S18986: A positive modulator of AMPA-receptors enhances (S)-AMPA-mediated BDNF mRNA and protein expression in rat primary cortical neuronal cultures

Lockhart, Brian P.; Rodriguez, Marianne; Mourlevat, Sophie; Péron, Philippe; Catesson, Sandra; Villain, Nadège; Galizzi, Jean‐Pierre; Boutin, Jean A.; Lestage, Pierre

doi:10.1016/j.ejphar.2007.01.030

Cited by 18 publications

(8 citation statements)

References 37 publications

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“…It is also known that the kinetics of AMPA-mediated BDNF activation are consistent with the known properties of AMPA receptors (Arai et al, 1996(Arai et al, , 2002Lockhart et al, 2007). In addition, sub-chronic administration of CX691 (an AMPA modulator) has been shown to elevate BDNF mRNA expression in both the whole and CA1 sub-region of the hippocampus (Woolley et al, 2009), while administration of another AMPA modulator (S18986) has been shown to enhance AMPA-mediated BDNF mRNA and protein expression in rat primary cortical neuronal cultures (Lockhart et al, 2007). These results along with ours suggest a close coupling of the AMPA receptor, BDNF and plasticity in the hippocampal-perirhinal projection.…”

Section: Wysssupporting

confidence: 53%

“…Furthermore, our results demonstrating an AMPA-mediated role in plasticity and BDNF changes perhaps should not be too surprising given that activation particularly of the non-NMDA receptors (AMPA and Kainate) result in an increased expression of neurotrophic factors, including BDNF (Zafra et al, 1990(Zafra et al, , 1992, while reciprocally BDNF via the TrkB receptor can increase the expression levels of AMPA receptors (Narisawa-Saito et al, 2002) which can enhance glutamatergic transmission in hippocampal cells (Lessmann et al, 1994;Levine et al, 1998). It is also known that the kinetics of AMPA-mediated BDNF activation are consistent with the known properties of AMPA receptors (Arai et al, 1996(Arai et al, , 2002Lockhart et al, 2007). In addition, sub-chronic administration of CX691 (an AMPA modulator) has been shown to elevate BDNF mRNA expression in both the whole and CA1 sub-region of the hippocampus (Woolley et al, 2009), while administration of another AMPA modulator (S18986) has been shown to enhance AMPA-mediated BDNF mRNA and protein expression in rat primary cortical neuronal cultures (Lockhart et al, 2007).…”

Section: Wyssmentioning

confidence: 83%

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Antagonism of glutamate receptors in the CA1 to perirhinal cortex projection prevents long-term potentiation and attenuates levels of brain-derived neurotrophic factor

Kealy

Commins

2009

Brain Research

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The CA1 to perirhinal cortex projection is one of multiple hippocampal-neocortical projections considered to be involved in memory consolidation. This projection has been shown to sustain long-term potentiation (LTP) following stimulation of CA1. Here we examined the pharmacological properties underpinning the plasticity observed in this projection. A stimulating electrode was inserted into the area CA1 and a recording electrode was inserted into the perirhinal cortex of urethane-anaesthetised Wistar rats. Rats (n = 6 in each drug group) were administered with either saline (0.09%), MK-801 (NMDA antagonist; 0.1 mg/kg) or CNQX (AMPA/kainate antagonist; 1.5 mg/kg). Baseline recordings were made for 10 min by stimulating area CA1 (0.05 Hz stimulation protocol). High-frequency stimulation (HFS; 250 Hz) was performed and post-HFS fEPSP recordings were made for 1 h (0.05 Hz, as above). Baseline and post-HFS paired-pulse facilitation (PPF) recordings were performed across six different interpulse intervals. CA1 and perirhinal cortex tissue samples were taken from the stimulated and unstimulated hemispheres of each rat brain and analysed using a brain-derived neurotrophic factor (BDNF) ELISA. Results indicate that LTP was induced in the saline and MK-801 groups but not in the CNQX group; fEPSPs in the latter group rapidly returned to baseline levels following a short period of post-tetanic potentiation. Drug treatment and HFS had no effect on PPF levels. Drug treatment IntroductionThe hippocampal formation is an important structure for learning and memory (Scoville and Milner, 1957;O'Keefe and Nadel, 1978;Squire, 1992). Although not the actual site of storage for long-term memory, the hippocampal formation acts as the site of association of sensory information (Rolls, 1996) and is required to form long-term memories. Long-term storage is believed to occur in the neocortex with the hippocampal formation acting in an integrative role (Squire et al., 1984;Squire, 1992;McClelland et al., 1995;Squire and Alvarez, 1995). Long-term potentiation (LTP) is a phenomenon first described in the rabbit hippocampus by Bliss and Lømo

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Section: Wysssupporting

confidence: 53%

Section: Wyssmentioning

confidence: 83%

Antagonism of glutamate receptors in the CA1 to perirhinal cortex projection prevents long-term potentiation and attenuates levels of brain-derived neurotrophic factor

Kealy

Commins

2009

Brain Research

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“…Using ELISA, Lockhart et al, (2007) reported that BDNF release remained below detection threshold after 5 h treatment with a different AMPA receptor modulator (S 18986). In contrast, our results indicated a robust CX614-dependent upregulation of BDNF release.…”

Section: Discussionmentioning

confidence: 99%

Positive AMPA Receptor Modulation Rapidly Stimulates BDNF Release and Increases Dendritic mRNA Translation

Jourdi¹,

Hsu²,

Zhou³

et al. 2009

Journal of Neuroscience

202

150

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“…As for its cellular effects, S18986, like other positive AMPAR modulators, would seem to be important for synaptic plasticity underlying learning and memory as it increases long-term potentiation (LTP) induction and maintenance in the hippocampus [1]. Moreover, the drug enhances the expression of cortical and hippocampal brain-derived neurotrophic factor (BDNF) (for references see [1,14]), which regulates neuronal plasticity. In addition to its effects on LTP and BDNF expression, the cognitive-enhancing properties of S18986 may reside in its ability to control the release of several neurotransmitters, as it enhances acetylcholine, noradrenaline and dopamine in the hippocampus and/or frontal cortex [13,17].…”

Section: Introductionmentioning

confidence: 99%

The AMPA receptor modulator S18986 in the prelimbic cortex enhances acquisition and retention of an odor-reward association

Yefimenko

Portero-Tresserra

Martí-Nicolovius

et al. 2013

Neuroscience Letters

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This is a postprint version of the following article: Yefimenko, N. ; Portero-Tresserra, M. ; Martí-Nicolovius, M. ; Gillazo-Blanch, G. ; Vale-Martínez, A. (2013 AbstractSystemic administration of S18986, a positive allosteric modulator of AMPA receptors, improves cognition. The present study further characterizes the drug's memory-enhancing properties and is the first to investigate its intracerebral effects on learning and memory. The results showed that rats receiving a single dose of S18986 (3µg / site) into the prelimbic cortex, prior to olfactory discrimination acquisition, exhibited significantly shorter latencies and fewer errors to make the correct response, both in the acquisition and two drug-free retention tests.Such findings corroborate the involvement of glutamate receptors in odor-reward learning and confirm the role of the AMPAkine S18986 as a cognitive enhancer.

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S18986: A positive modulator of AMPA-receptors enhances (S)-AMPA-mediated BDNF mRNA and protein expression in rat primary cortical neuronal cultures

Cited by 18 publications

References 37 publications

Antagonism of glutamate receptors in the CA1 to perirhinal cortex projection prevents long-term potentiation and attenuates levels of brain-derived neurotrophic factor

Antagonism of glutamate receptors in the CA1 to perirhinal cortex projection prevents long-term potentiation and attenuates levels of brain-derived neurotrophic factor

Positive AMPA Receptor Modulation Rapidly Stimulates BDNF Release and Increases Dendritic mRNA Translation

The AMPA receptor modulator S18986 in the prelimbic cortex enhances acquisition and retention of an odor-reward association

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