Topographic CA1 input shapes subicular spatial coding

2026 · doi:10.64898/2026.03.24.714092
preprint OA: closed CC-BY-NC-ND-4.0
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The study examined how hippocampal CA1-to-subiculum topographic projections contribute to spatial coding in latrophilin-2 conditional knockout mice, using selective disruption of CA1-to-subiculum topography. The authors found that disrupting precise topography changes the anatomical distribution of subicular spatial coding while largely preserving single-cell tuning. Boundary vector coding and long-term network stability were also selectively impaired, with the key caveat that the work focuses on a specific projection-level manipulation in this mouse genetic model. This paper does not explicitly discuss endometriosis or adenomyosis; it was included in the corpus via a keyword match in the upstream search index.

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Abstract

Topographic organization characterizes hippocampal circuits, yet its functional significance remains unclear. By selectively disrupting CA1-to-subiculum topographic projections in latrophilin-2 conditional knockout mice, we show that precise topography shapes the anatomical distribution of subicular spatial coding while preserving single-cell tuning. Disrupted topography also selectively impairs boundary vector coding and long-term network stability. Thus, CA1 inputs provide an indispensable scaffold for organizing subicular spatial maps and dynamics.
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Abstract Topographic organization characterizes hippocampal circuits, yet its functional significance remains unclear. By selectively disrupting CA1-to-subiculum topographic projections in latrophilin-2 conditional knockout mice, we show that precise topography shapes the anatomical distribution of subicular spatial coding while preserving single-cell tuning. Disrupted topography also selectively impairs boundary vector coding and long-term network stability. Thus, CA1 inputs provide an indispensable scaffold for organizing subicular spatial maps and dynamics. Competing Interest Statement The authors have declared no competing interest. Funder Information Declared National Institute of Health, K01DA058743, R01MH126904, R01MH130452, U19NS118284, P50DA042012, R01NS050580 National Institute of Health, R01NS104897, RF1AG065675 Simons Foundation, https://ror.org/01cmst727, 542987SPI, SCGB Fellows-to-Faculty award 00007396, SFARI Fellows-to-Faculty Award (DTP) Cancer Prevention and Research Institute of Texas, RR240082 Vallee Foundation, https://ror.org/05nmp3276, Lisa M Giocomo James S. McDonnell Foundation, https://ror.org/03dy4aq19, Lisa M Giocomo Howard Hughes Medical Institute, https://ror.org/006w34k90, Lisa M Giocomo, Liqun Luo Copyright The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY 4.0 International license.

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License: CC-BY-NC-ND-4.0