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<p>Olfactory bulbectomy in rodents is a wide-used model of cholinergic dysfunction, yet, the state of nerve growth factor system, crucial for cholinergic neurons survival, is poorly understood in this model. In the present study the effect of olfactory bulbectomy on nerve growth factor (NGF) forms levels in mouse brain regions was assessed. Levels of proNGF and mature NGF protein were evaluated in medial septal complex and hippocampus samples using Western blot. Also, hippocampal choline acetyltransferase activity was measured to assess cholinergic transmission state. Thirty days after bulbectomy, proNGF level was increased in the hippocampus but not in medial septal complex. Mature NGF levels remained unchanged. Hippocampal choline acetyltransferase activity was significantly decreased. This decrease in choline acetyltransferase activity was probably associated with predominant activation of pro-NGF signaling cascades triggered by p75 receptor.</p>

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Olfactory Bulbectomy in Mice Induces an Increase in Hippocampal Pro-Nerve Growth Factor Protein Levels

  • 期刊论文

  • 发表日期：

    2025年6月1日

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  • O. A. Nedogreeva,
  • M. Yu. Stepanichev

摘要

Olfactory bulbectomy in rodents is a wide-used model of cholinergic dysfunction, yet, the state of nerve growth factor system, crucial for cholinergic neurons survival, is poorly understood in this model. In the present study the effect of olfactory bulbectomy on nerve growth factor (NGF) forms levels in mouse brain regions was assessed. Levels of proNGF and mature NGF protein were evaluated in medial septal complex and hippocampus samples using Western blot. Also, hippocampal choline acetyltransferase activity was measured to assess cholinergic transmission state. Thirty days after bulbectomy, proNGF level was increased in the hippocampus but not in medial septal complex. Mature NGF levels remained unchanged. Hippocampal choline acetyltransferase activity was significantly decreased. This decrease in choline acetyltransferase activity was probably associated with predominant activation of pro-NGF signaling cascades triggered by p75 receptor.