Effects of estrogen on intracellular signaling pathways linked to activation of muscarinic acetylcholine receptors and on acetylcholinesterase activity in rat hippocampus
The aim of the present study was to investigate the effects of estrogen lack and estrogen replacement on the production of total [ 3H]inositol phosphate ([ 3H]IP) induced by the activation of muscarinic acetylcholine receptors (mAChRs) and on the mechanisms for inactivation of acetylcholine. Hippoca...
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| Published in: | Biochemical pharmacology Vol. 75; no. 9; pp. 1827 - 1834 |
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| Language: | English |
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| Abstract | The aim of the present study was to investigate the effects of estrogen lack and estrogen replacement on the production of total [
3H]inositol phosphate ([
3H]IP) induced by the activation of muscarinic acetylcholine receptors (mAChRs) and on the mechanisms for inactivation of acetylcholine. Hippocampi were obtained from rats in proestrus (PE), ovariectomized for 15 days (C15), ovariectomized for 15 days and then treated with 17β-estradiol for 7 days (E7) and ovariectomized and immediately treated with 17β-estradiol for 21 days (E21). Ovariectomy did not change the basal level of total [
3H]IP in the hippocampus. 17β-Estradiol replacement (E7 and E21) reduced the basal level of total [
3H]IP. In all experimental groups, carbachol (CCh) caused a concentration-dependent rise in total [
3H]IP. The maximum effect was reached with 10
−4
M CCh. The response to 10
−4
M CCh in the hippocampi from C15 and E7 rats was twofold higher than in hippocampi from PE and E21 animals and was blocked by pirenzepine, but not by methoctramine. Ovariectomy or 17β-estradiol treatment for 7 days did not change neither the total acetylcholinesterase (AChE) activity nor the relative amount of mono- and dimeric G
1/G
2 and tetrameric G
4 globular forms. Conversely, hormonal treatment for 21 days induced an increase in AChE activity of G
1/G
2 and G
4 forms, indicating that 17β-estradiol stimulates both synthesis and assembly of AChE molecular forms. The present results suggest that the duration and/or a critical period with regard to the initiation of estrogen therapy are important to regulate the function of mAChRs and AChE activity in female rat hippocampus. |
|---|---|
| AbstractList | The aim of the present study was to investigate the effects of estrogen lack and estrogen replacement on the production of total [3H]inositol phosphate ([3H]IP) induced by the activation of muscarinic acetylcholine receptors (mAChRs) and on the mechanisms for inactivation of acetylcholine. Hippocampi were obtained from rats in proestrus (PE), ovariectomized for 15 days (C15), ovariectomized for 15 days and then treated with 17beta-estradiol for 7 days (E7) and ovariectomized and immediately treated with 17beta-estradiol for 21 days (E21). Ovariectomy did not change the basal level of total [3H]IP in the hippocampus. 17beta-Estradiol replacement (E7 and E21) reduced the basal level of total [3H]IP. In all experimental groups, carbachol (CCh) caused a concentration-dependent rise in total [3H]IP. The maximum effect was reached with 10(-4) M CCh. The response to 10(-4) M CCh in the hippocampi from C15 and E7 rats was twofold higher than in hippocampi from PE and E21 animals and was blocked by pirenzepine, but not by methoctramine. Ovariectomy or 17beta-estradiol treatment for 7 days did not change neither the total acetylcholinesterase (AChE) activity nor the relative amount of mono- and dimeric G1/G2 and tetrameric G4 globular forms. Conversely, hormonal treatment for 21 days induced an increase in AChE activity of G1/G2 and G4 forms, indicating that 17beta-estradiol stimulates both synthesis and assembly of AChE molecular forms. The present results suggest that the duration and/or a critical period with regard to the initiation of estrogen therapy are important to regulate the function of mAChRs and AChE activity in female rat hippocampus. The aim of the present study was to investigate the effects of estrogen lack and estrogen replacement on the production of total [ 3H]inositol phosphate ([ 3H]IP) induced by the activation of muscarinic acetylcholine receptors (mAChRs) and on the mechanisms for inactivation of acetylcholine. Hippocampi were obtained from rats in proestrus (PE), ovariectomized for 15 days (C15), ovariectomized for 15 days and then treated with 17β-estradiol for 7 days (E7) and ovariectomized and immediately treated with 17β-estradiol for 21 days (E21). Ovariectomy did not change the basal level of total [ 3H]IP in the hippocampus. 17β-Estradiol replacement (E7 and E21) reduced the basal level of total [ 3H]IP. In all experimental groups, carbachol (CCh) caused a concentration-dependent rise in total [ 3H]IP. The maximum effect was reached with 10 −4 M CCh. The response to 10 −4 M CCh in the hippocampi from C15 and E7 rats was twofold higher than in hippocampi from PE and E21 animals and was blocked by pirenzepine, but not by methoctramine. Ovariectomy or 17β-estradiol treatment for 7 days did not change neither the total acetylcholinesterase (AChE) activity nor the relative amount of mono- and dimeric G 1/G 2 and tetrameric G 4 globular forms. Conversely, hormonal treatment for 21 days induced an increase in AChE activity of G 1/G 2 and G 4 forms, indicating that 17β-estradiol stimulates both synthesis and assembly of AChE molecular forms. The present results suggest that the duration and/or a critical period with regard to the initiation of estrogen therapy are important to regulate the function of mAChRs and AChE activity in female rat hippocampus. The aim of the present study was to investigate the effects of estrogen lack and estrogen replacement on the production of total [ super(3)H]inositol phosphate ([ super(3)H]IP) induced by the activation of muscarinic acetylcholine receptors (mAChRs) and on the mechanisms for inactivation of acetylcholine. Hippocampi were obtained from rats in proestrus (PE), ovariectomized for 15 days (C15), ovariectomized for 15 days and then treated with 17 beta -estradiol for 7 days (E7) and ovariectomized and immediately treated with 17 beta - estradiol for 21 days (E21). Ovariectomy did not change the basal level of total [ super(3)H]IP in the hippocampus. 17 beta -Estradiol replacement (E7 and E21) reduced the basal level of total [ super(3)H]IP. In all experimental groups, carbachol (CCh) caused a concentration-dependent rise in total [ super(3)H]IP. The maximum effect was reached with 10 super(-4) M CCh. The response to 10 super(-4) M CCh in the hippocampi from C15 and E7 rats was twofold higher than in hippocampi from PE and E21 animals and was blocked by pirenzepine, but not by methoctramine. Ovariectomy or 17 beta -estradiol treatment for 7 days did not change neither the total acetylcholinesterase (AChE) activity nor the relative amount of mono- and dimeric G sub(1)/G sub(2) and tetrameric G sub(4) globular forms. Conversely, hormonal treatment for 21 days induced an increase in AChE activity of G sub(1)/G sub(2) and G sub(4) forms, indicating that 17 beta -estradiol stimulates both synthesis and assembly of AChE molecular forms. The present results suggest that the duration and/or a critical period with regard to the initiation of estrogen therapy are important to regulate the function of mAChRs and AChE activity in female rat hippocampus. |
| Author | Porto, Catarina Segreti Abdalla, Fernando Maurício Francis Godinho, Rosely Oliveira Pereira, Renato Tavares dos Santos |
| Author_xml | – sequence: 1 givenname: Renato Tavares dos Santos surname: Pereira fullname: Pereira, Renato Tavares dos Santos organization: Laboratory of Pharmacology, Instituto Butantan, Av. Vital Brazil 1500, São Paulo, SP 05503-900, Brazil – sequence: 2 givenname: Catarina Segreti surname: Porto fullname: Porto, Catarina Segreti organization: Section of Experimental Endocrinology, Department of Pharmacology, Universidade Federal de São Paulo, Escola Paulista de Medicina, Brazil – sequence: 3 givenname: Rosely Oliveira surname: Godinho fullname: Godinho, Rosely Oliveira organization: Division of Cellular Pharmacology, Department of Pharmacology, Universidade Federal de São Paulo, Escola Paulista de Medicina, Brazil – sequence: 4 givenname: Fernando Maurício Francis surname: Abdalla fullname: Abdalla, Fernando Maurício Francis email: fabdalla@butantan.gov.br organization: Laboratory of Pharmacology, Instituto Butantan, Av. Vital Brazil 1500, São Paulo, SP 05503-900, Brazil |
| BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20302655$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/18329631$$D View this record in MEDLINE/PubMed |
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| Issue | 9 |
| Keywords | Inositol phosphate Ovariectomy Acetylcholinesterase Muscarinic acetylcholine receptors Hippocampus Estrogen Rat Central nervous system Esterases Encephalon Signal transduction Cholinergic receptor Signaling pathway Surgery Enzyme Rodentia Ovarian hormone Biological activity Carboxylic ester hydrolases Vertebrata Mammalia Treatment Animal Hydrolases Muscarinic receptor Sex steroid hormone |
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3H]inositol phosphate ([... The aim of the present study was to investigate the effects of estrogen lack and estrogen replacement on the production of total [3H]inositol phosphate... The aim of the present study was to investigate the effects of estrogen lack and estrogen replacement on the production of total [ super(3)H]inositol phosphate... |
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| SubjectTerms | Acetylcholinesterase Acetylcholinesterase - metabolism Animals Biological and medical sciences Estradiol - administration & dosage Estradiol - deficiency Estradiol - pharmacology Estrogen Estrogen Replacement Therapy Estrogens - administration & dosage Estrogens - deficiency Estrogens - pharmacology Female Hippocampus Hippocampus - drug effects Hippocampus - enzymology Hippocampus - metabolism Inositol phosphate Inositol Phosphates - metabolism Medical sciences Muscarinic acetylcholine receptors Ovariectomy Pharmacology. Drug treatments Rats Rats, Wistar Receptors, Muscarinic - metabolism Signal Transduction |
| Title | Effects of estrogen on intracellular signaling pathways linked to activation of muscarinic acetylcholine receptors and on acetylcholinesterase activity in rat hippocampus |
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