Selective immunolesion of cholinergic neurons leads to long-term changes in 5-HT2A receptor levels in hippocampus and frontal cortex.

Forskningsoutput: TidskriftsbidragArtikel i vetenskaplig tidskrift

Standard

Selective immunolesion of cholinergic neurons leads to long-term changes in 5-HT2A receptor levels in hippocampus and frontal cortex. / Severino, Maurizio; Pedersen, AF; Trajkovska, V; Christensen, E; Lohals, R; Veng, LM; Knudsen, GM; Aznar, S.

I: Neuroscience Letters, Vol. 428, Nr. 1, 2007, s. 47-51.

Forskningsoutput: TidskriftsbidragArtikel i vetenskaplig tidskrift

Harvard

Severino, M, Pedersen, AF, Trajkovska, V, Christensen, E, Lohals, R, Veng, LM, Knudsen, GM & Aznar, S 2007, 'Selective immunolesion of cholinergic neurons leads to long-term changes in 5-HT2A receptor levels in hippocampus and frontal cortex.', Neuroscience Letters, vol. 428, nr. 1, s. 47-51. https://doi.org/10.1016/j.neulet.2007.09.026

APA

Severino, M., Pedersen, AF., Trajkovska, V., Christensen, E., Lohals, R., Veng, LM., Knudsen, GM., & Aznar, S. (2007). Selective immunolesion of cholinergic neurons leads to long-term changes in 5-HT2A receptor levels in hippocampus and frontal cortex. Neuroscience Letters, 428(1), 47-51. https://doi.org/10.1016/j.neulet.2007.09.026

CBE

MLA

Vancouver

Author

Severino, Maurizio ; Pedersen, AF ; Trajkovska, V ; Christensen, E ; Lohals, R ; Veng, LM ; Knudsen, GM ; Aznar, S. / Selective immunolesion of cholinergic neurons leads to long-term changes in 5-HT2A receptor levels in hippocampus and frontal cortex. I: Neuroscience Letters. 2007 ; Vol. 428, Nr. 1. s. 47-51.

RIS

TY - JOUR

T1 - Selective immunolesion of cholinergic neurons leads to long-term changes in 5-HT2A receptor levels in hippocampus and frontal cortex.

AU - Severino, Maurizio

AU - Pedersen, AF

AU - Trajkovska, V

AU - Christensen, E

AU - Lohals, R

AU - Veng, LM

AU - Knudsen, GM

AU - Aznar, S

PY - 2007

Y1 - 2007

N2 - Although loss of cholinergic neurons in the basal forebrain is considered a key initial feature in Alzheimer's disease (AD), changes in other transmitter systems, including serotonin and 5-HT2A receptors, are also associated with early AD. The aim of this study was to investigate whether elimination of the cholinergic neurons in the basal forebrain directly affects 5-HT2A receptor levels. For this purpose intraventricular injection of the selective immunotoxin 192 IgG-Saporin was given to rats in doses of either 2.5 or 5 μg. The rats were sacrificed after 1, 2, 4 and 20 weeks. 5-HT2A protein levels were determined by western techniques in frontal cortex and hippocampus. A significant 70% downregulation in frontal cortex and a 100% upregulation in hippocampus of 5-HT2A receptor levels were observed 20 weeks after the cholinergic lesion when using the highest dose of 192 IgG-Saporin. Our results show that cholinergic deafferentation leads to decreased frontal cortex and increased hippoca

AB - Although loss of cholinergic neurons in the basal forebrain is considered a key initial feature in Alzheimer's disease (AD), changes in other transmitter systems, including serotonin and 5-HT2A receptors, are also associated with early AD. The aim of this study was to investigate whether elimination of the cholinergic neurons in the basal forebrain directly affects 5-HT2A receptor levels. For this purpose intraventricular injection of the selective immunotoxin 192 IgG-Saporin was given to rats in doses of either 2.5 or 5 μg. The rats were sacrificed after 1, 2, 4 and 20 weeks. 5-HT2A protein levels were determined by western techniques in frontal cortex and hippocampus. A significant 70% downregulation in frontal cortex and a 100% upregulation in hippocampus of 5-HT2A receptor levels were observed 20 weeks after the cholinergic lesion when using the highest dose of 192 IgG-Saporin. Our results show that cholinergic deafferentation leads to decreased frontal cortex and increased hippoca

U2 - 10.1016/j.neulet.2007.09.026

DO - 10.1016/j.neulet.2007.09.026

M3 - Article

VL - 428

SP - 47

EP - 51

JO - Neuroscience Letters

JF - Neuroscience Letters

SN - 0304-3940

IS - 1

ER -