MK-801 induced retrieval, but not acquisition, deficits for passive avoidance conditioning

Harrod, Steven B.; Flint, Robert W.; Riccio, David C.

doi:10.1016/s0091-3057(01)00565-2

Cited by 31 publications

(20 citation statements)

References 38 publications

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“…MK-801 has been shown to support state-dependent learning in other models. For example, rats treated with MK-801 (100 μg/kg ip) during place-footshock aversion conditioning appeared unable to express a place aversion when tested drug-free (Harrod et al, 2001). When tested immediately after MK-801 injection, however, the rats did express a place aversion.…”

Section: Discussionmentioning

confidence: 99%

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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Section: Discussionmentioning

confidence: 99%

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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“…If these steroids interacted mainly with GABA A receptors, or even NMDA receptors, blockade of which is also known to sustain StD (Jackson et al, 1992;Harrod et al, 2001), they would be expected to modify the brain chemical state in a way allowing the observation of StD. Their interaction with the s 1 receptor, known to occur at the dosage tested in the present study , may explain the lack of memory trace, further suggesting that acting through the s 1 receptor could also allow to modulate the chemical states induced by GABAergic or glutamatergic drugs.…”

Section: Influence Of Neuro(active) Steroids On Cocaine-induced Stdmentioning

confidence: 99%

“…Indeed, animals receiving a repeated treatment (vehicle solution/vehicle solution or drug/drug) before acquisition and retention showed optimal retention capacities, whereas animals receiving crossed treatments (vehicle/drug or drug/vehicle) showed significant deficits in retention parameters. Several drugs acting on specific neurotransmitter systems could elicit StD, including naloxone (Oberling et al, 1993), morphine (Bruins Slot and Colpaert, 1999a, b;Zarrindast and Rezayof, 2004), pentobarbital (Overton, 1966), muscimol, diazepam (Nakagawa et al, 1993;Nakagawa and Iwasaki, 1996), chlordiazepoxide (Colpaert, 1990), or dizocilpine (Jackson et al, 1992;Harrod et al, 2001). Endogenous agents may also sustain StD, such as the 3a-hydroxy-5-reduced metabolite of progesterone, pregnanolone (Bruins Slot et al, 1999), which acts as a positive modulator of the g-aminobutyric acid type A (GABA A ) receptor (Paul and Purdy, 1992).…”

Section: Introductionmentioning

confidence: 99%

σ1 Receptor Ligands and Related Neuroactive Steroids Interfere with the Cocaine-Induced State of Memory

Romieu

Lucas

Maurice

2005

Neuropsychopharmacol

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The present series of experiments examined the involvement of the s 1 receptor and related neuroactive steroids in the memory state induced by a very low dose of cocaine. Using a modified passive avoidance procedure in mice, we examined whether cocaine induces state-dependent (StD) learning. Animals trained and tested with saline or the same dose of cocaine (0.1 or 0.3 mg/kg) showed correct retention, measured using two independent parameters: the retention latency and a ratio between the retention latency and the last training latency. Animals trained with cocaine (0.1 mg/kg) and tested with saline or cocaine (0.03, 0.3 mg/kg), or trained with saline and tested with cocaine, showed altered retention parameters, demonstrating that StD occurred. Therefore, cocaine administered before training produced a chemical state used as an endogenous cue to insure optimal retention. Since s 1 receptor activation is an important event during the acquisition of cocaine reward, we tested several s 1 ligands and related neurosteroids. The s 1 agonist igmesine or antagonist BD1047 failed to produce StD, but modified the cocaine state. Among neuroactive steroids, pregnanolone and allopregnanolone, positive modulators of the g-aminobutyric acid type A (GABA A ) receptor, produced StD. However, steroids also acting as s 1 agonists, dehydroepiandrosterone (3b-hydroxy-5a-androsten-17-one (DHEA)), pregnenolone, or antagonist, progesterone, failed to induce StD but modified the cocaine state. Furthermore, optimal retention was observed with mice trained with (igmesine or DHEA) + cocaine and tested with a higher dose of cocaine, or with mice trained with (BD1047 or progesterone) + cocaine and tested with vehicle. This study demonstrated that: (i) low doses of cocaine induce a chemical state/memory trace sustaining StD; (ii) modulation of the s 1 receptor activation, although insufficient to provoke StD, modulates the cocaine state; (iii) neuroactive steroids exert a unique role in state-dependent vs state-independent learning, via GABA A or s 1 receptor modulation, and are able to affect the cocaine-induced mnesic trace at low brain concentrations.

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“…According to this view, a drug (or hormone)-induced memory reactivation would depend on the reinstatement of a sufficient number (or kind) of retrieval attributes that were present at, or immediately following, original learning. Some authors have argued that state dependence ensues because interoceptive states experienced in a given drug (or hormonal) state serve as contextual cues for retrieval (Harrod et al 2001;Izquierdo 1984;Izquierdo et al 1988), but others have cautioned against this view, since there is evidence that drugs can be discriminable in conditions in which they do not produce state dependency . In either case, one might consider the possibility that a retrograde modulation of memory may result from state dependency.…”

Section: Introductionmentioning

confidence: 99%

“…Regarding this point, it has been reported that NMDA antagonists induce state-dependent learning (Harrod et al 2001;Jackson et al 1992). Since polyamine binding site ligands interact with NMDA receptors, they could also produce a state on which the recall of the newly learned response is dependent.…”

Section: Introductionmentioning

confidence: 99%

Arcaine and MK-801 make recall state-dependent in rats

et al. 2008

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MK-801 induced retrieval, but not acquisition, deficits for passive avoidance conditioning

Cited by 31 publications

References 38 publications

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

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

σ1 Receptor Ligands and Related Neuroactive Steroids Interfere with the Cocaine-Induced State of Memory

Arcaine and MK-801 make recall state-dependent in rats

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