Introduction to the special issue on: A new view of hippocampal area <scp>CA2</scp>

Dudek, Serena M.; Alexander, Georgia M.; Farris, Shannon

doi:10.1002/hipo.23514

Cited by 1 publication

(1 citation statement)

References 62 publications

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“…Among these subregions, Cornu Ammonis 1 (CA1) occupies a significant portion of the hippocampus and receives inputs from CA3 pyramidal neurons, as well as direct input from CA2, the medial entorhinal cortex (MEC), and the lateral entorhinal cortex (LEC) [2][3][4][5]. Cornu Ammonis 2 (CA2), located between CA1 and CA3, exhibits distinct molecular characteristics, including increased expression of specific genes and proteins such as RGS14, TCP4, ACTN2, and PTPN5 [6,7].…”

Section: Introductionmentioning

confidence: 99%

E3 Ubiquitin Ligase Uhrf2 Knockout Reveals a Critical Role in Social Behavior and Synaptic Plasticity in the Hippocampus

Zhuang,

Li,

Zhao

et al. 2024

IJMS

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The hippocampal formation, particularly the CA2 subregion, is critical for social memory formation and memory processing, relying on synaptic plasticity—a fundamental mechanism by which synapses strengthen. Given the role of the ubiquitin–proteasome system (UPS) in various nervous system processes, including learning and memory, we were particularly interested in exploring the involvement of RING-type ubiquitin E3 ligases, such as UHRF2 (NIRF), in social behavior and synaptic plasticity. Our results revealed altered social behavior in mice with systemic Uhrf2 knockout, including changes in nest building, tube dominance, and the three-chamber social novelty test. In Uhrf2 knockout mice, the entorhinal cortex-CA2 circuit showed significant reductions in synaptic plasticity during paired-pulse facilitation and long-term potentiation, while the inability to evoke synaptic plasticity in the Schaffer-collateral CA2 synapses remained unaffected. These changes in synaptic plasticity correlated with significant changes in gene expression including genes related to vesicle trafficking and transcriptional regulation. The effects of Uhrf2 knockout on synaptic plasticity and the observed gene expression changes highlight UHRF2 as a regulator of learning and memory processes at both the cellular and systemic levels. Targeting E3 ubiquitin ligases, such as UHRF2, may hold therapeutic potential for memory-related disorders, warranting further investigation.

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