d-Cycloserine: Effects on Long-Term Retention of a Conditioned Response and on Memory for Contextual Attributes

Land, Cantey L.; Riccio, David C.

doi:10.1006/nlme.1998.3897

Cited by 55 publications

(43 citation statements)

References 28 publications

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“…A growing body of data supports the view that DCS facilitates the formation of extinction memory (Ledgerwood et al, 2003;Walker et al, 2002;Yamamoto et al, 2008); moreover, DCS facilitates learning and memory using a variety of learning paradigms in diverse animal species (Land and Riccio, 1999;Matsuoka and Aigner, 1996;Monahan et al, 1989;Pitkänen et al, 1995;Pussinen et al, 1997;Quartermain et al, 1994;Thompson et al, 1992). Our findings showed that DCS administration did not affect freezing during reactivation under the present treatment protocol as comparable levels of fear were observed between DCS-and SAL-treated animals, regardless whether animals were subjected to a threatening event before learning.…”

Section: Discussionsupporting

confidence: 75%

Previous Stress Attenuates the Susceptibility to Midazolam's Disruptive Effect on Fear Memory Reconsolidation: Influence of Pre-Reactivation D-Cycloserine Administration

Bustos

Giachero

Maldonado

et al. 2009

Neuropsychopharmacol

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It is well known that, under certain boundary conditions, the retrieval of a stable consolidated memory results into a labile one. During this unstable phase, memory can be vulnerable to interference by a number of pharmacological agents, including benzodiazepines. One of the goals of this study was to evaluate the vulnerability to midazolam (MDZ) after reactivation of recent and remote contextual fear memories in animals that experienced a stressful situation before learning. Animals were subjected to a restraint session and trained in a contextual fear paradigm the following day; consolidated memories were reactivated at different times after learning and different MDZ doses (1.5, 3.0 mg/kg) were administered to rats after reactivation. Our results show that MDZ did not affect memory reconsolidation in older-than-one-day memories of stressed animals, even after the administration of a higher MDZ dose and a longer reactivation session (5 min). In contrast, MDZ was effective in blocking reconsolidation at all memory ages in unstressed animals. In addition, the current research investigated whether activating NMDA sites before reactivation promotes the destabilization of resistant memories such as those of stressed animals. We tested the influence of pre-reactivation D-cycloserine (DCS), a partial NMDA agonist, on MDZ's effect on fear memory reconsolidation in stressed animals. Our findings indicate that DCS before reactivation promotes retrieval-induced lability in resistant memory traces, as MDZ-induced memory impairment in stressed rats became evident with pre-reactivation DCS but not after pre-reactivation sterile isotonic saline.

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Section: Discussionsupporting

confidence: 75%

Previous Stress Attenuates the Susceptibility to Midazolam's Disruptive Effect on Fear Memory Reconsolidation: Influence of Pre-Reactivation D-Cycloserine Administration

Bustos

Giachero

Maldonado

et al. 2009

Neuropsychopharmacol

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“…Therefore, DCS potentiated fear memory extinction, as has been demonstrated previously (Walker et al, 2002;Ledgerwood et al, 2003). Moreover, given that it is highly unlikely that the same infusion of DCS could both enhance and prevent extinction, and that DCS potentiates a range of learning processes (Monahan et al, 1989;Quartermain et al, 1994;Land and Riccio, 1999;Walker et al, 2002;Ledgerwood et al, 2003), the elevated freezing and lack of extinction after DCS infusion before short memory reactivation likely reflects a potentiation of conditioned fear memory reconsolidation. Reconsolidation and extinction have opposing effects on behavioral output, and so an enhancement of reconsolidation would act against the behavioral impact of extinction.…”

Section: Discussionsupporting

confidence: 64%

“…Not only does blockade of NMDA receptor transmission impair the acquisition of several forms of memory (Morris et al, 1986;Campeau et al, 1992;Burns et al, 1994;Maren et al, 1996;Ferry and Di Scala, 2000;Rodrigues et al, 2001;Goosens and Maren, 2004) and disrupt acutely the expression of previously acquired fear memories (Maren et al, 1996;Fendt, 2001;Lee et al, 2001) as observed here, but administration of partial NMDA receptor agonists also enhances learning (Monahan et al, 1989;Thompson et al, 1992;Quartermain et al, 1994;Land and Riccio, 1999). The extinction of conditioned fear memories, which involves new learning (Bouton and Bolles, 1979;Rescorla, 2001), has also been shown previously to be impaired by NMDA receptor antagonists (Falls et al, 1992;Baker and Azorlosa, 1996;Lee and Kim, 1998) and potentiated by the partial NMDA receptor agonist DCS (Walker et al, 2002;Ledgerwood et al, 2003), when these compounds are administered either systemically or directly into the BLA.…”

Section: Discussionsupporting

confidence: 52%

Reconsolidation and Extinction of Conditioned Fear: Inhibition and Potentiation

Lee¹,

Milton²,

Everitt³

2006

J. Neurosci.

444

426

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NMDA receptors are important for the acquisition, reconsolidation, and extinction of memories. NMDA receptor antagonists impair these memory processes, whereas the partial agonist D-cycloserine (DCS) potentiates both learning and extinction. Here, we used DCS and the noncompetitive NMDA receptor antagonist (ϩ)-5-methyl-10,11-dihydro-SH-dibenzo[a,d]cyclohepten-5,10-imine maleate (MK-801) to investigate the effects of enhancing and blocking NMDA receptor-mediated glutamatergic transmission on the reconsolidation and extinction of a conditioned fear memory. Either long extinction training or short memory reactivation sessions were used to preferentially engage extinction and reconsolidation processes, respectively. MK-801 blocked extinction to maintain high levels of conditioned freezing, and DCS potentiated extinction to reduce freezing, when they were administered before a long extinction training session. However, the opposite behavioral outcome was observed when the brief memory reactivation session was used: MK-801 administration impaired, whereas DCS increased, freezing, likely reflecting impairment and enhancement of reconsolidation, respectively. Finally, by using localized intracerebral infusions, we showed that the basolateral amygdala is a primary locus of action of systemically administered DCS. Thus, intrabasolateral amygdala DCS potentiated both the extinction and the reconsolidation of fear conditioning, depending on the length of the extinction/memory reactivation session. Therefore, memory reconsolidation can be both disrupted and enhanced, and extinction can be both potentiated and impaired, either to reduce or increase conditioned fear. These results have important implications for the use of reconsolidation blockade and potentiation of extinction as treatment strategies for maladaptive memory disorders.

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“…Our findings are in agreement with other studies in which DCS accelerated the rate of learning. For example, DCS has been shown in rats to enhance acquisition of spatial watermaze learning (Riekkinen and Riekkinen, 1997), inhibitory avoidance (Land and Riccio, 1999), and the extinction of fear-conditioning (Parnas et al, 2005) or fear-potentiated startle response (Walker et al, 2002). Relevant to gustatory learning, we have recently demonstrated that DCS potentiated acquisition of CTA (Houpt et al, 2005).…”

Section: Discussionmentioning

confidence: 95%

NMDA receptor in conditioned flavor-taste preference learning: Blockade by MK-801 and enhancement by D-cycloserine

Golden

Houpt

2007

Pharmacology Biochemistry and Behavior

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Conditioned flavor-taste preference (CFTP) is a robust form of learning in which animals acquire a preference for a flavor (e.g. Kool-Aid) previously mixed with a highly preferred tastant (e.g. fructose) over a flavor previously mixed with a less preferred tastant (e.g. saccharin). Here, the role of the Nmethyl-D-aspartate (NMDA) glutamate-glycine receptor (NR) was probed using systemic MK-801, a non-competitive antagonist, and D-cycloserine (DCS), a glycine agonist. Rats were injected with MK-801 (100 μg/kg) or vehicle 30 min prior to a daily 2-h conditioning session with 1-bottle access to a Kool-Aid flavor (grape or cherry) mixed with either 8% fructose (CS+/F) or 0.2% saccharin (CS −/S). CFTP expression was measured in 2-bottle preference tests between the Kool-Aid flavors mixed with 0.2% saccharin (CS+/S vs. CS−/S). While vehicle-treated rats acquired a preference for CS+/ S over CS−/S, MK-801 prior to conditioning completely blocked CFTP learning. The effect of MK-801 was specific to CFTP acquisition, because follow-up experiments demonstrated that MK-801 did not induce a conditioned taste aversion, cause state-dependent learning, or affect CFTP expression. In a second approach, rats were injected with DCS (15 mg/kg) 60 min prior to daily conditioning. In contrast to MK-801, adminstration of DCS prior to conditioning enhanced CFTP learning (but not reversal conditioning). These results demonstrate that NR neurotransmission is critical for CFTP learning. Furthermore, enhancement of CFTP learning by DCS suggests that endogenous levels of glycine or D-serine may be a limiting factor in CFTP learning.

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d-Cycloserine: Effects on Long-Term Retention of a Conditioned Response and on Memory for Contextual Attributes

Cited by 55 publications

References 28 publications

Previous Stress Attenuates the Susceptibility to Midazolam's Disruptive Effect on Fear Memory Reconsolidation: Influence of Pre-Reactivation D-Cycloserine Administration

Previous Stress Attenuates the Susceptibility to Midazolam's Disruptive Effect on Fear Memory Reconsolidation: Influence of Pre-Reactivation D-Cycloserine Administration

Reconsolidation and Extinction of Conditioned Fear: Inhibition and Potentiation

NMDA receptor in conditioned flavor-taste preference learning: Blockade by MK-801 and enhancement by D-cycloserine

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