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Serotonin (5-HT)1A receptor agonism and 5-HT7 receptor antagonism ameliorate the subchronic phencyclidine-induced deficit in executive functioning in mice

Rationale Reversal learning (RL), a type of executive function, dependent on prefrontal cortical function, is impaired in rodents by subchronic (sc) treatment with the N -methyl- d -aspartate receptor antagonist, phencyclidine (PCP), a widely studied model of cognitive impairment in schizophrenia (C... Full description

Journal Title: Psychopharmacology 2015-11-12, Vol.233 (4), p.649-660
Main Author: Rajagopal, Lakshmi
Other Authors: Massey, Bill W , Michael, Eric , Meltzer, Herbert Y
Format: Electronic Article Electronic Article
Language: English
Subjects:
Publisher: Berlin/Heidelberg: Springer Berlin Heidelberg
ID: ISSN: 0033-3158
Link: https://www.ncbi.nlm.nih.gov/pubmed/26558619
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title: Serotonin (5-HT)1A receptor agonism and 5-HT7 receptor antagonism ameliorate the subchronic phencyclidine-induced deficit in executive functioning in mice
format: Article
creator:
  • Rajagopal, Lakshmi
  • Massey, Bill W
  • Michael, Eric
  • Meltzer, Herbert Y
subjects:
  • Animals
  • Biomedical and Life Sciences
  • Biomedicine
  • Cognition Disorders - chemically induced
  • Cognition Disorders - drug therapy
  • Executive Function - drug effects
  • Executive Function - physiology
  • Isoindoles - pharmacology
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Neurosciences
  • Original Investigation
  • Pharmacology/Toxicology
  • Phencyclidine - administration & dosage
  • Phencyclidine - toxicity
  • Phenols - pharmacology
  • Phenols - therapeutic use
  • Piperazines - pharmacology
  • Psychiatry
  • Pyrimidines - pharmacology
  • Reaction Time - drug effects
  • Reaction Time - physiology
  • Receptor, Serotonin, 5-HT1A - physiology
  • Receptors, Serotonin - physiology
  • Reversal Learning - drug effects
  • Reversal Learning - physiology
  • Serotonin 5-HT1 Receptor Agonists - pharmacology
  • Serotonin 5-HT1 Receptor Agonists - therapeutic use
  • Serotonin Antagonists - pharmacology
  • Serotonin Antagonists - therapeutic use
  • Sulfonamides - pharmacology
  • Sulfonamides - therapeutic use
ispartof: Psychopharmacology, 2015-11-12, Vol.233 (4), p.649-660
description: Rationale Reversal learning (RL), a type of executive function, dependent on prefrontal cortical function, is impaired in rodents by subchronic (sc) treatment with the N -methyl- d -aspartate receptor antagonist, phencyclidine (PCP), a widely studied model of cognitive impairment in schizophrenia (CIS). Objective The principal objective of this study was to determine the ability of serotonin (5-HT) 1A partial agonism and 5-HT 7 receptor antagonism to improve RL in scPCP-treated mice. Methods Male C57BL/6J mice were trained on an operant RL (ORL) task, then received PCP, 10 mg/kg, or saline, bid, for 7 days, followed by a 7-day washout period. Results scPCP significantly diminished the percent correct responding, increased total incorrect trials, and total incorrect responses, in the reversal phase performance of the ORL task. Pre-treatment with the selective 5-HT 1A partial agonist, tandospirone, or the selective 5-HT 7 antagonist, SB269970, but not the 5-HT 7 agonist, AS 19, reversed the scPCP-induced deficit in RL. Pre-treatment with atypical antipsychotic drug lurasidone, which is a 5-HT 1A partial agonist and 5-HT 7 antagonist, as well as a 5-HT 2A and dopamine (D) 2 antagonist, also reversed RL deficit in the scPCP-treated mice. Furthermore, the selective 5-HT 1A antagonist, WAY100635, blocked the ability of lurasidone to reverse the scPCP-induced RL deficit. Conclusions These results indicate that 5-HT 7 antagonism and 5-HT 1A partial agonism contribute to restoration of RL in scPCP-treated mice. It is suggested that these two mechanisms are effective in restoring RL by decreasing excessive GABAergic inhibition of cortical pyramidal neurons following withdrawal of scPCP treatment.
language: eng
source:
identifier: ISSN: 0033-3158
fulltext: no_fulltext
issn:
  • 0033-3158
  • 1432-2072
url: Link


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titleSerotonin (5-HT)1A receptor agonism and 5-HT7 receptor antagonism ameliorate the subchronic phencyclidine-induced deficit in executive functioning in mice
creatorRajagopal, Lakshmi ; Massey, Bill W ; Michael, Eric ; Meltzer, Herbert Y
creatorcontribRajagopal, Lakshmi ; Massey, Bill W ; Michael, Eric ; Meltzer, Herbert Y
descriptionRationale Reversal learning (RL), a type of executive function, dependent on prefrontal cortical function, is impaired in rodents by subchronic (sc) treatment with the N -methyl- d -aspartate receptor antagonist, phencyclidine (PCP), a widely studied model of cognitive impairment in schizophrenia (CIS). Objective The principal objective of this study was to determine the ability of serotonin (5-HT) 1A partial agonism and 5-HT 7 receptor antagonism to improve RL in scPCP-treated mice. Methods Male C57BL/6J mice were trained on an operant RL (ORL) task, then received PCP, 10 mg/kg, or saline, bid, for 7 days, followed by a 7-day washout period. Results scPCP significantly diminished the percent correct responding, increased total incorrect trials, and total incorrect responses, in the reversal phase performance of the ORL task. Pre-treatment with the selective 5-HT 1A partial agonist, tandospirone, or the selective 5-HT 7 antagonist, SB269970, but not the 5-HT 7 agonist, AS 19, reversed the scPCP-induced deficit in RL. Pre-treatment with atypical antipsychotic drug lurasidone, which is a 5-HT 1A partial agonist and 5-HT 7 antagonist, as well as a 5-HT 2A and dopamine (D) 2 antagonist, also reversed RL deficit in the scPCP-treated mice. Furthermore, the selective 5-HT 1A antagonist, WAY100635, blocked the ability of lurasidone to reverse the scPCP-induced RL deficit. Conclusions These results indicate that 5-HT 7 antagonism and 5-HT 1A partial agonism contribute to restoration of RL in scPCP-treated mice. It is suggested that these two mechanisms are effective in restoring RL by decreasing excessive GABAergic inhibition of cortical pyramidal neurons following withdrawal of scPCP treatment.
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subjectAnimals ; Biomedical and Life Sciences ; Biomedicine ; Cognition Disorders - chemically induced ; Cognition Disorders - drug therapy ; Executive Function - drug effects ; Executive Function - physiology ; Isoindoles - pharmacology ; Male ; Mice ; Mice, Inbred C57BL ; Neurosciences ; Original Investigation ; Pharmacology/Toxicology ; Phencyclidine - administration & dosage ; Phencyclidine - toxicity ; Phenols - pharmacology ; Phenols - therapeutic use ; Piperazines - pharmacology ; Psychiatry ; Pyrimidines - pharmacology ; Reaction Time - drug effects ; Reaction Time - physiology ; Receptor, Serotonin, 5-HT1A - physiology ; Receptors, Serotonin - physiology ; Reversal Learning - drug effects ; Reversal Learning - physiology ; Serotonin 5-HT1 Receptor Agonists - pharmacology ; Serotonin 5-HT1 Receptor Agonists - therapeutic use ; Serotonin Antagonists - pharmacology ; Serotonin Antagonists - therapeutic use ; Sulfonamides - pharmacology ; Sulfonamides - therapeutic use
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descriptionRationale Reversal learning (RL), a type of executive function, dependent on prefrontal cortical function, is impaired in rodents by subchronic (sc) treatment with the N -methyl- d -aspartate receptor antagonist, phencyclidine (PCP), a widely studied model of cognitive impairment in schizophrenia (CIS). Objective The principal objective of this study was to determine the ability of serotonin (5-HT) 1A partial agonism and 5-HT 7 receptor antagonism to improve RL in scPCP-treated mice. Methods Male C57BL/6J mice were trained on an operant RL (ORL) task, then received PCP, 10 mg/kg, or saline, bid, for 7 days, followed by a 7-day washout period. Results scPCP significantly diminished the percent correct responding, increased total incorrect trials, and total incorrect responses, in the reversal phase performance of the ORL task. Pre-treatment with the selective 5-HT 1A partial agonist, tandospirone, or the selective 5-HT 7 antagonist, SB269970, but not the 5-HT 7 agonist, AS 19, reversed the scPCP-induced deficit in RL. Pre-treatment with atypical antipsychotic drug lurasidone, which is a 5-HT 1A partial agonist and 5-HT 7 antagonist, as well as a 5-HT 2A and dopamine (D) 2 antagonist, also reversed RL deficit in the scPCP-treated mice. Furthermore, the selective 5-HT 1A antagonist, WAY100635, blocked the ability of lurasidone to reverse the scPCP-induced RL deficit. Conclusions These results indicate that 5-HT 7 antagonism and 5-HT 1A partial agonism contribute to restoration of RL in scPCP-treated mice. It is suggested that these two mechanisms are effective in restoring RL by decreasing excessive GABAergic inhibition of cortical pyramidal neurons following withdrawal of scPCP treatment.
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13Pharmacology/Toxicology
14Phencyclidine - administration & dosage
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17Phenols - therapeutic use
18Piperazines - pharmacology
19Psychiatry
20Pyrimidines - pharmacology
21Reaction Time - drug effects
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23Receptor, Serotonin, 5-HT1A - physiology
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25Reversal Learning - drug effects
26Reversal Learning - physiology
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28Serotonin 5-HT1 Receptor Agonists - therapeutic use
29Serotonin Antagonists - pharmacology
30Serotonin Antagonists - therapeutic use
31Sulfonamides - pharmacology
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authorRajagopal, Lakshmi ; Massey, Bill W ; Michael, Eric ; Meltzer, Herbert Y
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31Sulfonamides - pharmacology
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abstractRationale Reversal learning (RL), a type of executive function, dependent on prefrontal cortical function, is impaired in rodents by subchronic (sc) treatment with the N -methyl- d -aspartate receptor antagonist, phencyclidine (PCP), a widely studied model of cognitive impairment in schizophrenia (CIS). Objective The principal objective of this study was to determine the ability of serotonin (5-HT) 1A partial agonism and 5-HT 7 receptor antagonism to improve RL in scPCP-treated mice. Methods Male C57BL/6J mice were trained on an operant RL (ORL) task, then received PCP, 10 mg/kg, or saline, bid, for 7 days, followed by a 7-day washout period. Results scPCP significantly diminished the percent correct responding, increased total incorrect trials, and total incorrect responses, in the reversal phase performance of the ORL task. Pre-treatment with the selective 5-HT 1A partial agonist, tandospirone, or the selective 5-HT 7 antagonist, SB269970, but not the 5-HT 7 agonist, AS 19, reversed the scPCP-induced deficit in RL. Pre-treatment with atypical antipsychotic drug lurasidone, which is a 5-HT 1A partial agonist and 5-HT 7 antagonist, as well as a 5-HT 2A and dopamine (D) 2 antagonist, also reversed RL deficit in the scPCP-treated mice. Furthermore, the selective 5-HT 1A antagonist, WAY100635, blocked the ability of lurasidone to reverse the scPCP-induced RL deficit. Conclusions These results indicate that 5-HT 7 antagonism and 5-HT 1A partial agonism contribute to restoration of RL in scPCP-treated mice. It is suggested that these two mechanisms are effective in restoring RL by decreasing excessive GABAergic inhibition of cortical pyramidal neurons following withdrawal of scPCP treatment.
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pmid26558619
doi10.1007/s00213-015-4137-1