Memory Formation in Day‐old Chicks Requires NMDA but not Non‐NMDA Glutamate Receptors

Burchuladze, R. A.; Rose, Steven

doi:10.1111/j.1460-9568.1992.tb00903.x

Cited by 75 publications

(38 citation statements)

References 40 publications

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“…In addition, NBQX shows very low affinity for NMDARs (IC 50 >90 µm) and glycine receptors (IC 50 >100 µm) unlike CNQX (IC 50 = 25 µm-NMDA; IC 50 = 14 µm-glycine) and DNQX (IC 50 = 40 µm-NMDA; IC 50 = 9.5 µm-glycine), which show higher affinity for those receptors. Interestingly, inhibitory avoidance conditioning of bead pecking in the chick has been shown to be disrupted by direct infusion of CNQX, but not by direct infusion of NBQX (Burchuladze and Rose 1992;Rickard et al 1994). Further, NBQX and another selective AMPAR antagonist, GYKI 52366, did not block LTP (Sato et al 1995;Kapus et al 2000).…”

Section: Ampar Antagonist Selectivitymentioning

confidence: 98%

Coantagonism of glutamate receptors and nicotinic acetylcholinergic receptors disrupts fear conditioning and latent inhibition of fear conditioning

Gould¹,

Lewis

2005

Learn. Mem.

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The present study investigated the hypothesis that both nicotinic acetylcholinergic receptors (nAChRs) and glutamate receptors (␣-amino-3-hydroxy-5-methyl-4-isoxazole propionate receptors (AMPARs) and N-methyl-Daspartate glutamate receptors (NMDARs)) are involved in fear conditioning, and may modulate similar processes. The effects of the nAChR antagonist mecamylamine administered alone, the AMPAR antagonist NBQX administered alone, and the NMDAR antagonist MK-801 administered alone on cued fear conditioning, contextual fear conditioning, and latent inhibition of cued fear conditioning were examined. In addition, the effects of coadministration of either mecamylamine and NBQX or mecamylamine and MK-801 on these behaviors were examined. Consistent with previous studies, neither mecamylamine nor NBQX administered alone disrupted any of the tasks. However, coadministration of mecamylamine and NBQX disrupted both contextual fear conditioning and latent inhibition of cued fear conditioning. In addition, coadministration of mecamylamine with a dose of MK-801 subthreshold for disrupting either task disrupted both contextual fear conditioning and latent inhibition of cued fear conditioning. Coadministration of mecamylamine and NBQX, and coadministration of mecamylamine with a dose of MK-801 subthreshold for disrupting fear conditioning had little effect on cued fear conditioning. These results suggest that nAChRs and glutamate receptors may support similar processes mediating acquisition of contextual fear conditioning and latent inhibition of fear conditioning.A large body of research has been directed at understanding the neural, cellular, and molecular processes that underlie fear conditioning and tasks that modulate conditioning, such as latent inhibition. This focus provides a means to not only understand the neurobiology of learning, but also to understand disease states that can be modeled with these tasks. Fear conditioning measures amygdala-and hippocampus-dependent learning (contextual fear conditioning), as well as amygdala-dependent and hippocampus-independent learning (cued fear conditioning) within the same subject (Kim and

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Section: Ampar Antagonist Selectivitymentioning

confidence: 98%

Coantagonism of glutamate receptors and nicotinic acetylcholinergic receptors disrupts fear conditioning and latent inhibition of fear conditioning

Gould¹,

Lewis

2005

Learn. Mem.

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“…There is increased release of the putative retrograde messenger arachidonic acid, in tissue prisms prepared 30-75 min post-training, though the onset time for amnesia if the arachidonic acid synthesis is blocked with phospholipase A 2 inhibitors is delayed until 75 min (Clements and Rose 1996;Holscher and Rose 1994). Interventive studies with MK801 (Burchuladze and Rose 1992), the N-type calcium channel blocker ⍀-conotoxin GVIA (Clements et al 1995), and PKC inhibitors such as mellitin and H7 (Burchuladze et al 1990), injected into …”

Section: The First Hourmentioning

confidence: 99%

God's Organism? The Chick as a Model System for Memory Studies

Rose¹

2000

Learn. Mem.

196

137

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The young chick is a powerful model system in which to study the biochemical and morphological processes underlying memory formation. Training chicks on a one trial passive avoidance task results in a molecular cascade in a specific brain region, the intermediate medial hyperstriatum ventrale. This cascade is initiated by glutamate release and engages a series of synaptic transients including increased calcium flux, up-regulation of NMDA-glutamate receptors, membrane protein phosphorylations, and the retrograde messenger NO. Expression of immediate early genes c-fos and c-jun precedes the synthesis, glycosylation, and redistribution, >4 hr downstream, of a number of synaptic membrane proteins, notably NCAM and L1. Other membrane proteins required in the early phase of memory formation include the amyloid precursor protein (APP) and apolipoprotein E. There are concomitant increases in dendritic spine number and changes in synaptic structure. Nonsynaptic factors, including corticosterone and BDNF, can modulate retention of the avoidance response, enhancing the salience of otherwise weakly retained memory. These results are discussed in relation to general concepts of memory formation and the spatio-temporal distribution of the putative memory trace.

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“…Although there is convincing evidence that activation of N-methyl-D-aspartate (NMDA) receptors is a key step in learning and memory formation (18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28) and that it is involved in the cellular events underlying synaptic plasticity in the hippocampus (29,30), memory storage in the neocortex (31), and activity-dependent development of neuronal connectivity in sensory systems (32)(33), a direct link between NMDA receptor activation and learning-related morphological synaptic changes, in particular, synaptic elimination, has not yet been revealed.…”

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confidence: 99%

Blockade of N -methyl- d -aspartate receptor activation suppresses learning-induced synaptic elimination

Bock

Braun

1999

Proc. Natl. Acad. Sci. U.S.A.

102

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Auditory filial imprinting in the domestic chicken is accompanied by a dramatic loss of spine synapses in two higher associative forebrain areas, the mediorostral neostriatum͞hyperstriatum ventrale (MNH) and the dorsocaudal neostriatum (Ndc). The cellular mechanisms that underlie this learning-induced synaptic reorganization are unclear. We found that local pharmacological blockade of N-methyl-D-aspartate (NMDA) receptors in the MNH, a manipulation that has been shown previously to impair auditory imprinting, suppresses the learning-induced spine reduction in this region. Chicks treated with the NMDA receptor antagonist 2-amino-5-phosphonovaleric acid (APV) during the behavioral training for imprinting (postnatal day 0-2) displayed similar spine frequencies at postnatal day 7 as naive control animals, which, in both groups, were significantly higher than in imprinted animals. Because the average dendritic length did not differ between the experimental groups, the reduced spine frequency can be interpreted as a reduction of the total number of spine synapses per neuron. In the Ndc, which is reciprocally connected with the MNH and not directly inf luenced by the injected drug, learning-induced spine elimination was partly suppressed. Spine frequencies of the APVtreated, behaviorally trained but nonimprinted animals were higher than in the imprinted animals but lower than in the naive animals. These results provide evidence that NMDA receptor activation is required for the learning-induced selective reduction of spine synapses, which may serve as a mechanism of information storage specific for juvenile emotional learning events.Spines are considered specialized structures subserving a biochemical compartmentalization to provide a protected microenvironment for calcium and other messengers and, therefore, to play a key role in the expression of synaptic plasticity (1-5). Changes in the numerical density of spine synapses are proposed to represent a principal cellular correlate of learning and memory formation (6-12). Auditory filial imprinting in the domestic chicken is associated with a reduction of spine synapses in two associative forebrain areas, the mediorostral neostriatum͞hyperstriatum ventrale (MNH) and the reciprocally connected dorsocaudal neostriatum (Ndc) (8,(12)(13)(14), an area that provides indirect auditory input into the MNH (15). Based on anatomical criteria, such as its glutamatergic thalamic afferents and its tegmental dopaminergic inputs, the MNH may be considered as the avian analogue of the mammalian prefrontal cortex, whereas the Ndc seems to correspond to second-order parasensory association areas in the mammalian parietotemporal cortex (15-17).The cellular and molecular mechanisms that trigger, regulate, and mediate proliferative and regressive changes of synaptic density in the course of this juvenile learning event are unclear. Although there is convincing evidence that activation of N-methyl-D-aspartate (NMDA) receptors is a key step in learning and memory formation (18-28) and t...

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Memory Formation in Day‐old Chicks Requires NMDA but not Non‐NMDA Glutamate Receptors

Cited by 75 publications

References 40 publications

Coantagonism of glutamate receptors and nicotinic acetylcholinergic receptors disrupts fear conditioning and latent inhibition of fear conditioning

Coantagonism of glutamate receptors and nicotinic acetylcholinergic receptors disrupts fear conditioning and latent inhibition of fear conditioning

God's Organism? The Chick as a Model System for Memory Studies

Blockade of N -methyl- d -aspartate receptor activation suppresses learning-induced synaptic elimination

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