Serotonin depletion results in a decrease of the neuronal activation caused by rivastigmine in the rat hippocampus

Research output: Contribution to journalJournal articleResearchpeer-review

Standard

Serotonin depletion results in a decrease of the neuronal activation caused by rivastigmine in the rat hippocampus. / Kornum, Birgitte R; Weikop, Pia; Moller, Arne; Ronn, Lars C B; Knudsen, Gitte M; Aznar, Susana.

In: Brain Research Reviews, Vol. 1073-1074, 16.02.2006, p. 262-8.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Kornum, BR, Weikop, P, Moller, A, Ronn, LCB, Knudsen, GM & Aznar, S 2006, 'Serotonin depletion results in a decrease of the neuronal activation caused by rivastigmine in the rat hippocampus', Brain Research Reviews, vol. 1073-1074, pp. 262-8. https://doi.org/10.1016/j.brainres.2005.12.030

APA

Kornum, B. R., Weikop, P., Moller, A., Ronn, L. C. B., Knudsen, G. M., & Aznar, S. (2006). Serotonin depletion results in a decrease of the neuronal activation caused by rivastigmine in the rat hippocampus. Brain Research Reviews, 1073-1074, 262-8. https://doi.org/10.1016/j.brainres.2005.12.030

Vancouver

Kornum BR, Weikop P, Moller A, Ronn LCB, Knudsen GM, Aznar S. Serotonin depletion results in a decrease of the neuronal activation caused by rivastigmine in the rat hippocampus. Brain Research Reviews. 2006 Feb 16;1073-1074:262-8. https://doi.org/10.1016/j.brainres.2005.12.030

Author

Kornum, Birgitte R ; Weikop, Pia ; Moller, Arne ; Ronn, Lars C B ; Knudsen, Gitte M ; Aznar, Susana. / Serotonin depletion results in a decrease of the neuronal activation caused by rivastigmine in the rat hippocampus. In: Brain Research Reviews. 2006 ; Vol. 1073-1074. pp. 262-8.

Bibtex

@article{a0eddc24e2a94b3a82801fa24dcebcf4,
title = "Serotonin depletion results in a decrease of the neuronal activation caused by rivastigmine in the rat hippocampus",
abstract = "Interactions between the serotonergic and cholinergic systems are known to occur and are believed to play a role in the mechanism underlying both major depression and Alzheimer's disease. On a molecular level, studies suggest that acetylcholine (ACh) increases serotonin (5-HT) release through nicotinic receptors located at nerve terminals. The aim of the present study was to determine in which areas and to what extent 5-HT mediates the neuronal response to ACh release. For this purpose, neuronal activity was measured in rats with rivastigmine-induced elevated ACh levels after a 95{\%} 5-HT depletion obtained by dosing p-chlorophenylalanine followed by D,L-fenfluramine. Neuronal activation was quantified by stereological measurements of c-Fos immunoreactivity. The brain areas examined were medial prefrontal cortex, septum, dorsal hippocampus, and dorsal raphe nucleus. Rivastigmine significantly increased c-Fos immunoreactivity in medial prefrontal cortex and the hippocampus, but not in the septum and dorsal raphe nucleus. 5-HT depletion decreased ACh-induced c-Fos immunoreactivity in the dentate gyrus. By contrast, 5-HT depletion had no effect on the ACh-induced activity in the other brain areas examined. It is concluded that 5-HT mediates part of the ACh-induced hippocampal neuronal activation, possibly mediated via locally released 5-HT.",
keywords = "Acetylcholine/metabolism, Animals, Cell Count/methods, Chromatography, High Pressure Liquid/methods, Drug Interactions, Fenclonine/pharmacology, Fenfluramine/pharmacology, Gene Expression/drug effects, Hippocampus/cytology, Hydroxyindoleacetic Acid/metabolism, Immunohistochemistry/methods, Male, Neurons/drug effects, Neuroprotective Agents/pharmacology, Phenylcarbamates/pharmacology, Proto-Oncogene Proteins c-fos/metabolism, Rats, Rats, Sprague-Dawley, Rivastigmine, Serotonin/deficiency, Serotonin Uptake Inhibitors/pharmacology",
author = "Kornum, {Birgitte R} and Pia Weikop and Arne Moller and Ronn, {Lars C B} and Knudsen, {Gitte M} and Susana Aznar",
year = "2006",
month = "2",
day = "16",
doi = "10.1016/j.brainres.2005.12.030",
language = "English",
volume = "1073-1074",
pages = "262--8",
journal = "Brain Research Reviews",
issn = "0165-0173",
publisher = "Elsevier",

}

RIS

TY - JOUR

T1 - Serotonin depletion results in a decrease of the neuronal activation caused by rivastigmine in the rat hippocampus

AU - Kornum, Birgitte R

AU - Weikop, Pia

AU - Moller, Arne

AU - Ronn, Lars C B

AU - Knudsen, Gitte M

AU - Aznar, Susana

PY - 2006/2/16

Y1 - 2006/2/16

N2 - Interactions between the serotonergic and cholinergic systems are known to occur and are believed to play a role in the mechanism underlying both major depression and Alzheimer's disease. On a molecular level, studies suggest that acetylcholine (ACh) increases serotonin (5-HT) release through nicotinic receptors located at nerve terminals. The aim of the present study was to determine in which areas and to what extent 5-HT mediates the neuronal response to ACh release. For this purpose, neuronal activity was measured in rats with rivastigmine-induced elevated ACh levels after a 95% 5-HT depletion obtained by dosing p-chlorophenylalanine followed by D,L-fenfluramine. Neuronal activation was quantified by stereological measurements of c-Fos immunoreactivity. The brain areas examined were medial prefrontal cortex, septum, dorsal hippocampus, and dorsal raphe nucleus. Rivastigmine significantly increased c-Fos immunoreactivity in medial prefrontal cortex and the hippocampus, but not in the septum and dorsal raphe nucleus. 5-HT depletion decreased ACh-induced c-Fos immunoreactivity in the dentate gyrus. By contrast, 5-HT depletion had no effect on the ACh-induced activity in the other brain areas examined. It is concluded that 5-HT mediates part of the ACh-induced hippocampal neuronal activation, possibly mediated via locally released 5-HT.

AB - Interactions between the serotonergic and cholinergic systems are known to occur and are believed to play a role in the mechanism underlying both major depression and Alzheimer's disease. On a molecular level, studies suggest that acetylcholine (ACh) increases serotonin (5-HT) release through nicotinic receptors located at nerve terminals. The aim of the present study was to determine in which areas and to what extent 5-HT mediates the neuronal response to ACh release. For this purpose, neuronal activity was measured in rats with rivastigmine-induced elevated ACh levels after a 95% 5-HT depletion obtained by dosing p-chlorophenylalanine followed by D,L-fenfluramine. Neuronal activation was quantified by stereological measurements of c-Fos immunoreactivity. The brain areas examined were medial prefrontal cortex, septum, dorsal hippocampus, and dorsal raphe nucleus. Rivastigmine significantly increased c-Fos immunoreactivity in medial prefrontal cortex and the hippocampus, but not in the septum and dorsal raphe nucleus. 5-HT depletion decreased ACh-induced c-Fos immunoreactivity in the dentate gyrus. By contrast, 5-HT depletion had no effect on the ACh-induced activity in the other brain areas examined. It is concluded that 5-HT mediates part of the ACh-induced hippocampal neuronal activation, possibly mediated via locally released 5-HT.

KW - Acetylcholine/metabolism

KW - Animals

KW - Cell Count/methods

KW - Chromatography, High Pressure Liquid/methods

KW - Drug Interactions

KW - Fenclonine/pharmacology

KW - Fenfluramine/pharmacology

KW - Gene Expression/drug effects

KW - Hippocampus/cytology

KW - Hydroxyindoleacetic Acid/metabolism

KW - Immunohistochemistry/methods

KW - Male

KW - Neurons/drug effects

KW - Neuroprotective Agents/pharmacology

KW - Phenylcarbamates/pharmacology

KW - Proto-Oncogene Proteins c-fos/metabolism

KW - Rats

KW - Rats, Sprague-Dawley

KW - Rivastigmine

KW - Serotonin/deficiency

KW - Serotonin Uptake Inhibitors/pharmacology

U2 - 10.1016/j.brainres.2005.12.030

DO - 10.1016/j.brainres.2005.12.030

M3 - Journal article

C2 - 16426583

VL - 1073-1074

SP - 262

EP - 268

JO - Brain Research Reviews

JF - Brain Research Reviews

SN - 0165-0173

ER -

ID: 196169018