TY - JOUR
T1 - Ketamine as a pharmacological tool for the preclinical study of memory deficit in schizophrenia
AU - Suárez Santiago, José Eduardo
AU - Roldán, Gabriel Roldán
AU - Picazo, Ofir
N1 - Publisher Copyright:
Copyright © 2022 Wolters Kluwer Health, Inc. All rights reserved.
PY - 2023/4/1
Y1 - 2023/4/1
N2 - Schizophrenia is a serious neuropsychiatric disorder characterized by the presence of positive symptoms (hallucinations, delusions, and disorganization of thought and language), negative symptoms (abulia, alogia, and affective flattening), and cognitive impairment (attention deficit, impaired declarative memory, and deficits in social cognition). Dopaminergic hyperactivity seems to explain the positive symptoms, but it does not completely clarify the appearance of negative and cognitive clinical manifestations. Preclinical data have demonstrated that acute and subchronic treatment with NMDA receptor antagonists such as ketamine (KET) represents a useful model that resembles the schizophrenia symptomatology, including cognitive impairment. This latter has been explained as a hypofunction of NMDA receptors located on the GABA parvalbumin-positive interneurons (near to the cortical pyramidal cells), thus generating an imbalance between the inhibitory and excitatory activity in the corticomesolimbic circuits. The use of behavioral models to explore alterations in different domains of memory is vital to learn more about the neurobiological changes that underlie schizophrenia. Thus, to better understand the neurophysiological mechanisms involved in cognitive impairment related to schizophrenia, the purpose of this review is to analyze the most recent findings regarding the effect of KET administration on these processes.
AB - Schizophrenia is a serious neuropsychiatric disorder characterized by the presence of positive symptoms (hallucinations, delusions, and disorganization of thought and language), negative symptoms (abulia, alogia, and affective flattening), and cognitive impairment (attention deficit, impaired declarative memory, and deficits in social cognition). Dopaminergic hyperactivity seems to explain the positive symptoms, but it does not completely clarify the appearance of negative and cognitive clinical manifestations. Preclinical data have demonstrated that acute and subchronic treatment with NMDA receptor antagonists such as ketamine (KET) represents a useful model that resembles the schizophrenia symptomatology, including cognitive impairment. This latter has been explained as a hypofunction of NMDA receptors located on the GABA parvalbumin-positive interneurons (near to the cortical pyramidal cells), thus generating an imbalance between the inhibitory and excitatory activity in the corticomesolimbic circuits. The use of behavioral models to explore alterations in different domains of memory is vital to learn more about the neurobiological changes that underlie schizophrenia. Thus, to better understand the neurophysiological mechanisms involved in cognitive impairment related to schizophrenia, the purpose of this review is to analyze the most recent findings regarding the effect of KET administration on these processes.
KW - GABA
KW - NMDA
KW - ketamine
KW - rat
KW - recognition memory
KW - schizophrenia
KW - spatial memory
UR - http://www.scopus.com/inward/record.url?scp=85150001383&partnerID=8YFLogxK
U2 - 10.1097/FBP.0000000000000689
DO - 10.1097/FBP.0000000000000689
M3 - Artículo de revisión
C2 - 36094064
AN - SCOPUS:85150001383
SN - 0955-8810
VL - 34
SP - 80
EP - 91
JO - Behavioural Pharmacology
JF - Behavioural Pharmacology
IS - 2-3
ER -