Abstract
In this study, we investigated the neuronal activity of hippocampal slices from the β-amyloid protein-infused (300 pmol/day for 10-11 days) rats using the extracellular recording technique. Perfusion of nicotine (50 μM) reduced the amplitude of electrically evoked population spikes in the CA1 pyramidal cells of the vehicle control rats, but not in those of the β-amyloid protein-infused rats, suggesting the impairment of nicotinic signaling in the β-amyloid protein-infused rats. Long-term potentiation induced by tetanic stimulations in CA1 pyramidal cells, which was readily observed in the vehicle control rats, was also impaired in the β-amyloid protein-infused rats. Nicotinic blockade by adding hexamethonium into the perfused solution inhibited long-term potentiation induction. Taken together, our previous and present results suggest that β-amyloid protein infusion impairs the signal transduction mechanisms via nicotinic acetylcholine receptors. This dysfunction may be responsible, at least in part, for the impairment of long-term potentiation induction and may lead to learning deficits. Copyright (C) 1999 Elsevier Science B.V.
| Original language | English |
|---|---|
| Pages (from-to) | 167-175 |
| Number of pages | 9 |
| Journal | European Journal of Pharmacology |
| Volume | 382 |
| Issue number | 3 |
| DOIs | |
| Publication status | Published - 15-10-1999 |
| Externally published | Yes |
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All Science Journal Classification (ASJC) codes
- Pharmacology
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Impairments of long-term potentiation in hippocampal slices of β-amyloid-infused rats. / Itoh, Akio; Akaike, Tadashi; Sokabe, Masahiro; Nitta, Atsumi; Iida, Ryuichi; Olariu, Ana; Yamada, Kiyofumi; Nabeshima, Toshitaka.
In: European Journal of Pharmacology, Vol. 382, No. 3, 15.10.1999, p. 167-175.Research output: Contribution to journal › Article
TY - JOUR
T1 - Impairments of long-term potentiation in hippocampal slices of β-amyloid-infused rats
AU - Itoh, Akio
AU - Akaike, Tadashi
AU - Sokabe, Masahiro
AU - Nitta, Atsumi
AU - Iida, Ryuichi
AU - Olariu, Ana
AU - Yamada, Kiyofumi
AU - Nabeshima, Toshitaka
PY - 1999/10/15
Y1 - 1999/10/15
N2 - In this study, we investigated the neuronal activity of hippocampal slices from the β-amyloid protein-infused (300 pmol/day for 10-11 days) rats using the extracellular recording technique. Perfusion of nicotine (50 μM) reduced the amplitude of electrically evoked population spikes in the CA1 pyramidal cells of the vehicle control rats, but not in those of the β-amyloid protein-infused rats, suggesting the impairment of nicotinic signaling in the β-amyloid protein-infused rats. Long-term potentiation induced by tetanic stimulations in CA1 pyramidal cells, which was readily observed in the vehicle control rats, was also impaired in the β-amyloid protein-infused rats. Nicotinic blockade by adding hexamethonium into the perfused solution inhibited long-term potentiation induction. Taken together, our previous and present results suggest that β-amyloid protein infusion impairs the signal transduction mechanisms via nicotinic acetylcholine receptors. This dysfunction may be responsible, at least in part, for the impairment of long-term potentiation induction and may lead to learning deficits. Copyright (C) 1999 Elsevier Science B.V.
AB - In this study, we investigated the neuronal activity of hippocampal slices from the β-amyloid protein-infused (300 pmol/day for 10-11 days) rats using the extracellular recording technique. Perfusion of nicotine (50 μM) reduced the amplitude of electrically evoked population spikes in the CA1 pyramidal cells of the vehicle control rats, but not in those of the β-amyloid protein-infused rats, suggesting the impairment of nicotinic signaling in the β-amyloid protein-infused rats. Long-term potentiation induced by tetanic stimulations in CA1 pyramidal cells, which was readily observed in the vehicle control rats, was also impaired in the β-amyloid protein-infused rats. Nicotinic blockade by adding hexamethonium into the perfused solution inhibited long-term potentiation induction. Taken together, our previous and present results suggest that β-amyloid protein infusion impairs the signal transduction mechanisms via nicotinic acetylcholine receptors. This dysfunction may be responsible, at least in part, for the impairment of long-term potentiation induction and may lead to learning deficits. Copyright (C) 1999 Elsevier Science B.V.
UR - http://www.scopus.com/inward/record.url?scp=0032754051&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0032754051&partnerID=8YFLogxK
U2 - 10.1016/S0014-2999(99)00601-9
DO - 10.1016/S0014-2999(99)00601-9
M3 - Article
C2 - 10556667
AN - SCOPUS:0032754051
VL - 382
SP - 167
EP - 175
JO - European Journal of Pharmacology
JF - European Journal of Pharmacology
SN - 0014-2999
IS - 3
ER -