Very delayed neuronal loss occurs in the glomerular layer of the main olfactory bulb following transient ischemia in gerbils

In Koo Hwang; Jae Chul Lee; Jun Hwi Cho; Ki Yeon Yoo; Duk Soo Kim; Young Sam Nam; Won Ki Kim; In Se Lee; Tae Cheon Kang; Moo Ho Won

doi:10.1016/j.neulet.2004.05.071

Very delayed neuronal loss occurs in the glomerular layer of the main olfactory bulb following transient ischemia in gerbils

In Koo Hwang, Jae Chul Lee, Jun Hwi Cho, Ki Yeon Yoo, Duk Soo Kim, Young Sam Nam, Won Ki Kim, In Se Lee, Tae Cheon Kang, Moo Ho Won

Research output: Contribution to journal › Article

12 Citations (Scopus)

Abstract

Olfactory dysfunction could happen following various insults such as ischemic-hypoxic state. Neurons of the main olfactory bulb (MOB) are resistant to ischemic damage. In the present study, we investigated the ischemia-related changes of neurons and glial cells in the glomerular layer (GL) of the gerbil MOB after transient ischemia. The number of NeuN-immunoreactive neurons became to decrease from 10 days after ischemic insult. Fifteen days after ischemic insult, astrocytes and microglia were increased in number. By 60 days after ischemia, NeuN-immunoreactive neurons were significantly decreased by 42% per glomerulus. At this time period, astrocytes and microglia were pronouncedly increased. This result indicates that neuronal loss must be much delayed in the GL following transient ischemia.

Original language	English
Pages (from-to)	272-276
Number of pages	5
Journal	Neuroscience Letters
Volume	366
Issue number	3
DOIs	https://doi.org/10.1016/j.neulet.2004.05.071
Publication status	Published - 2004 Aug 19
Externally published	Yes

Keywords

Gerbil
Gliosis
Glomerular layer
Main olfactory bulb
NeuN
Transient forebrain ischemia

ASJC Scopus subject areas

Neuroscience(all)

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Very delayed neuronal loss occurs in the glomerular layer of the main olfactory bulb following transient ischemia in gerbils. / Hwang, In Koo; Lee, Jae Chul; Cho, Jun Hwi; Yoo, Ki Yeon; Kim, Duk Soo; Nam, Young Sam; Kim, Won Ki; Lee, In Se; Kang, Tae Cheon; Won, Moo Ho.

In: Neuroscience Letters, Vol. 366, No. 3, 19.08.2004, p. 272-276.

Research output: Contribution to journal › Article

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abstract = "Olfactory dysfunction could happen following various insults such as ischemic-hypoxic state. Neurons of the main olfactory bulb (MOB) are resistant to ischemic damage. In the present study, we investigated the ischemia-related changes of neurons and glial cells in the glomerular layer (GL) of the gerbil MOB after transient ischemia. The number of NeuN-immunoreactive neurons became to decrease from 10 days after ischemic insult. Fifteen days after ischemic insult, astrocytes and microglia were increased in number. By 60 days after ischemia, NeuN-immunoreactive neurons were significantly decreased by 42% per glomerulus. At this time period, astrocytes and microglia were pronouncedly increased. This result indicates that neuronal loss must be much delayed in the GL following transient ischemia.",

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AU - Hwang, In Koo

AU - Lee, Jae Chul

AU - Cho, Jun Hwi

AU - Yoo, Ki Yeon

AU - Kim, Duk Soo

AU - Nam, Young Sam

AU - Kim, Won Ki

AU - Lee, In Se

AU - Kang, Tae Cheon

AU - Won, Moo Ho

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AB - Olfactory dysfunction could happen following various insults such as ischemic-hypoxic state. Neurons of the main olfactory bulb (MOB) are resistant to ischemic damage. In the present study, we investigated the ischemia-related changes of neurons and glial cells in the glomerular layer (GL) of the gerbil MOB after transient ischemia. The number of NeuN-immunoreactive neurons became to decrease from 10 days after ischemic insult. Fifteen days after ischemic insult, astrocytes and microglia were increased in number. By 60 days after ischemia, NeuN-immunoreactive neurons were significantly decreased by 42% per glomerulus. At this time period, astrocytes and microglia were pronouncedly increased. This result indicates that neuronal loss must be much delayed in the GL following transient ischemia.

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KW - Gliosis

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KW - Main olfactory bulb

KW - NeuN

KW - Transient forebrain ischemia

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