Combined loss of brevican, neurocan, tenascin-C and tenascin-R leads to impaired fear retrieval due to perineuronal net loss.

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Tác giả: Verian Bader, Andreas Faissner, Melanie D Mark, Cornelius Mueller-Buehl, Johanna Pakusch, Konstanze F Winklhofer

Ngôn ngữ: eng

Ký hiệu phân loại: 546.734 *Iodine

Thông tin xuất bản: England : Scientific reports , 2025

Mô tả vật lý:

Bộ sưu tập: NCBI

ID: 103253

In conditions such as neurodegenerative diseases, posttraumatic stress disorder (PTSD), addiction and spinal cord injuries, restricted synaptic plasticity hinders the formation of new neuronal connections, preventing the compensation and treatment of adverse behaviors. Perineuronal nets (PNNs) significantly restrict synaptic plasticity by inhibiting synapse formation. The digestion of PNNs has been associated with short-term cognitive improvements and reduced long-term memory, offering potential therapeutic benefits in PTSD. This study investigates the correlation between PNNs and fear memory processes in extracellular matrix (ECM) mutant mice, particularly focusing on the amygdala-medial prefrontal cortex (mPFC) circuit, which is crucial for fear memory generation and maintenance. Fear conditioning was conducted on mice lacking four key ECM-molecules: brevican, neurocan, tenascin-C and tenascin-R (4x KO). These mice exhibited severe impairments in memory consolidation, as evident by their inability to retrieve previously learned fear memories, coupled with reduced PNN density and disturbed synaptic integrity along their PNNs. Additionally, changes in neural activity in the basolateral amygdala (BL) and reductions in VGAT
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