ATP-sensitive potassium-channel inhibitor glibenclamide attenuates HPA axis hyperactivity, depression- and anxiety-related symptoms in a rat model of Alzheimer's disease

•Aβ25-35 microinjection induced anxiety- and depression-like behaviors in rats.•Aβ25-35 microinjection increased corticosterone and HPA axis activity in rats.•Glibenclamide decreased Aβ25-35-induced behavioral abnormalities in rats.•Glibenclamide reduced Aβ25-35-induced HPA axis hyperactivity in rat...

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Bibliographic Details
Published inBrain research bulletin Vol. 137; pp. 265 - 276
Main Authors Esmaeili, Mohammad Hossein, Bahari, Behnam, Salari, Ali-Akbar
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 01.03.2018
Subjects
Alzheimer disease
Alzheimer Disease - drug therapy
Alzheimer Disease - physiopathology
Alzheimer Disease - psychology
Amyloid beta-Peptides
Animals
Anxiety - drug therapy
Anxiety - physiopathology
ATP-sensitive potassium channel
Aβ25-35
Corticosterone - metabolism
Depression - drug therapy
Depression - physiopathology
Disease Models, Animal
Glibenclamide
Glyburide - pharmacology
HPA axis
Hypothalamo-Hypophyseal System - drug effects
Hypothalamo-Hypophyseal System - physiopathology
KATP Channels - antagonists & inhibitors
KATP Channels - metabolism
Nootropic Agents - pharmacology
Peptide Fragments
Pituitary-Adrenal System - drug effects
Pituitary-Adrenal System - physiopathology
Potassium Channel Blockers - pharmacology
Rats, Wistar
Stress, Psychological - drug therapy
Stress, Psychological - physiopathology
HPA axis
Glibenclamide
Alzheimer disease
Aβ25-35
ATP-sensitive potassium channel
Online AccessGet full text
ISSN0361-9230
1873-2747
1873-2747
DOI10.1016/j.brainresbull.2018.01.001

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Abstract •Aβ25-35 microinjection induced anxiety- and depression-like behaviors in rats.•Aβ25-35 microinjection increased corticosterone and HPA axis activity in rats.•Glibenclamide decreased Aβ25-35-induced behavioral abnormalities in rats.•Glibenclamide reduced Aβ25-35-induced HPA axis hyperactivity in rats.•Glibenclamide, a KATP channel inhibitor, may be a therapeutic target for AD. Affective disorders including depression and anxiety are among the most prevalent behavioral abnormalities in patients with Alzheimer's disease (AD), which affect the quality of life and progression of the disease. Dysregulation of the hypothalamic-pituitary-adrenal-(HPA) axis has been reported in affective disorders and AD. Recent studies revealed that current antidepressant drugs are not completely effective for treating anxiety- and depression-related disorders in people with dementia. ATP-sensitive-potassium-(KATP) channels are well-known to be involved in AD pathophysiology, HPA axis function and the pathogenesis of depression and anxiety-related behaviors. Thus, targeting of KATP channel may be a potential therapeutic strategy in AD. Hence, we investigated the effects of intracerebroventricular injection of Aβ25-35 alone or in combination with glibenclamide, KATP channel inhibitor on depression- and anxiety-related behaviors as well as HPA axis response to stress in rats. To do this, non-Aβ25-35- and Aβ25-35-treated rats were orally treated with glibenclamide, then the behavioral consequences were assessed using sucrose preference, forced swim, light-dark box and plus maze tests. Stress-induced corticosterone levels following forced swim and plus maze tests were also evaluated as indicative of abnormal HPA-axis-function. Aβ25-35 induced HPA axis hyperreactivity and increased depression- and anxiety-related symptoms in rats. Our results showed that blockade of KATP channels with glibenclamide decreased depression- and anxiety-related behaviors by normalizing HPA axis activity in Aβ25-35-treated rats. This study provides additional evidence that Aβ administration can induce depression- and anxiety-like symptoms in rodents, and suggests that KATP channel inhibitors may be a plausible therapeutic strategy for treating affective disorders in AD patients.
AbstractList •Aβ25-35 microinjection induced anxiety- and depression-like behaviors in rats.•Aβ25-35 microinjection increased corticosterone and HPA axis activity in rats.•Glibenclamide decreased Aβ25-35-induced behavioral abnormalities in rats.•Glibenclamide reduced Aβ25-35-induced HPA axis hyperactivity in rats.•Glibenclamide, a KATP channel inhibitor, may be a therapeutic target for AD. Affective disorders including depression and anxiety are among the most prevalent behavioral abnormalities in patients with Alzheimer's disease (AD), which affect the quality of life and progression of the disease. Dysregulation of the hypothalamic-pituitary-adrenal-(HPA) axis has been reported in affective disorders and AD. Recent studies revealed that current antidepressant drugs are not completely effective for treating anxiety- and depression-related disorders in people with dementia. ATP-sensitive-potassium-(KATP) channels are well-known to be involved in AD pathophysiology, HPA axis function and the pathogenesis of depression and anxiety-related behaviors. Thus, targeting of KATP channel may be a potential therapeutic strategy in AD. Hence, we investigated the effects of intracerebroventricular injection of Aβ25-35 alone or in combination with glibenclamide, KATP channel inhibitor on depression- and anxiety-related behaviors as well as HPA axis response to stress in rats. To do this, non-Aβ25-35- and Aβ25-35-treated rats were orally treated with glibenclamide, then the behavioral consequences were assessed using sucrose preference, forced swim, light-dark box and plus maze tests. Stress-induced corticosterone levels following forced swim and plus maze tests were also evaluated as indicative of abnormal HPA-axis-function. Aβ25-35 induced HPA axis hyperreactivity and increased depression- and anxiety-related symptoms in rats. Our results showed that blockade of KATP channels with glibenclamide decreased depression- and anxiety-related behaviors by normalizing HPA axis activity in Aβ25-35-treated rats. This study provides additional evidence that Aβ administration can induce depression- and anxiety-like symptoms in rodents, and suggests that KATP channel inhibitors may be a plausible therapeutic strategy for treating affective disorders in AD patients.
Affective disorders including depression and anxiety are among the most prevalent behavioral abnormalities in patients with Alzheimer's disease (AD), which affect the quality of life and progression of the disease. Dysregulation of the hypothalamic-pituitary-adrenal-(HPA) axis has been reported in affective disorders and AD. Recent studies revealed that current antidepressant drugs are not completely effective for treating anxiety- and depression-related disorders in people with dementia. ATP-sensitive-potassium-(K ) channels are well-known to be involved in AD pathophysiology, HPA axis function and the pathogenesis of depression and anxiety-related behaviors. Thus, targeting of K channel may be a potential therapeutic strategy in AD. Hence, we investigated the effects of intracerebroventricular injection of Aβ25-35 alone or in combination with glibenclamide, K channel inhibitor on depression- and anxiety-related behaviors as well as HPA axis response to stress in rats. To do this, non-Aβ25-35- and Aβ25-35-treated rats were orally treated with glibenclamide, then the behavioral consequences were assessed using sucrose preference, forced swim, light-dark box and plus maze tests. Stress-induced corticosterone levels following forced swim and plus maze tests were also evaluated as indicative of abnormal HPA-axis-function. Aβ25-35 induced HPA axis hyperreactivity and increased depression- and anxiety-related symptoms in rats. Our results showed that blockade of K channels with glibenclamide decreased depression- and anxiety-related behaviors by normalizing HPA axis activity in Aβ25-35-treated rats. This study provides additional evidence that Aβ administration can induce depression- and anxiety-like symptoms in rodents, and suggests that K channel inhibitors may be a plausible therapeutic strategy for treating affective disorders in AD patients.
Affective disorders including depression and anxiety are among the most prevalent behavioral abnormalities in patients with Alzheimer's disease (AD), which affect the quality of life and progression of the disease. Dysregulation of the hypothalamic-pituitary-adrenal-(HPA) axis has been reported in affective disorders and AD. Recent studies revealed that current antidepressant drugs are not completely effective for treating anxiety- and depression-related disorders in people with dementia. ATP-sensitive-potassium-(KATP) channels are well-known to be involved in AD pathophysiology, HPA axis function and the pathogenesis of depression and anxiety-related behaviors. Thus, targeting of KATP channel may be a potential therapeutic strategy in AD. Hence, we investigated the effects of intracerebroventricular injection of Aβ25-35 alone or in combination with glibenclamide, KATP channel inhibitor on depression- and anxiety-related behaviors as well as HPA axis response to stress in rats. To do this, non-Aβ25-35- and Aβ25-35-treated rats were orally treated with glibenclamide, then the behavioral consequences were assessed using sucrose preference, forced swim, light-dark box and plus maze tests. Stress-induced corticosterone levels following forced swim and plus maze tests were also evaluated as indicative of abnormal HPA-axis-function. Aβ25-35 induced HPA axis hyperreactivity and increased depression- and anxiety-related symptoms in rats. Our results showed that blockade of KATP channels with glibenclamide decreased depression- and anxiety-related behaviors by normalizing HPA axis activity in Aβ25-35-treated rats. This study provides additional evidence that Aβ administration can induce depression- and anxiety-like symptoms in rodents, and suggests that KATP channel inhibitors may be a plausible therapeutic strategy for treating affective disorders in AD patients.Affective disorders including depression and anxiety are among the most prevalent behavioral abnormalities in patients with Alzheimer's disease (AD), which affect the quality of life and progression of the disease. Dysregulation of the hypothalamic-pituitary-adrenal-(HPA) axis has been reported in affective disorders and AD. Recent studies revealed that current antidepressant drugs are not completely effective for treating anxiety- and depression-related disorders in people with dementia. ATP-sensitive-potassium-(KATP) channels are well-known to be involved in AD pathophysiology, HPA axis function and the pathogenesis of depression and anxiety-related behaviors. Thus, targeting of KATP channel may be a potential therapeutic strategy in AD. Hence, we investigated the effects of intracerebroventricular injection of Aβ25-35 alone or in combination with glibenclamide, KATP channel inhibitor on depression- and anxiety-related behaviors as well as HPA axis response to stress in rats. To do this, non-Aβ25-35- and Aβ25-35-treated rats were orally treated with glibenclamide, then the behavioral consequences were assessed using sucrose preference, forced swim, light-dark box and plus maze tests. Stress-induced corticosterone levels following forced swim and plus maze tests were also evaluated as indicative of abnormal HPA-axis-function. Aβ25-35 induced HPA axis hyperreactivity and increased depression- and anxiety-related symptoms in rats. Our results showed that blockade of KATP channels with glibenclamide decreased depression- and anxiety-related behaviors by normalizing HPA axis activity in Aβ25-35-treated rats. This study provides additional evidence that Aβ administration can induce depression- and anxiety-like symptoms in rodents, and suggests that KATP channel inhibitors may be a plausible therapeutic strategy for treating affective disorders in AD patients.
Author Esmaeili, Mohammad Hossein
Salari, Ali-Akbar
Bahari, Behnam
Author_xml – sequence: 1
  givenname: Mohammad Hossein
  surname: Esmaeili
  fullname: Esmaeili, Mohammad Hossein
  organization: Cellular and Molecular Research Center & Department of Physiology, Qazvin University of Medical Sciences, Qazvin, Iran
– sequence: 2
  givenname: Behnam
  surname: Bahari
  fullname: Bahari, Behnam
  organization: Drug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
– sequence: 3
  givenname: Ali-Akbar
  surname: Salari
  fullname: Salari, Ali-Akbar
  email: aa.salari@yahoo.com
  organization: Drug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
BackLink https://www.ncbi.nlm.nih.gov/pubmed/29307659$$D View this record in MEDLINE/PubMed
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Tue Aug 26 16:34:25 EDT 2025
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Keywords HPA axis
Glibenclamide
Alzheimer disease
Aβ25-35
ATP-sensitive potassium channel
Language English
License Copyright © 2018 Elsevier Inc. All rights reserved.
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PublicationTitle Brain research bulletin
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SSID ssj0006856
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Snippet •Aβ25-35 microinjection induced anxiety- and depression-like behaviors in rats.•Aβ25-35 microinjection increased corticosterone and HPA axis activity in...
Affective disorders including depression and anxiety are among the most prevalent behavioral abnormalities in patients with Alzheimer's disease (AD), which...
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StartPage 265
SubjectTerms Alzheimer disease
Alzheimer Disease - drug therapy
Alzheimer Disease - physiopathology
Alzheimer Disease - psychology
Amyloid beta-Peptides
Animals
Anxiety - drug therapy
Anxiety - physiopathology
ATP-sensitive potassium channel
Aβ25-35
Corticosterone - metabolism
Depression - drug therapy
Depression - physiopathology
Disease Models, Animal
Glibenclamide
Glyburide - pharmacology
HPA axis
Hypothalamo-Hypophyseal System - drug effects
Hypothalamo-Hypophyseal System - physiopathology
KATP Channels - antagonists & inhibitors
KATP Channels - metabolism
Nootropic Agents - pharmacology
Peptide Fragments
Pituitary-Adrenal System - drug effects
Pituitary-Adrenal System - physiopathology
Potassium Channel Blockers - pharmacology
Rats, Wistar
Stress, Psychological - drug therapy
Stress, Psychological - physiopathology
Title ATP-sensitive potassium-channel inhibitor glibenclamide attenuates HPA axis hyperactivity, depression- and anxiety-related symptoms in a rat model of Alzheimer's disease
URI https://www.clinicalkey.com/#!/content/1-s2.0-S0361923017305142
https://dx.doi.org/10.1016/j.brainresbull.2018.01.001
https://www.ncbi.nlm.nih.gov/pubmed/29307659
https://www.proquest.com/docview/1989542804
Volume 137
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