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Recovery from ketamine-induced amnesia by blockade of GABA-A receptor in the medial prefrontal cortex of mice.
Neuroscience. 2017 03 06; 344:48-55.N

Abstract

Ketamine and other noncompetitive N-methyl-d-aspartate (NMDA) receptor antagonists are known to induce deficits in learning and cognitive performance sensitive to prefrontal cortex (PFC) functions. The interaction of a glutamatergic and GABAergic systems is essential for many cognitive behaviors. In order to understand the effect of γ-aminobutyric acid (GABA)/glutamate interactions on learning and memory, we investigated the effects of intra medial prefrontal cortex (mPFC) injections of GABAergic agents on ketamine-induced amnesia using a one-trial passive avoidance task in mice. Pre-training systemic administration of ketamine (5, 10 and 15mg/kg, i.p.) dose-dependently decreased the memory acquisition of a one-trial passive avoidance task. Pre-training intra-mPFC injection of muscimol, GABAA receptor agonist (0.05, 0.1 and 0.2μg/mouse) and baclofen GABAB receptor agonist (0.05, 0.1, 0.5 and 1μg/mouse), impaired memory acquisition. However, co-pretreatment of different doses of muscimol and baclofen with a lower dose of ketamine (5mg/kg), which did not induce amnesia by itself, caused inhibition of memory formation. Our data showed that sole pre-training administration of bicuculline, GABA-A receptor antagonist and phaclofen GABA-B receptor antagonist into the mPFC, did not affect memory acquisition. In addition, the amnesia induced by pre-training ketamine (15mg/kg) was significantly decreased by the pretreatment of bicuculline (0.005, 0.1 and 0.5μg/mouse). It can be concluded that GABAergic system of the mPFC is involved in the ketamine-induced impairment of memory acquisition.

Authors+Show Affiliations

Department of Neuroscience, School of Advanced Medical Technologies, Tehran University of Medical Sciences, Tehran, Iran; Iranian National Center for Addiction Studies, Tehran University of Medical Sciences, Tehran, Iran.Iranian National Center for Addiction Studies, Tehran University of Medical Sciences, Tehran, Iran; Department of Basic Sciences, Faculty of Veterinary Medicine, Islamic Azad University, Garmsar Branch, Semnan, Iran.Department of Neuroscience, School of Advanced Medical Technologies, Tehran University of Medical Sciences, Tehran, Iran; Iranian National Center for Addiction Studies, Tehran University of Medical Sciences, Tehran, Iran.Department of Neuroscience, School of Advanced Medical Technologies, Tehran University of Medical Sciences, Tehran, Iran; Iranian National Center for Addiction Studies, Tehran University of Medical Sciences, Tehran, Iran; Department of Pharmacology, Tehran University of Medical Sciences, Tehran, Iran; Institute for Cognitive Science Studies (ICSS), Tehran, Iran; Cognitive and Neuroscience Research Center (CNRC), Medical Genomics Research Center and School of Advanced Sciences in Medicine, Islamic Azad University, Tehran Medical Sciences Branch, Tehran, Iran; School of Cognitive Sciences, Institute for Research in Fundamental Sciences (IPM), Tehran, Iran. Electronic address: zarinmr@ams.ac.ir.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

26944606

Citation

Farahmandfar, Maryam, et al. "Recovery From Ketamine-induced Amnesia By Blockade of GABA-A Receptor in the Medial Prefrontal Cortex of Mice." Neuroscience, vol. 344, 2017, pp. 48-55.
Farahmandfar M, Akbarabadi A, Bakhtazad A, et al. Recovery from ketamine-induced amnesia by blockade of GABA-A receptor in the medial prefrontal cortex of mice. Neuroscience. 2017;344:48-55.
Farahmandfar, M., Akbarabadi, A., Bakhtazad, A., & Zarrindast, M. R. (2017). Recovery from ketamine-induced amnesia by blockade of GABA-A receptor in the medial prefrontal cortex of mice. Neuroscience, 344, 48-55. https://doi.org/10.1016/j.neuroscience.2016.02.056
Farahmandfar M, et al. Recovery From Ketamine-induced Amnesia By Blockade of GABA-A Receptor in the Medial Prefrontal Cortex of Mice. Neuroscience. 2017 03 6;344:48-55. PubMed PMID: 26944606.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Recovery from ketamine-induced amnesia by blockade of GABA-A receptor in the medial prefrontal cortex of mice. AU - Farahmandfar,Maryam, AU - Akbarabadi,Ardeshir, AU - Bakhtazad,Atefeh, AU - Zarrindast,Mohammad-Reza, Y1 - 2016/03/02/ PY - 2015/10/05/received PY - 2016/02/23/revised PY - 2016/02/23/accepted PY - 2016/3/6/pubmed PY - 2017/11/10/medline PY - 2016/3/6/entrez KW - GABAergic system KW - ketamine KW - medial prefrontal cortex KW - mice KW - passive avoidance SP - 48 EP - 55 JF - Neuroscience JO - Neuroscience VL - 344 N2 - Ketamine and other noncompetitive N-methyl-d-aspartate (NMDA) receptor antagonists are known to induce deficits in learning and cognitive performance sensitive to prefrontal cortex (PFC) functions. The interaction of a glutamatergic and GABAergic systems is essential for many cognitive behaviors. In order to understand the effect of γ-aminobutyric acid (GABA)/glutamate interactions on learning and memory, we investigated the effects of intra medial prefrontal cortex (mPFC) injections of GABAergic agents on ketamine-induced amnesia using a one-trial passive avoidance task in mice. Pre-training systemic administration of ketamine (5, 10 and 15mg/kg, i.p.) dose-dependently decreased the memory acquisition of a one-trial passive avoidance task. Pre-training intra-mPFC injection of muscimol, GABAA receptor agonist (0.05, 0.1 and 0.2μg/mouse) and baclofen GABAB receptor agonist (0.05, 0.1, 0.5 and 1μg/mouse), impaired memory acquisition. However, co-pretreatment of different doses of muscimol and baclofen with a lower dose of ketamine (5mg/kg), which did not induce amnesia by itself, caused inhibition of memory formation. Our data showed that sole pre-training administration of bicuculline, GABA-A receptor antagonist and phaclofen GABA-B receptor antagonist into the mPFC, did not affect memory acquisition. In addition, the amnesia induced by pre-training ketamine (15mg/kg) was significantly decreased by the pretreatment of bicuculline (0.005, 0.1 and 0.5μg/mouse). It can be concluded that GABAergic system of the mPFC is involved in the ketamine-induced impairment of memory acquisition. SN - 1873-7544 UR - https://www.unboundmedicine.com/medline/citation/26944606/Recovery_from_ketamine_induced_amnesia_by_blockade_of_GABA_A_receptor_in_the_medial_prefrontal_cortex_of_mice_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0306-4522(16)00196-2 DB - PRIME DP - Unbound Medicine ER -