How does prolonged caloric restriction ameliorate age-related impairment of long-term potentiation in the hippocampus?

Mitsuko Okada, Hiroshi Nakanishi, Toshiaki Amamoto, Ryuji Urae, Susumu Ando, Kazuyoshi Yazawa, Michihiro Fujiwara

Research output: Contribution to journalArticle

18 Citations (Scopus)

Abstract

Prolonged dietary restriction has been reported to suppress age-induced phenomena. In order to investigate how prolonged caloric restriction reduces age-related deterioration of hippocampal synaptic transmission, we compared the levels of major hippocampal polyunsaturated fatty acids, arachidonic acid and docosahexaenoic acid between 4- and 26-month-old rats. The Ca2+ responses upon perfusion of NMDA or 30 mM K+ between 4- and 26-month-old rats with prolonged dietary restriction were also compared using the fluorescent probe Fura-2. A decrease in membrane arachidonic acid is thought to be a major causal factor in the age-related impairment of long-term potentiation. Long-term caloric restriction seems to increase arachidonic acid levels regardless of age. However, there is no significant difference of hippocampal arachidonic acid levels between in freely feeding 4- and 26-month-old rats. Similar results were obtained from the measurement of hippocampal docosahexaenoic acid levels. Under caloric restriction, the 500 μM N-methyl-D-aspartate-induced Ca2+ response was greatly reduced by aging, while the 30 mM K+-induced Ca2+ response was not affected. In our preliminary data, the amplitude of the population spike after tetanic stimulation did not differ between 4- and 26-month-old rats under caloric restriction, while 50 μM of 2-amino-5-phosphonovaleric acid, a N-methyl-D-aspartate antagonist, markedly inhibited a potentiation of the population spike in 4-month-old rats, but with negligible inhibition in 26-month-old rats. From these results, an age-related impairment of hippocampal excitatory synaptic transmission may not be solely due to the reduction of membrane arachidonic acid. Caloric restriction might prevent age-related reduction in hippocampal synaptic transmission by enhancing non-N-methyl-D-aspartate mechanisms.

Original languageEnglish
Pages (from-to)175-181
Number of pages7
JournalMolecular Brain Research
Volume111
Issue number1-2
DOIs
Publication statusPublished - Mar 17 2003

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Caloric Restriction
Long-Term Potentiation
Hippocampus
Arachidonic Acid
N-Methylaspartate
Synaptic Transmission
Docosahexaenoic Acids
2-Amino-5-phosphonovalerate
D-Aspartic Acid
Membranes
Fura-2
Age Factors
Unsaturated Fatty Acids
Fluorescent Dyes
Population
Perfusion

All Science Journal Classification (ASJC) codes

  • Molecular Biology
  • Cellular and Molecular Neuroscience

Cite this

How does prolonged caloric restriction ameliorate age-related impairment of long-term potentiation in the hippocampus? / Okada, Mitsuko; Nakanishi, Hiroshi; Amamoto, Toshiaki; Urae, Ryuji; Ando, Susumu; Yazawa, Kazuyoshi; Fujiwara, Michihiro.

In: Molecular Brain Research, Vol. 111, No. 1-2, 17.03.2003, p. 175-181.

Research output: Contribution to journalArticle

Okada, Mitsuko ; Nakanishi, Hiroshi ; Amamoto, Toshiaki ; Urae, Ryuji ; Ando, Susumu ; Yazawa, Kazuyoshi ; Fujiwara, Michihiro. / How does prolonged caloric restriction ameliorate age-related impairment of long-term potentiation in the hippocampus?. In: Molecular Brain Research. 2003 ; Vol. 111, No. 1-2. pp. 175-181.
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