Acute Effects of Ketamine on Memory Systems and Psychotic Symptoms in Healthy Volunteers

Morgan, Philip G.; Mofeez, Ali; Brandner, Brigitta; Bromley, Lesley; Curran, H. Valerie

doi:10.1038/sj.npp.1300342

Cited by 244 publications

(200 citation statements)

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“…[45][46][47][48][49] Interestingly, increased response to acute AMPH treatment has been directly implicated in the positive symptoms of schizophrenia, 47 whereas acute pharmacological treatment with NMDA receptor antagonists may additionally induce memory impairments related to the cognitive symptoms of schizophrenia. 50, 51 Prenatal immune activation by the inflammatory agent PolyI:C in mice thus precipitates a wide spectrum of adult behavioral and pharmacological abnormalities related especially to the symptom profiles in schizophrenia.…”

Section: Discussionmentioning

confidence: 99%

Adult behavioral and pharmacological dysfunctions following disruption of the fetal brain balance between pro-inflammatory and IL-10-mediated anti-inflammatory signaling

et al. 2007

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Maternal infections during pregnancy increase the risk for schizophrenia and related disorders of putative neurodevelopmental origin in the offspring. This association has been attributed to enhanced expression of pro-inflammatory cytokines in the fetal environment in response to maternal immunological stimulation. In contrast, the specific roles of anti-inflammatory cytokines are virtually unknown in this context. Here, we demonstrate that genetically enforced expression of the anti-inflammatory cytokine interleukin (IL)-10 by macrophages attenuates the long-term behavioral and pharmacological consequences of prenatal immune activation in a mouse model of prenatal viral-like infection by polyriboinosinic-polyribocytidilic acid (PolyI:C; 2 mg/kg, intravenously). In the absence of a discrete prenatal inflammatory stimulus, however, enhanced levels of IL-10 at the maternal-fetal interface by itself also precipitates specific behavioral abnormalities in the grown offspring. This highlights that in addition to the disruptive effects of excess pro-inflammatory molecules, a shift toward enhanced antiinflammatory signaling in prenatal life can similarly affect cognitive and behavioral development. Hence, shifts of the balance between pro-and anti-inflammatory cytokine classes may be a critical determinant of the final impact on neurodevelopment following early life infection or innate immune imbalances.

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Section: Discussionmentioning

confidence: 99%

Adult behavioral and pharmacological dysfunctions following disruption of the fetal brain balance between pro-inflammatory and IL-10-mediated anti-inflammatory signaling

et al. 2007

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“…7 A research line that is largely ignored in Dalenberg et al's review is the psychopharmacology of dissociative symptoms. Some drugs, notably ketamine, have been shown to produce severe dissociative symptoms along with memory dysfunctions in healthy volunteers (e.g., Morgan, Mofeez, Brandner, Bromley, & Curran, 2004). We consider this type of study important insofar as it may shed light on the issue of whether dissociative reactions may occur in the absence of a history of trauma.…”

Section: Commentmentioning

confidence: 99%

The trauma model of dissociation: Inconvenient truths and stubborn fictions. Comment on Dalenberg et al. (2012).

Lynn

Lilienfeld

Merckelbach

et al. 2014

Psychological Bulletin

129

130

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Dalenberg et al. (2012) argued that convincing evidence (a) supports the longstanding trauma model (TM), which posits that early trauma plays a key role in the genesis of dissociation; and (b) refutes the fantasy model (FM), which posits that fantasy proneness, suggestibility, cognitive failures, and other variables foster dissociation. We review evidence bearing on Dalenberg et al.'s 8 predictions and find them largely wanting in empirical support. We contend that the authors repeat errors committed by many previous proponents of the TM, such as attributing a central etiological role to trauma in the absence of sufficient evidence. Specifically, Dalenberg et al. leap too quickly from correlational data to causal conclusions, do not adequately consider the lack of corroboration of abuse in many studies, and underestimate the relation between dissociation and false memories. Nevertheless, we identify points of agreement between the TM and FM regarding potential moderators and mediators of dissociative symptoms (e.g., family environment, biological vulnerabilities) and the hypothesis that dissociative identity disorder is a disorder of self-understanding. We acknowledge that trauma may play a causal role in dissociation but that this role is less central and specific than Dalenberg et al. contend. Finally, although a key assumption of the TM is dissociative amnesia, the notion that people can encode traumatic experiences without being able to recall them lacks strong empirical support. Accordingly, we conclude that the field should now abandon the simple trauma-dissociation model and embrace multifactorial models that accommodate the diversity of causes of dissociation and dissociative disorders.Keywords: dissociation, dissociative disorder, dissociative identity disorder, trauma, sociocognitive modelThe notion that people dissociate to cope with trauma has its roots in the writings of Janet (1889/1973). This trauma model (TM) remains influential among some clinical scholars (e.g., Dalenberg et al., 2012), who contend that trauma is the key player in the genesis of dissociation. Nevertheless, as we discuss later, advocates of the TM have often neglected to articulate trauma's precise role in the cause of dissociation. Critics of the TM (e.g., Giesbrecht, Lynn, Lilienfeld, & Merckelbach, 2008, 2010Lynn, Lilienfeld, Merckelbach, Giesbrecht, & van der Kloet, 2012;Pope & Hudson, 1995) Correspondence concerning this article should be addressed to Steven Jay Lynn, Psychology Department, Binghamton University (SUNY), Binghamton, NY 13902. E-mail: stevenlynn100@gmail.com This document is copyrighted by the American Psychological Association or one of its allied publishers.This article is intended solely for the personal use of the individual user and is not to be disseminated broadly.Psychological Bulletin © 2014 American Psychological Association 2014 0033-2909/14/$12.00 DOI: 10.1037/a0035570 896 etiology of dissociation and dissociative disorders. 1 An early alternative to the TM, the sociocognitive model (SCM; Lili...

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“…Human evidence indicates that pharmacologic blockade of NMDA receptors impairs learning and memory (Morgan et al, 2004;Rockstroh et al, 1996), whereas post-learning administration of an NMDA agonist facilitates consolidation of fearful memories (Kalisch et al, 2009). …”

Section: Glutamatergic Modulation Of Episodic Memorymentioning

confidence: 99%

Dopamine and glutamate receptor genes interactively influence episodic memory in old age

Papenberg¹,

Li²,

Nagel³

et al. 2014

Neurobiology of Aging

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a b s t r a c tBoth the dopaminergic and glutamatergic systems modulate episodic memory consolidation. Evidence from animal studies suggests that these two neurotransmitters may interact in influencing memory performance. Given that individual differences in episodic memory are heritable, we investigated whether variations of the dopamine D2 receptor gene (rs6277, C957T) and the N-methyl-D-aspartate 3A (NR3A) gene, coding for the N-methyl-D-aspartate 3A subunit of the glutamate N-methyl-D-aspartate receptor (rs10989591, Val362Met), interactively modulate episodic memory in large samples of younger (20e31 years; n ¼ 670) and older (59e71 years; n ¼ 832) adults. We found a reliable gene-gene interaction, which was observed in older adults only: older individuals carrying genotypes associated with greater D2 and N-methyl-D-aspartate receptor efficacy showed better episodic performance. These results are in line with findings showing magnification of genetic effects on memory in old age, presumably as a consequence of reduced brain resources. Our findings underscore the need for investigating interactive effects of multiple genes to understand individual difference in episodic memory.

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Acute Effects of Ketamine on Memory Systems and Psychotic Symptoms in Healthy Volunteers

Cited by 244 publications

References 43 publications

Adult behavioral and pharmacological dysfunctions following disruption of the fetal brain balance between pro-inflammatory and IL-10-mediated anti-inflammatory signaling

Adult behavioral and pharmacological dysfunctions following disruption of the fetal brain balance between pro-inflammatory and IL-10-mediated anti-inflammatory signaling

The trauma model of dissociation: Inconvenient truths and stubborn fictions. Comment on Dalenberg et al. (2012).

Dopamine and glutamate receptor genes interactively influence episodic memory in old age

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