The antagonism of amino acid‐induced excitations of rat hippocampal CA1 neurones in vitro.

Collingridge, Graham L.; Kehl, Steven J.; McLennan, H.

doi:10.1113/jphysiol.1983.sp014477

Cited by 349 publications

(134 citation statements)

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“…Schaeffer collateral LTP is considered a post-synaptic form of LTP in which activation of NMDA receptors leads to calcium entry, which then induces LTP [6,24,28]. We observed that APP/PS1KI mice with only one mutant PS1 allele, wildtype and PS1KI mice showed a normal LTP pattern at 6 months.…”

Section: Discussionmentioning

confidence: 79%

APP/PS1KI bigenic mice develop early synaptic deficits and hippocampus atrophy

et al. 2009

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Abeta accumulation has an important function in the etiology of Alzheimer's disease (AD) with its typical clinical symptoms, like memory impairment and changes in personality. However, the mode of this toxic activity is still a matter of scientific debate. We used the APP/PS1KI mouse model for AD, because it is the only model so far which develops 50% hippocampal CA1 neuron loss at the age of 1 year. Previously, we have shown that this model develops severe learning deficits occurring much earlier at the age of 6 months. This observation prompted us to study the anatomical and cellular basis at this time point in more detail. In the current report, we observed that at 6 months of age there is already a 33% CA1 neuron loss and an 18% atrophy of the hippocampus, together with a drastic reduction of long-term potentiation and disrupted paired pulse facilitation. Interestingly, at 4 months of age, there was no long-term potentiation deficit in CA1. This was accompanied by reduced levels of pre-and post-synaptic markers. We also observed that intraneuronal and total amount of different Abeta peptides including N-modified, fibrillar and oligomeric Abeta species increased and coincided well with CA1 neuron loss. Overall, these data provide the basis for the observed robust working memory deficits in this mouse model for AD at 6 months of age.

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Section: Discussionmentioning

confidence: 79%

APP/PS1KI bigenic mice develop early synaptic deficits and hippocampus atrophy

et al. 2009

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“…In all respects the mechanism is similar to that by which activation of mGluRs inhibits Ca2+ currents (Lester & Jahr, 1990). This potentiation may have a physiological role in forms of synaptic plasticity which are dependent on the activation of NMDA receptors, such LTP in the Schaffer collateral commissural pathway (Collingridge et al, 1983). In particular, it can explain how a mixture of IS,3R-ACPD and IR,3S-ACPD rapidly enhances STP (the initial phase of LTP) (McGuinness et al, 1991).…”

Section: Discussionmentioning

confidence: 85%

Signal transduction pathways involved in the acute potentiation of NMDA responses by 1S,3R‐ACPD in rat hippocampal slices

Harvey

Collingridge

1993

British J Pharmacology

135

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1 A grease-gap recording technique has been used to investigate the mechanisms underlying the acute potentiation of N-methyl-D-aspartate (NMDA) responses by aminocyclopentane-1S,3R-dicarboxylic acid (IS,3R-ACPD) in area CAI of rat hippocampal slices.2 1S,3R-ACPD (1OM), but not IR,3S-ACPD (1OEM), potentiated submaximal responses to NMDA (dose-ratio of 0.81 ± 0.02 (mean ± s.e.mean); n = 55), but not to a-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), in a readily reversible manner. Potentiation also occurred in slices treated with 0.2 tLM tetrodotoxin, and in slices perfused with Mg2"-free medium.3 IS,3R-ACPD-induced potentiation was unaffected by the protein kinase inhibitors K-252b (0.1 tLM) and staurosporine (1 gM) and the intracellular Ca2+ store depletor, thapsigargin (10 gM). Coapplication of staurosporine and thapsigargin was also without effect. 4 IS,3R-ACPD-induced potentiation was unaffected by inhibitors of arachidonic acid formation, bromophenacyl bromide (50 tM) and RG80267 (100 gM). Arachidonic acid (10-50 gM) depressed reversibly NMDA-induced responses. The potentiation was unaffected by 8-bromo cyclic AMP (500 jAM) or the PKA inhibitor Rp-adenosine 3,5-cyclic monophosphothioate triethylamine (Rp-cAMPS; 50 jAM). 5 IS,3R-ACPD-induced potentiation was abolished in slices perfused with Ca2+-free medium. The potentiation was also blocked by phorbol-12,13-diacetate (1 gM), in a staurosporine-sensitive manner.6 It is concluded that the potentiation of NMDA responses by IS,3R-ACPD is not mediated by protein kinase A or C, by release of Ca2+ from intracellular stores or by arachidonic acid. It involves a Ca2+-sensitive process and is negatively regulated by protein kinase C.

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“…Activation of NMDA receptors and the resultant Ca 2+ influx are necessary for LTP induction in area CA1 (Collingridge et al 1983;Malenka et al 1988). Spatial enrichment may facilitate induction of LTP by increasing NMDA receptor currents or by enhancing neuronal membrane excitability.…”

Section: Glutamatergic Synaptic Currents and Spike Frequency Accommodmentioning

confidence: 99%

Environmental Enrichment Modifies the PKA-Dependence of Hippocampal LTP and Improves Hippocampus-Dependent Memory

Duffy

Craddock²,

Abel³

et al. 2001

Learn. Mem.

300

211

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cAMP-dependent protein kinase (PKA) is critical for the expression of some forms of long-term potentiation (LTP) in area CA1 of the mouse hippocampus and for hippocampus-dependent memory. Exposure to spatially enriched environments can modify LTP and improve behavioral memory in rodents, but the molecular bases for the enhanced memory performance seen in enriched animals are undefined. We tested the hypothesis that exposure to a spatially enriched environment may alter the PKA dependence of hippocampal LTP. Hippocampal slices from enriched mice showed enhanced LTP following a single burst of 100-Hz stimulation in the Schaffer collateral pathway of area CA1. In slices from nonenriched mice, this single-burst form of LTP was less robust and was unaffected by Rp-cAMPS, an inhibitor of PKA. In contrast, the enhanced LTP in enriched mice was attenuated by Rp-cAMPS. Enriched slices expressed greater forskolin-induced, cAMP-dependent synaptic facilitation than did slices from nonenriched mice. Enriched mice showed improved memory for contextual fear conditioning, whereas memory for cued fear conditioning was unaffected following enrichment. Our data indicate that exposure of mice to spatial enrichment alters the PKA dependence of LTP and enhances one type of hippocampus-dependent memory. Environmental enrichment can transform the pharmacological profile of hippocampal LTP, possibly by altering the threshold for activity-dependent recruitment of the cAMP-PKA signaling pathway following electrical and chemical stimulation. We suggest that experience-dependent plasticity of the PKA dependence of hippocampal LTP may be important for regulating the efficacy of hippocampus-based memory.

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The antagonism of amino acid‐induced excitations of rat hippocampal CA1 neurones in vitro.

Cited by 349 publications

References 39 publications

APP/PS1KI bigenic mice develop early synaptic deficits and hippocampus atrophy

APP/PS1KI bigenic mice develop early synaptic deficits and hippocampus atrophy

Signal transduction pathways involved in the acute potentiation of NMDA responses by 1S,3R‐ACPD in rat hippocampal slices

Environmental Enrichment Modifies the PKA-Dependence of Hippocampal LTP and Improves Hippocampus-Dependent Memory

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