Scholarlink

<p>The study objective was descriptive, qualitative and quantitative texture analysis of ultrastructural research of the dendritic domain, especially dendrites, within the cerebellar dentate nucleus (DN) in an experimental model of hyperthermia-induced seizures (HS) developed at our Center, conducted on young Wistar rats. Specimens (1&#xa0;mm³) collected from the DN in both experimental and control groups, and fixed via transcardial perfusion with paraformaldehyde and glutaraldehyde solutions, were routinely processed for transmission electron microscopy. Ultrastructural studies, including morphometric assessment of dendrites across the DN in the experimental model of hyperthermia-induced seizures (HS), revealed distinctive and easily recognizable morphological signs of aponecrosis, manifested as “dark” dendroplasm degeneration (“dark dendrites”), resulting in significant disturbances in the cerebro-cerebellar function in animals subjected to hyperthermic stress. The aponecrotic lesions affecting the dendritic tree were characterized by shrunken, dark, nearly black, homogeneous dendroplasm exhibiting intense degenerative changes up to and including necrosis, which fully correlated with the quantitative analysis. Lethally damaged large dendrites displayed clear signs of cytoskeletal disintegration within the dendrites, particularly affecting microtubules, which are critical structures involved in numerous cellular processes, as well as cytoplasmic organelles. Our current and previous pioneering qualitative and quantitative ultrastructural investigations into the cellular mechanisms underlying the experimental model of HS indicate that damage to the somatodendritic domain of DN, including dendritic arborization and neuronal somata, characterized by aponecrosis, may play a major role in the morphogenesis of heat stress-induced convulsions.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Pioneering ultrastructural texture analysis of dendrites in the cerebellar dentate nucleus: an experimental rat model of hyperthermia-induced seizures

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年4月6日

查看全文
  • Joanna Maria Łotowska,
  • Marta Borowska,
  • Milena Żochowska-Sobaniec,
  • Maria Elżbieta Sobaniec-Łotowska,
  • Piotr Sobaniec

摘要

The study objective was descriptive, qualitative and quantitative texture analysis of ultrastructural research of the dendritic domain, especially dendrites, within the cerebellar dentate nucleus (DN) in an experimental model of hyperthermia-induced seizures (HS) developed at our Center, conducted on young Wistar rats. Specimens (1 mm³) collected from the DN in both experimental and control groups, and fixed via transcardial perfusion with paraformaldehyde and glutaraldehyde solutions, were routinely processed for transmission electron microscopy. Ultrastructural studies, including morphometric assessment of dendrites across the DN in the experimental model of hyperthermia-induced seizures (HS), revealed distinctive and easily recognizable morphological signs of aponecrosis, manifested as “dark” dendroplasm degeneration (“dark dendrites”), resulting in significant disturbances in the cerebro-cerebellar function in animals subjected to hyperthermic stress. The aponecrotic lesions affecting the dendritic tree were characterized by shrunken, dark, nearly black, homogeneous dendroplasm exhibiting intense degenerative changes up to and including necrosis, which fully correlated with the quantitative analysis. Lethally damaged large dendrites displayed clear signs of cytoskeletal disintegration within the dendrites, particularly affecting microtubules, which are critical structures involved in numerous cellular processes, as well as cytoplasmic organelles. Our current and previous pioneering qualitative and quantitative ultrastructural investigations into the cellular mechanisms underlying the experimental model of HS indicate that damage to the somatodendritic domain of DN, including dendritic arborization and neuronal somata, characterized by aponecrosis, may play a major role in the morphogenesis of heat stress-induced convulsions.