Glutamate receptor function in learning and memory

Riedel, Gernot; Platt, Bettina; Micheau, Jacques

doi:10.1016/s0166-4328(02)00272-3

Cited by 858 publications

(559 citation statements)

References 512 publications

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“…For technical reasons related to the behavioral paradigm used in these studies (fear-potentiated startle), it was not possible to assess the effects of NMDAR blockade during extinction learning. Given the role of NMDARs in the induction of synaptic plasticity (Martin et al, 2000;Riedel et al, 2003), the most likely interpretation of these results is that the synaptic plasticity required for the acquisition of fear extinction was disrupted. However, two studies (Santini et al, 2001;Suzuki et al, 2004), using a different measure of fear (freezing rather than potentiated startle) and systemic infusions of the non-subunit selective NMDAR antagonist CPP ((7)-3-(2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid), found that whereas the retention of extinction was impaired, there was no apparent impairment during the acquisition of extinction.…”

Section: Introductionmentioning

confidence: 99%

Acquisition of Fear Extinction Requires Activation of NR2B-Containing NMDA Receptors in the Lateral Amygdala

Sotres-Bayón

Bush

LeDoux

2007

Neuropsychopharmacol

257

207

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N-methyl-D-aspartate receptors (NMDARs) contribute to synaptic plasticity underlying learning in a variety of brain systems. Fear extinction, which involves learning to suppress the expression of previously learned fear, appears to require NMDAR activation in the amygdala. However, it is unclear whether amygdala NMDARs are required for the acquisition of extinction learning, and it is unknown whether NR2B-containing NMDARs are required in fear extinction. Here, we assessed the effects of selective NR2B blockade with ifenprodil on fear extinction learning, and found that both systemic and intra-amygdala ifenprodil treatment, given before extinction training, impaired the initial acquisition, and subsequent retrieval of fear extinction. These results confirm previous evidence showing that NMDARs in the amygdala are involved in fear extinction, and additionally show that NR2B-containing NMDARs are required. Contrary to the conclusion of previous studies, our findings demonstrate NMDARs are required for the initial acquisition, rather than only the retention, of fear extinction learning. Thus, our results support a previously not known role for NMDA-dependent plasticity in the lateral amygdala during the acquisition of fear extinction.

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Section: Introductionmentioning

confidence: 99%

Acquisition of Fear Extinction Requires Activation of NR2B-Containing NMDA Receptors in the Lateral Amygdala

Sotres-Bayón

Bush

LeDoux

2007

Neuropsychopharmacol

257

207

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“…Glutamate neurotransmission appears essential to brain plasticity including learning and memory processes (for a recent review see Riedel et al, 2003). While mesocorticolimbic dopamine systems are involved in opiate reward (Wise, 2004) including reinstatement phenomena (Shaham et al, 2003), these systems are under the control of glutamate afferents (Siggins et al, 2003;Sesack et al, 2003), expressing among others NMDA receptors (Gracy et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

Reinstatement of Morphine-Conditioned Reward is Blocked by Memantine

Popik

Wróbel

Bisaga

2005

Neuropsychopharmacol

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Protection of abstinent individuals from relapse is the main goal of drug dependence treatment. Relapse is frequently precipitated by exposure to small doses of the drug of abuse or exposure to the environment that was previously associated with the drug. Mice exposed to morphine (10 mg/kg) in a unique test-box environment display a conditioned place preference for this environment. Such preference can be extinguished by subsequent pairing of physiological saline administration with the same environment. Once extinguished, the original place preference can be reinstated after a priming dose (1-2.5 mg/kg) of morphine is given. However, mice treated with 7.5 (but not 3.75) mg/kg of memantine (the glutamate/NMDA receptor antagonist) during the extinction phase were insensitive to morphine's ability to reinstate the place preference 2 days after extinction conditionings. Effect of memantine was also observed when priming dose of morphine was given 21 days after extinction conditionings. In contrast, morphine's ability to reinstate conditioned response was not affected by treatment with 10 mg/kg of chlordiazepoxide, 0.5 mg/kg of LSD-25, or 1 mg/kg of morphine given during extinction conditionings. A separate experiment demonstrated that memantine (7.5 mg/kg) treatment did not affect learning. We show for the first time that memantine treatment during extinction conditionings may abolish the ability of drug-related cues to evoke reinstatement, suggesting that this NMDA receptor antagonist can be useful in preventing relapse in opioid dependent individuals.

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“…L-Glutamate plays important roles in many fields including bioprocess monitoring [1,2], biomedical application [3,4] and food processing [5]. As a functional amino acid, it is a crucial excitatory neurotransmitter in the central nervous system.…”

Section: Introductionmentioning

confidence: 99%