Effect of WAY-100135 on the hippocampal acetylcholine release potentiated by 8-OH-DPAT, a serotonin,, receptor agonist, in normal and p-chlorophenylalanine-treated rats as measured by in vivo microdialysis

Katsuhiko Nakai, Takeshi Fujii, Kazuko Fujimoto, Takeshi Suzuki, Koichiro Kawashima

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29 Citations (Scopus)

Abstract

The mechanisms involved in the enhancement of acetylcholine (ACh) release in the rat hippocampus by 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), a serotonin (5-HT)(1A) receptor agonist, were investigated using in vivo microdialysis. Administration of p-chlorophenylalanine (PCPA, 300 mg/kg, i.p.), a tryptophan hydroxylase inhibitor, 3 days before the dialysis experiments reduced the hippocampal 5-HT content to 30% of that in saline-treated rats, but did not affect basal ACh release in the hippocampus. 8-OH-DPAT administered systemically (0.5 mg/kg, s.c.) or applied locally (30 μM) into the hippocampus through the dialysis probe significantly enhanced the release of ACh in the hippocampus of PCPA-treated rats to the same degree as that in saline-treated rats. Pretreatment with (+)WAY-100135 (5 mg/kg, i.p.), a selective 5-HT)(1A) receptor antagonist, completely eliminated the enhancement of ACh release induced by locally applied 8-OH-DPAT, but only partially reduced the effects induced by systemically administered 8-OH-DPAT, in both groups of rats. Systemically administered 8-OH-DPAT induced hyperlocomotion in the both saline- and PCPA-treated rats, but this was not eliminated by (+)WAY-100135. 8-OH-DPAT applied locally into the hippocampus did not elicit hyperlocomotion in either group of rats. These results suggest that the modification of endogenous 5-HT release via the 5-HT)(1A) autoreceptor is not involved in the 8-OH-DPAT-induced increase of hippocampal ACh release, and that the increase of ACh release induced by locally applied 8-OH-DPAT involves mainly hippocampal postsynaptic 5-HT)(1A) receptor stimulation. In addition, a possibility that subtypes of 5-HT receptors other than the 5-HT)(1A) receptor, probably 5-HT7 receptor in the septum as well as postsynaptic 5-HT)(1A) receptor in the hippocampus, are involved in the increased hippocampal ACh release induced by systemically administered 8-OH-DPAT is discussed.

Original languageEnglish
Pages (from-to)23-29
Number of pages7
JournalNeuroscience Research
Volume31
Issue number1
DOIs
Publication statusPublished - 1998 May

Fingerprint

Fenclonine
8-Hydroxy-2-(di-n-propylamino)tetralin
Serotonin Receptor Agonists
Microdialysis
Acetylcholine
Receptor, Serotonin, 5-HT1A
Hippocampus
Serotonin
Dialysis
hydroxide ion
WAY 100135
Tryptophan Hydroxylase
Autoreceptors
Serotonin Receptors

Keywords

  • (+)WAY-100135
  • 8-hydroxy-2-(di-n-propylamino)tetralin
  • Acetylcholine
  • Hippocampus
  • Microdialysis
  • Radioimmunoassay
  • Serotonin(1A) receptor

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

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title = "Effect of WAY-100135 on the hippocampal acetylcholine release potentiated by 8-OH-DPAT, a serotonin,, receptor agonist, in normal and p-chlorophenylalanine-treated rats as measured by in vivo microdialysis",
abstract = "The mechanisms involved in the enhancement of acetylcholine (ACh) release in the rat hippocampus by 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), a serotonin (5-HT)(1A) receptor agonist, were investigated using in vivo microdialysis. Administration of p-chlorophenylalanine (PCPA, 300 mg/kg, i.p.), a tryptophan hydroxylase inhibitor, 3 days before the dialysis experiments reduced the hippocampal 5-HT content to 30{\%} of that in saline-treated rats, but did not affect basal ACh release in the hippocampus. 8-OH-DPAT administered systemically (0.5 mg/kg, s.c.) or applied locally (30 μM) into the hippocampus through the dialysis probe significantly enhanced the release of ACh in the hippocampus of PCPA-treated rats to the same degree as that in saline-treated rats. Pretreatment with (+)WAY-100135 (5 mg/kg, i.p.), a selective 5-HT)(1A) receptor antagonist, completely eliminated the enhancement of ACh release induced by locally applied 8-OH-DPAT, but only partially reduced the effects induced by systemically administered 8-OH-DPAT, in both groups of rats. Systemically administered 8-OH-DPAT induced hyperlocomotion in the both saline- and PCPA-treated rats, but this was not eliminated by (+)WAY-100135. 8-OH-DPAT applied locally into the hippocampus did not elicit hyperlocomotion in either group of rats. These results suggest that the modification of endogenous 5-HT release via the 5-HT)(1A) autoreceptor is not involved in the 8-OH-DPAT-induced increase of hippocampal ACh release, and that the increase of ACh release induced by locally applied 8-OH-DPAT involves mainly hippocampal postsynaptic 5-HT)(1A) receptor stimulation. In addition, a possibility that subtypes of 5-HT receptors other than the 5-HT)(1A) receptor, probably 5-HT7 receptor in the septum as well as postsynaptic 5-HT)(1A) receptor in the hippocampus, are involved in the increased hippocampal ACh release induced by systemically administered 8-OH-DPAT is discussed.",
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author = "Katsuhiko Nakai and Takeshi Fujii and Kazuko Fujimoto and Takeshi Suzuki and Koichiro Kawashima",
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T1 - Effect of WAY-100135 on the hippocampal acetylcholine release potentiated by 8-OH-DPAT, a serotonin,, receptor agonist, in normal and p-chlorophenylalanine-treated rats as measured by in vivo microdialysis

AU - Nakai, Katsuhiko

AU - Fujii, Takeshi

AU - Fujimoto, Kazuko

AU - Suzuki, Takeshi

AU - Kawashima, Koichiro

PY - 1998/5

Y1 - 1998/5

N2 - The mechanisms involved in the enhancement of acetylcholine (ACh) release in the rat hippocampus by 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), a serotonin (5-HT)(1A) receptor agonist, were investigated using in vivo microdialysis. Administration of p-chlorophenylalanine (PCPA, 300 mg/kg, i.p.), a tryptophan hydroxylase inhibitor, 3 days before the dialysis experiments reduced the hippocampal 5-HT content to 30% of that in saline-treated rats, but did not affect basal ACh release in the hippocampus. 8-OH-DPAT administered systemically (0.5 mg/kg, s.c.) or applied locally (30 μM) into the hippocampus through the dialysis probe significantly enhanced the release of ACh in the hippocampus of PCPA-treated rats to the same degree as that in saline-treated rats. Pretreatment with (+)WAY-100135 (5 mg/kg, i.p.), a selective 5-HT)(1A) receptor antagonist, completely eliminated the enhancement of ACh release induced by locally applied 8-OH-DPAT, but only partially reduced the effects induced by systemically administered 8-OH-DPAT, in both groups of rats. Systemically administered 8-OH-DPAT induced hyperlocomotion in the both saline- and PCPA-treated rats, but this was not eliminated by (+)WAY-100135. 8-OH-DPAT applied locally into the hippocampus did not elicit hyperlocomotion in either group of rats. These results suggest that the modification of endogenous 5-HT release via the 5-HT)(1A) autoreceptor is not involved in the 8-OH-DPAT-induced increase of hippocampal ACh release, and that the increase of ACh release induced by locally applied 8-OH-DPAT involves mainly hippocampal postsynaptic 5-HT)(1A) receptor stimulation. In addition, a possibility that subtypes of 5-HT receptors other than the 5-HT)(1A) receptor, probably 5-HT7 receptor in the septum as well as postsynaptic 5-HT)(1A) receptor in the hippocampus, are involved in the increased hippocampal ACh release induced by systemically administered 8-OH-DPAT is discussed.

AB - The mechanisms involved in the enhancement of acetylcholine (ACh) release in the rat hippocampus by 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), a serotonin (5-HT)(1A) receptor agonist, were investigated using in vivo microdialysis. Administration of p-chlorophenylalanine (PCPA, 300 mg/kg, i.p.), a tryptophan hydroxylase inhibitor, 3 days before the dialysis experiments reduced the hippocampal 5-HT content to 30% of that in saline-treated rats, but did not affect basal ACh release in the hippocampus. 8-OH-DPAT administered systemically (0.5 mg/kg, s.c.) or applied locally (30 μM) into the hippocampus through the dialysis probe significantly enhanced the release of ACh in the hippocampus of PCPA-treated rats to the same degree as that in saline-treated rats. Pretreatment with (+)WAY-100135 (5 mg/kg, i.p.), a selective 5-HT)(1A) receptor antagonist, completely eliminated the enhancement of ACh release induced by locally applied 8-OH-DPAT, but only partially reduced the effects induced by systemically administered 8-OH-DPAT, in both groups of rats. Systemically administered 8-OH-DPAT induced hyperlocomotion in the both saline- and PCPA-treated rats, but this was not eliminated by (+)WAY-100135. 8-OH-DPAT applied locally into the hippocampus did not elicit hyperlocomotion in either group of rats. These results suggest that the modification of endogenous 5-HT release via the 5-HT)(1A) autoreceptor is not involved in the 8-OH-DPAT-induced increase of hippocampal ACh release, and that the increase of ACh release induced by locally applied 8-OH-DPAT involves mainly hippocampal postsynaptic 5-HT)(1A) receptor stimulation. In addition, a possibility that subtypes of 5-HT receptors other than the 5-HT)(1A) receptor, probably 5-HT7 receptor in the septum as well as postsynaptic 5-HT)(1A) receptor in the hippocampus, are involved in the increased hippocampal ACh release induced by systemically administered 8-OH-DPAT is discussed.

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KW - 8-hydroxy-2-(di-n-propylamino)tetralin

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KW - Hippocampus

KW - Microdialysis

KW - Radioimmunoassay

KW - Serotonin(1A) receptor

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DO - 10.1016/S0168-0102(98)00019-4

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