LongCovid #MECFS #hippocampus

Link to plos.org:

journals.plos.org/plosone/arti

journals.plos.orgHippocampal subfield volume alterations and associations with severity measures in long COVID and ME/CFS: A 7T MRI studyLong COVID and Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) patients share similar symptoms including post-exertional malaise, neurocognitive impairment, and memory loss. The neurocognitive impairment in both conditions might be linked to alterations in the hippocampal subfields. Therefore, this study compared alterations in hippocampal subfields of 17 long COVID, 29 ME/CFS patients, and 15 healthy controls (HC). Structural MRI data was acquired with sub-millimeter isotropic resolution on a 7 Telsa MRI scanner and hippocampal subfield volumes were then estimated for each participant using FreeSurfer software. Our study found significantly larger volumes in the left hippocampal subfields of both long COVID and ME/CFS patients compared to HC. These included the left subiculum head (long COVID; p = 0.01, ME/CFS; p = 0.002,), presubiculum head (long COVID; p = 0.004, ME/CFS; p = 0.005), molecular layer hippocampus head (long COVID; p = 0.014, ME/CFS; p = 0.011), and whole hippocampal head (long COVID; p = 0.01, ME/CFS; p = 0.01). Notably, hippocampal subfield volumes were similar between long COVID and ME/CFS patients. Additionally, we found significant associations between hippocampal subfield volumes and severity measures of ‘Pain’, ‘Duration of illness’, ‘Severity of fatigue’, ‘Impaired concentration’, ‘Unrefreshing sleep’, and ‘Physical function’ in both conditions. These findings suggest that hippocampal alterations may contribute to the neurocognitive impairment experienced by long COVID and ME/CFS patients. Furthermore, our study highlights similarities between these two conditions.