The effect of ketamine on the consolidation and extinction of contextual fear memory. Clifton, N., E., Thomas, K., L., & Hall, J. Journal of Psychopharmacology, 32(2):156-162, SAGE PublicationsSage UK: London, England, 1, 2018. ![The effect of ketamine on the consolidation and extinction of contextual fear memory [pdf]](https://bibbase.org/img/filetypes/pdf.svg "pdf")
Paper ![The effect of ketamine on the consolidation and extinction of contextual fear memory [link]](https://bibbase.org/img/filetypes/link.svg "link")
Website abstract bibtex Ketamine, principally an antagonist of
N
-methyl-
ᴅ
-aspartate receptors, induces schizophrenia-like symptoms in adult humans, warranting its use in the
investigation of psychosis-related phenotypes in animal models. Genomic studies further implicate
N
-methyl-
ᴅ
-aspartate receptor-mediated processes
in schizophrenia pathology, together with more broadly-defined synaptic plasticity and associative learning processes. Strong pathophysiological
links have been demonstrated between fear learning and psychiatric disorders such as schizophrenia. To further investigate the impact of ketamine
on associative fear learning, we studied the effects of pre- and post-training ketamine on the consolidation and extinction of contextual fear memory
in rats. Administration of 25 mg/kg ketamine prior to fear conditioning did not affect consolidation when potentially confounding effects of state
dependency were controlled for. Pre-training ketamine (25 mg/kg) impaired the extinction of the conditioned fear response, which was mirrored with
the use of a lower dose (8 mg/kg). Post-training ketamine (25 mg/kg) had no effect on the consolidation or extinction of conditioned fear. These
observations implicate processes relating to the extinction of contextual fear memory in the manifestation of ketamine-induced phenotypes, and are
consistent with existing hypotheses surrounding abnormal associative learning in schizophrenia.
@article{
title = {The effect of ketamine on the consolidation and extinction of contextual fear memory},
type = {article},
year = {2018},
identifiers = {[object Object]},
keywords = {Contextual fear conditioning,N-methyl-ᴅ-aspartate receptor,extinction learning,ketamine,schizophrenia},
pages = {156-162},
volume = {32},
websites = {http://journals.sagepub.com/doi/10.1177/0269881117748903},
month = {1},
publisher = {SAGE PublicationsSage UK: London, England},
day = {17},
id = {575590c2-4722-3f42-9efe-1e58a3a6f3f6},
created = {2018-01-22T19:06:08.290Z},
accessed = {2018-01-22},
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last_modified = {2018-05-31T16:53:52.387Z},
tags = {OA},
read = {false},
starred = {false},
authored = {false},
confirmed = {true},
hidden = {false},
citation_key = {Clifton2018},
private_publication = {false},
abstract = {Ketamine, principally an antagonist of
N
-methyl-
ᴅ
-aspartate receptors, induces schizophrenia-like symptoms in adult humans, warranting its use in the
investigation of psychosis-related phenotypes in animal models. Genomic studies further implicate
N
-methyl-
ᴅ
-aspartate receptor-mediated processes
in schizophrenia pathology, together with more broadly-defined synaptic plasticity and associative learning processes. Strong pathophysiological
links have been demonstrated between fear learning and psychiatric disorders such as schizophrenia. To further investigate the impact of ketamine
on associative fear learning, we studied the effects of pre- and post-training ketamine on the consolidation and extinction of contextual fear memory
in rats. Administration of 25 mg/kg ketamine prior to fear conditioning did not affect consolidation when potentially confounding effects of state
dependency were controlled for. Pre-training ketamine (25 mg/kg) impaired the extinction of the conditioned fear response, which was mirrored with
the use of a lower dose (8 mg/kg). Post-training ketamine (25 mg/kg) had no effect on the consolidation or extinction of conditioned fear. These
observations implicate processes relating to the extinction of contextual fear memory in the manifestation of ketamine-induced phenotypes, and are
consistent with existing hypotheses surrounding abnormal associative learning in schizophrenia.},
bibtype = {article},
author = {Clifton, Nicholas E. and Thomas, Kerrie L. and Hall, Jeremy},
journal = {Journal of Psychopharmacology},
number = {2}
}
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