Carbon monoxide-induced delayed amnesia, delayed neuronal death and change in acetylcholine concentration in mice

Toshitaka Nabeshima, A. Katoh, H. Ishimaru, Y. Yoneda, K. Ogita, K. Murase, H. Ohtsuka, K. Inari, T. Fukuta, T. Kameyama

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Abstract

We investigated the interrelationship of delayed amnesia, delayed neuronal death and changes in acetylcholine concentration induced by carbon monoxide (CO)-exposure in mice. In the test for retention of the passive avoidance task, amnesia was observed 5 and 7 days after CO-exposure when the mice were exposed to CO 1 day after training; in the case when the mice were exposed to CO 5 and 7 days before training, amnesia was also observed in a retention test given 1 day after training. The number of pyramidal cells in the hippocampal CA1 subfield was lower than that of the control 3,5 and 7 days after CO-exposure. But the neurodegeneration in the parietal cortex, area 1, was not observed until 7 days after CO-exposure. The findings indicated that the amnesia and the neuronal death were produced after a delay when the mice were exposed to CO. In addition, the delayed amnesia was closely related to the delayed neuronal death in the hippocampal CA1 subfield. Moreover, [3H]glutamate and [3H]glycine binding sites did not change after CO-exposure but, 7 days after CO-exposure, the concentration of acetylcholine and the binding of [3H]quinuclidinyl benzilate in the frontal cortex and the striatum were found to have significantly changed, but those in the hippocampus did not show significant change. Therefore, we suggest that delayed amnesia induced by CO-exposure may result from delayed neuronal death in the hippocampal CA1 subfield and dysfunction in the acetylcholinergic neurons, in the frontal cortex, the striatum and/or the hippocampus.

Original languageEnglish
Pages (from-to)378-384
Number of pages7
JournalJournal of Pharmacology and Experimental Therapeutics
Volume256
Issue number1
Publication statusPublished - 01-01-1991
Externally publishedYes

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Amnesia
Carbon Monoxide
Acetylcholine
Frontal Lobe
Hippocampus
Quinuclidinyl Benzilate
Parietal Lobe
Pyramidal Cells
Glycine
Glutamic Acid
Binding Sites
Neurons

All Science Journal Classification (ASJC) codes

  • Molecular Medicine
  • Pharmacology

Cite this

Nabeshima, Toshitaka ; Katoh, A. ; Ishimaru, H. ; Yoneda, Y. ; Ogita, K. ; Murase, K. ; Ohtsuka, H. ; Inari, K. ; Fukuta, T. ; Kameyama, T. / Carbon monoxide-induced delayed amnesia, delayed neuronal death and change in acetylcholine concentration in mice. In: Journal of Pharmacology and Experimental Therapeutics. 1991 ; Vol. 256, No. 1. pp. 378-384.
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Nabeshima, T, Katoh, A, Ishimaru, H, Yoneda, Y, Ogita, K, Murase, K, Ohtsuka, H, Inari, K, Fukuta, T & Kameyama, T 1991, 'Carbon monoxide-induced delayed amnesia, delayed neuronal death and change in acetylcholine concentration in mice', Journal of Pharmacology and Experimental Therapeutics, vol. 256, no. 1, pp. 378-384.

Carbon monoxide-induced delayed amnesia, delayed neuronal death and change in acetylcholine concentration in mice. / Nabeshima, Toshitaka; Katoh, A.; Ishimaru, H.; Yoneda, Y.; Ogita, K.; Murase, K.; Ohtsuka, H.; Inari, K.; Fukuta, T.; Kameyama, T.

In: Journal of Pharmacology and Experimental Therapeutics, Vol. 256, No. 1, 01.01.1991, p. 378-384.

Research output: Contribution to journalArticle

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T1 - Carbon monoxide-induced delayed amnesia, delayed neuronal death and change in acetylcholine concentration in mice

AU - Nabeshima, Toshitaka

AU - Katoh, A.

AU - Ishimaru, H.

AU - Yoneda, Y.

AU - Ogita, K.

AU - Murase, K.

AU - Ohtsuka, H.

AU - Inari, K.

AU - Fukuta, T.

AU - Kameyama, T.

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N2 - We investigated the interrelationship of delayed amnesia, delayed neuronal death and changes in acetylcholine concentration induced by carbon monoxide (CO)-exposure in mice. In the test for retention of the passive avoidance task, amnesia was observed 5 and 7 days after CO-exposure when the mice were exposed to CO 1 day after training; in the case when the mice were exposed to CO 5 and 7 days before training, amnesia was also observed in a retention test given 1 day after training. The number of pyramidal cells in the hippocampal CA1 subfield was lower than that of the control 3,5 and 7 days after CO-exposure. But the neurodegeneration in the parietal cortex, area 1, was not observed until 7 days after CO-exposure. The findings indicated that the amnesia and the neuronal death were produced after a delay when the mice were exposed to CO. In addition, the delayed amnesia was closely related to the delayed neuronal death in the hippocampal CA1 subfield. Moreover, [3H]glutamate and [3H]glycine binding sites did not change after CO-exposure but, 7 days after CO-exposure, the concentration of acetylcholine and the binding of [3H]quinuclidinyl benzilate in the frontal cortex and the striatum were found to have significantly changed, but those in the hippocampus did not show significant change. Therefore, we suggest that delayed amnesia induced by CO-exposure may result from delayed neuronal death in the hippocampal CA1 subfield and dysfunction in the acetylcholinergic neurons, in the frontal cortex, the striatum and/or the hippocampus.

AB - We investigated the interrelationship of delayed amnesia, delayed neuronal death and changes in acetylcholine concentration induced by carbon monoxide (CO)-exposure in mice. In the test for retention of the passive avoidance task, amnesia was observed 5 and 7 days after CO-exposure when the mice were exposed to CO 1 day after training; in the case when the mice were exposed to CO 5 and 7 days before training, amnesia was also observed in a retention test given 1 day after training. The number of pyramidal cells in the hippocampal CA1 subfield was lower than that of the control 3,5 and 7 days after CO-exposure. But the neurodegeneration in the parietal cortex, area 1, was not observed until 7 days after CO-exposure. The findings indicated that the amnesia and the neuronal death were produced after a delay when the mice were exposed to CO. In addition, the delayed amnesia was closely related to the delayed neuronal death in the hippocampal CA1 subfield. Moreover, [3H]glutamate and [3H]glycine binding sites did not change after CO-exposure but, 7 days after CO-exposure, the concentration of acetylcholine and the binding of [3H]quinuclidinyl benzilate in the frontal cortex and the striatum were found to have significantly changed, but those in the hippocampus did not show significant change. Therefore, we suggest that delayed amnesia induced by CO-exposure may result from delayed neuronal death in the hippocampal CA1 subfield and dysfunction in the acetylcholinergic neurons, in the frontal cortex, the striatum and/or the hippocampus.

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