A Pertussis Toxin-Sensitive G Protein in Hippocampal Long-Term Potentiation

Goh, Joanne W.; Pennefather, Peter

doi:10.1126/science.2543072

Cited by 112 publications

(35 citation statements)

References 36 publications

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“…Recent evidence shows that mGluR is involved in the long-term potentiation (LTP) of the excitatory postsynaptic potential (EPSP) in the hippocampal CAl region (Reymann & Matthies, 1989;Izumi et al 1991). Since IAP treatment inhibits LTP induction in hippocampal slices (Goh & Pennefather, 1989), the IAPinsensitive, mGluR-induced IK(ca) in the present preparation might not be involved in LTP. Though it has been reported that 10-5 M tACPD potentiated LTP in the CAl region (McGuinness et al 1991), the concentration used in that work is near the threshold concentration (Fig.…”

Section: Discussionmentioning

confidence: 87%

Metabotropic glutamate response in acutely dissociated hippocampal CA1 pyramidal neurones of the rat.

Shirasaki

Harata

Akaike

1994

The Journal of Physiology

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1. The metabotropic glutamate (mGlu) response was investigated in dissociated rat hippocampal CAI pyramidal neurones using conventional and nystatin-perforated whole-cell modes of the patch recording configuration. 2. In the perforated patch recording configuration, the application of glutamate (Glu), quisqualate (QA), aspartate (Asp) and N-methyl-D-aspartate (NMDA) induced a slow outward current superimposed on a fast ionotropic inward current, whereas a-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) and kainate (KA) induced only an ionotropic inward current at a holding potential (VH) of -20 mV. A specific agonist of the mGlu receptor (mGluR), trans-1-aminocyclopentane-1,3-dicarboxylate (tACPD), induced an outward current in -80 % of the neurones tested. Asp-and NMDA-induced outward currents were antagonized by D-2-amino-5-phosphonopentanoate (D-AP5) whereas Glu-, QA-and tACPD-induced outward currents were not antagonized by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), 6,7-dinitroquinoxaline-2,3-dione (DNQX) and D-AP5, indicating that the mGlu response is an outward current component. 3. L-2-Amino-3-phosphonopropionate (L-AP3) and DL-2-amino-4-phosphonobutyrate (AP4) did not block the mGlu response. 4. The relative potencies of mGlu agonists were QA > Glu > tACPD. The threshold and EC50 values of metabotropic outward currents were 10-100 times lower than those of the ionotropic inward current (iGlu response).5. The reversal potential of the mGlu response (Emaju) was close to EK (K+ equilibrium potential), and it shifted 59*5 mV for a tenfold change in extracellular K+ concentration.6. In Ca2"-free external solution, the mGlu response was elicited by an initial application of Glu, but subsequent applications failed to induce the response. There was also an increase in the intracellular free Ca21 concentration ([Ca2+]1) during the application of Glu and QA but not of AMPA, indicating Ca2" release from an intracellular Ca2+ store. 7. During the activation of a Ca2"-dependent K+ current (IK(ca)) by inositol trisphosphate (IP3) in the internal solution, the mGlu response was suppressed. Addition of GDP-,b-S, neomycin or heparin to the internal solution also suppressed the mGlu response, but staurosporine had no effect. The mGlu response was abolished by pretreatment with either caffeine or ryanodine, but treatment with pertussis toxin (IAP) for 6-8 h had no effect.

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Section: Discussionmentioning

confidence: 87%

Metabotropic glutamate response in acutely dissociated hippocampal CA1 pyramidal neurones of the rat.

Shirasaki

Harata

Akaike

1994

The Journal of Physiology

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“…Infusions were 1 mL/side at 0.4 mL/ min, and the injection cannula was left in place for 30 sec before the mouse was returned to its home cage. Because studies indicate that the effects of PTx are best evaluated 3 d after infusion (Goh and Pennefather 1989;Stratton et al 1989), PTx was infused 3 d before testing. To minimize potential effects of PTx on conditioning, training was administered the day after PTx infusion, and testing was performed 2 d after training.…”

Section: Dorsal Hippocampus Infusionmentioning

confidence: 99%

“…Because PTx can take several days to be fully effective in the hippocampus in vivo (Goh and Pennefather 1989;Stratton et al 1989), PTx was infused into the DH 1 d before fear conditioning to minimize potential effects on acquisition and consolidation. Mice were then tested 2 d after conditioning.…”

Section: Pertussis Toxin Blocks the Impairing Effects Of Xamoterol Onmentioning

confidence: 99%

Xamoterol impairs hippocampus-dependent emotional memory retrieval via G_i/o-coupled β₂-adrenergic signaling

Schutsky¹,

Ouyang²,

Thomas³

2011

Learn. Mem.

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Xamoterol, a partial b 1 -adrenergic receptor agonist, has been reported to impair the retrieval of hippocampus-dependent spatial reference memory in rats. In contrast, xamoterol restores memory retrieval in gene-targeted mice lacking norepinephrine (NE) and in a transgenic mouse model of Down syndrome in which NE levels are reduced. Restoration of retrieval by xamoterol in these two models complements the observation that NE and b 1 signaling are required for hippocampusdependent retrieval of contextual and spatial reference memory in wild-type mice and rats. Additional evidence indicates that cAMP-mediated PKA and Epac signaling are required for the retrieval of hippocampus-dependent memory. As a result, we hypothesized that xamoterol has effects in addition to the stimulation of b 1 receptors that, at higher doses, act to counter the effects of b 1 signaling. Here we report that xamoterol-induced disruption of memory retrieval depends on b 2 -adrenergic receptor signaling. Interestingly, the impairment of memory retrieval by xamoterol is blocked by pretreatment with pertussis toxin, an uncoupling agent for G i/o signaling, suggesting that b 2 signaling opposes b 1 signaling during memory retrieval at the level of G protein and cAMP signaling. Finally, similar to the time-dependent roles for NE, b 1 , and cAMP signaling in hippocampus-dependent memory retrieval, xamoterol only impairs retrieval for several days after training, indicating that its effects are also limited by the age of the memory. We conclude that the disruption of memory retrieval by xamoterol is mediated by G i/o -coupled b 2 signaling, which opposes the G s -coupled b 1 signaling that is transiently required for hippocampus-dependent emotional memory retrieval.

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“…They are composed of three subunits, namely Gα, Gβ, and Gγ. In mammals, signals transduced by these components are essential for a broad range of biological events, such as long term potentiation in neural communication (Goh and Pennefather, 1989) and immune responses (Ngai et al, 2008) as well as endocrine regulation (Landis et al, 1989). In rice plants, mutants of the Gα gene (RGA1), which is a single copy gene in the rice genome (Ishikawa et al, 1995), are called d1 (Ashikari et al, 1999;Fujisawa et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

Study of novel d1 alleles, defective mutants of the .ALPHA. subunit of heterotrimeric G-protein in rice

et al. 2009

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It has been shown that the disruption of the α-subunit gene of heterotorimeric G-proteins (Gα) results in dwarf traits, the erection of leaves and the setting of small seeds in rice. These mutants are called d1. We have studied the expression profiles of the transcripts and translation products of rice Gα in ten alleles of d1 including five additional alleles newly identified. By RT-PCR, the transcripts of the Gα gene were detected in the all d1 alleles. By western blot, the Gα proteins were not detected in the plasma membrane fractions of the d1 alleles with the exception of d1-4. In d1-4, one amino acid change in the GTP-binding box A of the Gα protein was occurred and even in this case the Gα protein was only just detectable in the plasma membrane fraction. Given that the Gα protein did not accumulate in the plasma membrane fraction in d1-8 which has a deletion of just a single amino acid in the Gα protein, it is likely that a proper conformation of the Gα is necessary for accumulation of Gα protein in the plasma membrane. Nine alleles of d1 showed a severer phenotype whilst d1-4 exhibited a mild phenotype with respect to seed size and elongation pattern of internodes. As brassinosteroid signaling was known to be partially impaired in d1s, the sensitivity to 24-epibrassinolide (24-epiBL) was compared among d1 alleles in a T65 genetic background. Only d1-4 showed responses similar to wild type rice. The results show that the d1-4 mutant is a mild allele in terms of the phenotype and mild hyposensitivity to the exogenously applied 24-epiBL.

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A Pertussis Toxin-Sensitive G Protein in Hippocampal Long-Term Potentiation

Cited by 112 publications

References 36 publications

Metabotropic glutamate response in acutely dissociated hippocampal CA1 pyramidal neurones of the rat.

Metabotropic glutamate response in acutely dissociated hippocampal CA1 pyramidal neurones of the rat.

Xamoterol impairs hippocampus-dependent emotional memory retrieval via G_i/o-coupled β₂-adrenergic signaling

Study of novel d1 alleles, defective mutants of the .ALPHA. subunit of heterotrimeric G-protein in rice

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A Pertussis Toxin-Sensitive G Protein in Hippocampal Long-Term Potentiation

Cited by 112 publications

References 36 publications

Metabotropic glutamate response in acutely dissociated hippocampal CA1 pyramidal neurones of the rat.

Metabotropic glutamate response in acutely dissociated hippocampal CA1 pyramidal neurones of the rat.

Xamoterol impairs hippocampus-dependent emotional memory retrieval via Gi/o-coupled β2-adrenergic signaling

Study of novel d1 alleles, defective mutants of the .ALPHA. subunit of heterotrimeric G-protein in rice

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Xamoterol impairs hippocampus-dependent emotional memory retrieval via G_i/o-coupled β₂-adrenergic signaling