Quantal analysis of paired-pulse facilitation in guinea pig hippocampal slices

Hess, Grzegorz; Kuhnt, U.; Voronin, L. L.

doi:10.1016/0304-3940(87)90584-2

Cited by 121 publications

(72 citation statements)

References 11 publications

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“…Paired-pulse facilitation, a short-term synaptic plasticity relying on presynaptic mechanisms (Hess et al, 1987), was unchanged in Thy 1/ PN-1 mice as well. These results suggest that overexpression of PN-1 does not interfere with presynaptic release processes.…”

Section: Ltp In Thy 1/pn-1 Micementioning

confidence: 90%

Endogenous Serine Protease Inhibitor Modulates Epileptic Activity and Hippocampal Long-Term Potentiation

et al. 1997

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Protease nexin-1 (PN-1), a member of the serpin superfamily, controls the activity of extracellular serine proteases and is expressed in the brain. Mutant mice overexpressing PN-1 in brain under the control of the Thy-1 promoter (Thy 1/PN-1) or lacking PN-1 (PN-1Ϫ/Ϫ) were found to develop epileptic activity in vivo and in vitro. Theta burst-induced long-term potentiation (LTP) and NMDA receptor-mediated synaptic transmission in the CA1 field of hippocampal slices were augmented in Thy 1/PN-1 mice and reduced in PN-1Ϫ/Ϫ mice. Compensatory changes in GABA-mediated inhibition in Thy 1/PN-1 mice suggest that altered brain PN-1 levels lead to an imbalance between excitatory and inhibitory synaptic transmission.

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Section: Ltp In Thy 1/pn-1 Micementioning

confidence: 90%

Endogenous Serine Protease Inhibitor Modulates Epileptic Activity and Hippocampal Long-Term Potentiation

et al. 1997

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“…Evidence for this comes from examining quantal parameters (5,(31)(32)(33)(34)(35), presynaptic calcium transients during PPF (36), and the effect of altering membrane potential (37), and from finding that maneuvers that alter p are associated with changes in PPF (11,12,38). However, there is also evidence for a postsynaptic component to its expression (39).…”

Section: Resultsmentioning

confidence: 99%

Long-term potentiation involves increases in the probability of neurotransmitter release

Schulz

1997

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

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Biochemistry. In the article ''Identification by mass spectrometry of the phosphorylated residue responsible for activation of the catalytic domain of myosin I heavy chain kinase, a member of the PAK͞STE20 family'' by Joanna Szczepanowska, Xiaolong Zhang, Christopher J. Herring, Jun Qin, Edward D. Korn, and Hanna Brzeska, which appeared in number 16, August 5, 1997, of Proc. Natl. Acad. Sci. USA (94,(8503)(8504)(8505)(8506)(8507)(8508), the authors wish to note that in Fig. 3, the ions of m͞z 1345.3 and 1247.1 were incorrectly identified as b 13 and b 13 ⌬ , respectively, produced by cleavage of the peptide AS(Pi)VVGTTYW-MAPEVVK between E and V (Fig. 3 Inset). In fact, these ions are b 12 and b 12 ⌬ , produced by cleavage of the peptide between P and E. This correction has no effect on the conclusion that the phosphorylated residue is serine. Also, in Table 2, reference numbers 22-24 should be 21-23 (the reference in the legend is cited correctly) and the MIHCK sequence is from residue 624 to residue 638.Cell Biology. In the article ''Subtraction hybridization identifies a transformation progression-associated gene PEG-3 with sequence homology to a growth arrest and DNA damageinducible gene'' by Zao

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“…PPF is widely regarded to be a measure of presynaptic efficacy (Hess et al, 1987;Zucker and Regehr, 2002). Thus, the small increase in PPF in ␤-adducin knock-out mice is likely to represent an increase in presynaptic neurotransmitter release.…”

Section: Discussionmentioning

confidence: 99%

Impaired Synaptic Plasticity and Learning in Mice Lacking β-Adducin, an Actin-Regulating Protein

Rabenstein¹,

Addy²,

Caldarone³

et al. 2005

J. Neurosci.

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The adducin family of proteins interacts with the actin cytoskeleton and the plasma membrane in a calcium-and cAMP-dependent manner. Thus, adducins may be involved in changes in cytoskeletal organization resulting from synaptic stimulation. ␤-Adducin knockout mice were examined in physiological and behavioral paradigms related to synaptic plasticity to elucidate the role the adducin family plays in processes underlying learning and memory. In situ hybridization for ␣-and ␤-adducin demonstrates that these mRNAs are found throughout the brain, with high levels of expression in the hippocampus. Schaffer collateral-CA1 tetanic long-term potentiation decayed rapidly in acute hippocampal slices from ␤-adducin knock-out mice, although baseline spine morphology and postsynaptic density were normal. Interestingly, the input-output relationship was significantly increased in hippocampal slices from ␤-adducin knock-out mice. Furthermore, ␤-adducin knock-out mice were impaired in performance of fear conditioning and the water maze paradigm. The current results indicate that ␤-adducin may play an important role in the cellular mechanisms underlying activitydependent synaptic plasticity associated with learning and memory.

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Quantal analysis of paired-pulse facilitation in guinea pig hippocampal slices

Cited by 121 publications

References 11 publications

Endogenous Serine Protease Inhibitor Modulates Epileptic Activity and Hippocampal Long-Term Potentiation

Endogenous Serine Protease Inhibitor Modulates Epileptic Activity and Hippocampal Long-Term Potentiation

Long-term potentiation involves increases in the probability of neurotransmitter release

Impaired Synaptic Plasticity and Learning in Mice Lacking β-Adducin, an Actin-Regulating Protein

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