Study reveals that learning triggers a series of molecular events including DNA damage and repair in hippocampal neurons, mediated by TLR9, crucial for memory formation.
By Dr. Chinta SidharthanMar 31 2024Reviewed by Susha Cheriyedath, M.Sc. In a recent study published in the journal Nature, researchers found that the recruitment of neurons to memory circuits is preceded by a cascade of molecular events induced during learning, which includes double-stranded deoxyribonucleic acid damage in hippocampal neuronal clusters and repair mediated by toll-like receptor 9 .
Studies have also explored the role of intrinsic neuronal and pre-existing developmental programs in memory formation and have found that transcriptional factors such as cyclic adenosine monophosphate -response element binding protein are involved in the process. Recent research has also focused on understanding how interneuronal perineuronal nets control inhibitory inputs to neuronal assemblies to stabilize memory circuits.
Given that transient breaks in double-stranded DNA are known to be induced during neuronal activity for the induction of immediate early gene expression, they hypothesized that the DNA damage induced by learning activity might be more extensive and sustained in discrete populations of neurons.
Additionally, single nuclear RNA sequencing was performed to characterize gene expression changes in neuronal and non-neuronal hippocampal cell populations due to the impact of contextual fear conditioning and neuron-specific knockout of TLR9. The researchers also examined the contributions of infiltrating immune cells and cell-free DNA from blood in memory formation and the upregulation of TLR9 signaling.
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