Differential vulnerability in the hindbrain neurons and local cerebral blood flow during bilateral vertebral occlusion in gerbils

Ryuji Hata, M. Matsumoto, T. Hatakeyama, T. Ohtsuki, N. Handa, M. Niinobe, K. Mikoshiba, S. Sakaki, T. Nishimura, T. Yanagihara, T. Kamada

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Abstract

Differential vulnerability in the hindbrain neurons was examined immunohistochemically during hindbrain ischemia in the gerbil. Hindbrain ischemia was produced by extracranial occlusion of the bilateral vertebral arteries just before their entry into the transverse foramen of the cervical vertebra. Local cerebral blood flow was measured by quantitative autoradiographic technique after 5 min of ischemia and was reduced to less than 5 ml/100 g per min in the cerebellum, the pons, and the medulla, indicating that severe and reproducible hindbrain ischemia was induced immediately after occlusion. For immunohistochemical investigation, four gerbils each were used for each ischemie period of 5, 10, 15, and 30 min. Immunohistochemical lesions, detected by the reaction for microtubule-associated protein 2, were visible in the lateral vestibular nucleus and the cerebellar interpositus nucleus even after 5 min of ischemia. These results suggested that these areas were more vulnerable than others, although blood flow was markedly reduced in various regions of the hindbrain. In contrast, areas related to respiratory or cardiovascular control were rather resistant to ischemia. The present study suggests that selective vulnerability during hindbrain ischemia depends mainly on different metabolic characteristics inherent to various neurons in the hindbrain.

Original languageEnglish
Pages (from-to)423-439
Number of pages17
JournalNeuroscience
Volume56
Issue number2
DOIs
Publication statusPublished - 01-01-1993

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Cerebrovascular Circulation
Rhombencephalon
Gerbillinae
Ischemia
Neurons
Lateral Vestibular Nucleus
Cervical Vertebrae
Cerebellar Nuclei
Microtubule-Associated Proteins
Pons
Vertebral Artery
Cerebellum

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)

Cite this

Hata, Ryuji ; Matsumoto, M. ; Hatakeyama, T. ; Ohtsuki, T. ; Handa, N. ; Niinobe, M. ; Mikoshiba, K. ; Sakaki, S. ; Nishimura, T. ; Yanagihara, T. ; Kamada, T. / Differential vulnerability in the hindbrain neurons and local cerebral blood flow during bilateral vertebral occlusion in gerbils. In: Neuroscience. 1993 ; Vol. 56, No. 2. pp. 423-439.
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Hata, R, Matsumoto, M, Hatakeyama, T, Ohtsuki, T, Handa, N, Niinobe, M, Mikoshiba, K, Sakaki, S, Nishimura, T, Yanagihara, T & Kamada, T 1993, 'Differential vulnerability in the hindbrain neurons and local cerebral blood flow during bilateral vertebral occlusion in gerbils', Neuroscience, vol. 56, no. 2, pp. 423-439. https://doi.org/10.1016/0306-4522(93)90343-E

Differential vulnerability in the hindbrain neurons and local cerebral blood flow during bilateral vertebral occlusion in gerbils. / Hata, Ryuji; Matsumoto, M.; Hatakeyama, T.; Ohtsuki, T.; Handa, N.; Niinobe, M.; Mikoshiba, K.; Sakaki, S.; Nishimura, T.; Yanagihara, T.; Kamada, T.

In: Neuroscience, Vol. 56, No. 2, 01.01.1993, p. 423-439.

Research output: Contribution to journalArticle

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AU - Yanagihara, T.

AU - Kamada, T.

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N2 - Differential vulnerability in the hindbrain neurons was examined immunohistochemically during hindbrain ischemia in the gerbil. Hindbrain ischemia was produced by extracranial occlusion of the bilateral vertebral arteries just before their entry into the transverse foramen of the cervical vertebra. Local cerebral blood flow was measured by quantitative autoradiographic technique after 5 min of ischemia and was reduced to less than 5 ml/100 g per min in the cerebellum, the pons, and the medulla, indicating that severe and reproducible hindbrain ischemia was induced immediately after occlusion. For immunohistochemical investigation, four gerbils each were used for each ischemie period of 5, 10, 15, and 30 min. Immunohistochemical lesions, detected by the reaction for microtubule-associated protein 2, were visible in the lateral vestibular nucleus and the cerebellar interpositus nucleus even after 5 min of ischemia. These results suggested that these areas were more vulnerable than others, although blood flow was markedly reduced in various regions of the hindbrain. In contrast, areas related to respiratory or cardiovascular control were rather resistant to ischemia. The present study suggests that selective vulnerability during hindbrain ischemia depends mainly on different metabolic characteristics inherent to various neurons in the hindbrain.

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