Roles of adrenergic α1 and dopamine D1 and D2 receptors in the mediation of the desynchronization effects of modafinil in a mouse EEG synchronization model.
BACKGROUND: Synchronized electroencephalogram (EEG) activity is observed in pathological stages of cognitive impairment and epilepsy. Modafinil, known to increase the release of catecholamines, is a potent wake-promoting agent, and has shown some abilities to desynchronize EEG,but its receptor mecha...
Main Authors: | , , , , , |
---|---|
Format: | Article |
Language: | English |
Published: |
Public Library of Science (PLoS)
2013-01-01
|
Series: | PLoS ONE |
Online Access: | http://europepmc.org/articles/PMC3792106?pdf=render |
id |
doaj-42a44a364598436bbbc16c5e829a1895 |
---|---|
record_format |
Article |
spelling |
doaj-42a44a364598436bbbc16c5e829a18952020-11-25T01:26:18ZengPublic Library of Science (PLoS)PLoS ONE1932-62032013-01-01810e7610210.1371/journal.pone.0076102Roles of adrenergic α1 and dopamine D1 and D2 receptors in the mediation of the desynchronization effects of modafinil in a mouse EEG synchronization model.Chang-Rui ChenSu-Rong YangYuan-Yuan LiuWei-Min QuYoshihiro UradeZhi-Li HuangBACKGROUND: Synchronized electroencephalogram (EEG) activity is observed in pathological stages of cognitive impairment and epilepsy. Modafinil, known to increase the release of catecholamines, is a potent wake-promoting agent, and has shown some abilities to desynchronize EEG,but its receptor mechanisms by which modafinil induces desynchoronization remain to be elucidated. Here we used a pharmacological EEG synchronization model to investigate the involvement of adrenergic α1 receptors (R, α1R) and dopamine (DA) D1 and D2 receptors (D1Rs and D2Rs) on modafinil-induced desynchronization in mice. METHODOLOGY/PRINCIPAL FINDINGS: Mice were treated with cholinergic receptor antagonist scopolamine and monoamine depletor reserpine to produce experimental EEG synchronization characterized by continuous large-amplitude synchronized activity, with prominent increased delta and decreased theta, alpha, and beta power density. The results showed that modafinil produced an EEG desynchronization in the model. This was characterized by a general decrease in amplitude of all the frequency bands between 0 and 20 Hz, a prominent reduction in delta power density, and an increase in theta power density. Adrenergic α1R antagonist terazosin (1 mg/kg, i.p.) completely antagonized the EEG desynchronization effects of modafinil at 90 mg/kg. However, DA D1R and D2R blockers partially attenuated the effects of modafinil. The modafinil-induced decrease in the amplitudes of the delta, theta, alpha, and beta waves and in delta power density were completely abolished by pretreatment with a combination of the D1R antagonist SCH 23390 (30 µg/kg) and the D2R antagonist raclopride (2 mg/kg, i.p.). CONCLUSIONS/SIGNIFICANCE: These results suggest that modafinil-mediated desynchronization may be attributed to the activation of adrenergic α1R, and dopaminergic D1R and D2R in a model of EEG synchronization.http://europepmc.org/articles/PMC3792106?pdf=render |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Chang-Rui Chen Su-Rong Yang Yuan-Yuan Liu Wei-Min Qu Yoshihiro Urade Zhi-Li Huang |
spellingShingle |
Chang-Rui Chen Su-Rong Yang Yuan-Yuan Liu Wei-Min Qu Yoshihiro Urade Zhi-Li Huang Roles of adrenergic α1 and dopamine D1 and D2 receptors in the mediation of the desynchronization effects of modafinil in a mouse EEG synchronization model. PLoS ONE |
author_facet |
Chang-Rui Chen Su-Rong Yang Yuan-Yuan Liu Wei-Min Qu Yoshihiro Urade Zhi-Li Huang |
author_sort |
Chang-Rui Chen |
title |
Roles of adrenergic α1 and dopamine D1 and D2 receptors in the mediation of the desynchronization effects of modafinil in a mouse EEG synchronization model. |
title_short |
Roles of adrenergic α1 and dopamine D1 and D2 receptors in the mediation of the desynchronization effects of modafinil in a mouse EEG synchronization model. |
title_full |
Roles of adrenergic α1 and dopamine D1 and D2 receptors in the mediation of the desynchronization effects of modafinil in a mouse EEG synchronization model. |
title_fullStr |
Roles of adrenergic α1 and dopamine D1 and D2 receptors in the mediation of the desynchronization effects of modafinil in a mouse EEG synchronization model. |
title_full_unstemmed |
Roles of adrenergic α1 and dopamine D1 and D2 receptors in the mediation of the desynchronization effects of modafinil in a mouse EEG synchronization model. |
title_sort |
roles of adrenergic α1 and dopamine d1 and d2 receptors in the mediation of the desynchronization effects of modafinil in a mouse eeg synchronization model. |
publisher |
Public Library of Science (PLoS) |
series |
PLoS ONE |
issn |
1932-6203 |
publishDate |
2013-01-01 |
description |
BACKGROUND: Synchronized electroencephalogram (EEG) activity is observed in pathological stages of cognitive impairment and epilepsy. Modafinil, known to increase the release of catecholamines, is a potent wake-promoting agent, and has shown some abilities to desynchronize EEG,but its receptor mechanisms by which modafinil induces desynchoronization remain to be elucidated. Here we used a pharmacological EEG synchronization model to investigate the involvement of adrenergic α1 receptors (R, α1R) and dopamine (DA) D1 and D2 receptors (D1Rs and D2Rs) on modafinil-induced desynchronization in mice. METHODOLOGY/PRINCIPAL FINDINGS: Mice were treated with cholinergic receptor antagonist scopolamine and monoamine depletor reserpine to produce experimental EEG synchronization characterized by continuous large-amplitude synchronized activity, with prominent increased delta and decreased theta, alpha, and beta power density. The results showed that modafinil produced an EEG desynchronization in the model. This was characterized by a general decrease in amplitude of all the frequency bands between 0 and 20 Hz, a prominent reduction in delta power density, and an increase in theta power density. Adrenergic α1R antagonist terazosin (1 mg/kg, i.p.) completely antagonized the EEG desynchronization effects of modafinil at 90 mg/kg. However, DA D1R and D2R blockers partially attenuated the effects of modafinil. The modafinil-induced decrease in the amplitudes of the delta, theta, alpha, and beta waves and in delta power density were completely abolished by pretreatment with a combination of the D1R antagonist SCH 23390 (30 µg/kg) and the D2R antagonist raclopride (2 mg/kg, i.p.). CONCLUSIONS/SIGNIFICANCE: These results suggest that modafinil-mediated desynchronization may be attributed to the activation of adrenergic α1R, and dopaminergic D1R and D2R in a model of EEG synchronization. |
url |
http://europepmc.org/articles/PMC3792106?pdf=render |
work_keys_str_mv |
AT changruichen rolesofadrenergica1anddopamined1andd2receptorsinthemediationofthedesynchronizationeffectsofmodafinilinamouseeegsynchronizationmodel AT surongyang rolesofadrenergica1anddopamined1andd2receptorsinthemediationofthedesynchronizationeffectsofmodafinilinamouseeegsynchronizationmodel AT yuanyuanliu rolesofadrenergica1anddopamined1andd2receptorsinthemediationofthedesynchronizationeffectsofmodafinilinamouseeegsynchronizationmodel AT weiminqu rolesofadrenergica1anddopamined1andd2receptorsinthemediationofthedesynchronizationeffectsofmodafinilinamouseeegsynchronizationmodel AT yoshihirourade rolesofadrenergica1anddopamined1andd2receptorsinthemediationofthedesynchronizationeffectsofmodafinilinamouseeegsynchronizationmodel AT zhilihuang rolesofadrenergica1anddopamined1andd2receptorsinthemediationofthedesynchronizationeffectsofmodafinilinamouseeegsynchronizationmodel |
_version_ |
1725109852926115840 |