Marco Capogna

Presynaptic enhancement of inhibitory synaptic transmission by protein kinases A and C in the rat hippocampus in vitro

Research output: Contribution to journal/Conference contribution in journal/Contribution to newspaperJournal articleResearchpeer-review

Standard

Presynaptic enhancement of inhibitory synaptic transmission by protein kinases A and C in the rat hippocampus in vitro. / Capogna, M; Gähwiler, B H; Thompson, S M.

In: The Journal of neuroscience : the official journal of the Society for Neuroscience, Vol. 15, No. 2, 02.1995, p. 1249-60.

Research output: Contribution to journal/Conference contribution in journal/Contribution to newspaperJournal articleResearchpeer-review

Harvard

Capogna, M, Gähwiler, BH & Thompson, SM 1995, 'Presynaptic enhancement of inhibitory synaptic transmission by protein kinases A and C in the rat hippocampus in vitro', The Journal of neuroscience : the official journal of the Society for Neuroscience, vol. 15, no. 2, pp. 1249-60.

APA

Capogna, M., Gähwiler, B. H., & Thompson, S. M. (1995). Presynaptic enhancement of inhibitory synaptic transmission by protein kinases A and C in the rat hippocampus in vitro. The Journal of neuroscience : the official journal of the Society for Neuroscience, 15(2), 1249-60.

CBE

Capogna M, Gähwiler BH, Thompson SM. 1995. Presynaptic enhancement of inhibitory synaptic transmission by protein kinases A and C in the rat hippocampus in vitro. The Journal of neuroscience : the official journal of the Society for Neuroscience. 15(2):1249-60.

MLA

Capogna, M, B H Gähwiler and S M Thompson. "Presynaptic enhancement of inhibitory synaptic transmission by protein kinases A and C in the rat hippocampus in vitro". The Journal of neuroscience : the official journal of the Society for Neuroscience. 1995, 15(2). 1249-60.

Vancouver

Capogna M, Gähwiler BH, Thompson SM. Presynaptic enhancement of inhibitory synaptic transmission by protein kinases A and C in the rat hippocampus in vitro. The Journal of neuroscience : the official journal of the Society for Neuroscience. 1995 Feb;15(2):1249-60.

Author

Capogna, M ; Gähwiler, B H ; Thompson, S M. / Presynaptic enhancement of inhibitory synaptic transmission by protein kinases A and C in the rat hippocampus in vitro. In: The Journal of neuroscience : the official journal of the Society for Neuroscience. 1995 ; Vol. 15, No. 2. pp. 1249-60.

Bibtex

@article{18062cd4194047699a58ce54a2e8c0aa,
title = "Presynaptic enhancement of inhibitory synaptic transmission by protein kinases A and C in the rat hippocampus in vitro",
abstract = "The protein kinase C activator phorbol 12,13-dibutyrate (0.5 microM, PDBu) and the protein kinase A activator forskolin (20 microM) each increased evoked monosynaptic inhibitory postsynaptic current (IPSC) amplitude, without affecting its reversal potential, and increased the frequency of miniature IPSCs (mIPSCs), without affecting their amplitude or kinetics, as assessed with whole-cell recording form CA3 pyramidal cells in hippocampal slice cultures. The effects of forskolin and PDBu on both evoked IPSC amplitude and mIPSC frequency were additive and were antagonized by inhibitors of protein kinases A and C, respectively. The kinase activator-induced increases in mIPSC frequency were quantitatively comparable to the increases in evoked IPSC amplitude. The increases in mIPSC frequency were not attenuated by the voltage-dependent calcium channel blocker Cd2+ (100 microM). We conclude that stimulation of protein kinases A and C potentiates hippocampal inhibitory synaptic transmission through independent presynaptic mechanisms of action. Kinase-induced potentiation of spontaneous release does not require modulation of axon terminal Ca2+ channels. This mechanism may also contribute substantially to the potentiation of evoked release.",
keywords = "Animals, Cadmium/pharmacology, Colforsin/pharmacology, Cyclic AMP-Dependent Protein Kinases/physiology, Drug Synergism, Electrophysiology, Hippocampus/physiology, In Vitro Techniques, Kinetics, Neural Inhibition/physiology, Phorbol 12,13-Dibutyrate/pharmacology, Presynaptic Terminals/physiology, Protein Kinase C/physiology, Rats, Synaptic Transmission/physiology",
author = "M Capogna and G{\"a}hwiler, {B H} and Thompson, {S M}",
year = "1995",
month = feb,
language = "English",
volume = "15",
pages = "1249--60",
journal = "The Journal of neuroscience : the official journal of the Society for Neuroscience",
issn = "0270-6474",
publisher = "Society for Neuroscience",
number = "2",

}

RIS

TY - JOUR

T1 - Presynaptic enhancement of inhibitory synaptic transmission by protein kinases A and C in the rat hippocampus in vitro

AU - Capogna, M

AU - Gähwiler, B H

AU - Thompson, S M

PY - 1995/2

Y1 - 1995/2

N2 - The protein kinase C activator phorbol 12,13-dibutyrate (0.5 microM, PDBu) and the protein kinase A activator forskolin (20 microM) each increased evoked monosynaptic inhibitory postsynaptic current (IPSC) amplitude, without affecting its reversal potential, and increased the frequency of miniature IPSCs (mIPSCs), without affecting their amplitude or kinetics, as assessed with whole-cell recording form CA3 pyramidal cells in hippocampal slice cultures. The effects of forskolin and PDBu on both evoked IPSC amplitude and mIPSC frequency were additive and were antagonized by inhibitors of protein kinases A and C, respectively. The kinase activator-induced increases in mIPSC frequency were quantitatively comparable to the increases in evoked IPSC amplitude. The increases in mIPSC frequency were not attenuated by the voltage-dependent calcium channel blocker Cd2+ (100 microM). We conclude that stimulation of protein kinases A and C potentiates hippocampal inhibitory synaptic transmission through independent presynaptic mechanisms of action. Kinase-induced potentiation of spontaneous release does not require modulation of axon terminal Ca2+ channels. This mechanism may also contribute substantially to the potentiation of evoked release.

AB - The protein kinase C activator phorbol 12,13-dibutyrate (0.5 microM, PDBu) and the protein kinase A activator forskolin (20 microM) each increased evoked monosynaptic inhibitory postsynaptic current (IPSC) amplitude, without affecting its reversal potential, and increased the frequency of miniature IPSCs (mIPSCs), without affecting their amplitude or kinetics, as assessed with whole-cell recording form CA3 pyramidal cells in hippocampal slice cultures. The effects of forskolin and PDBu on both evoked IPSC amplitude and mIPSC frequency were additive and were antagonized by inhibitors of protein kinases A and C, respectively. The kinase activator-induced increases in mIPSC frequency were quantitatively comparable to the increases in evoked IPSC amplitude. The increases in mIPSC frequency were not attenuated by the voltage-dependent calcium channel blocker Cd2+ (100 microM). We conclude that stimulation of protein kinases A and C potentiates hippocampal inhibitory synaptic transmission through independent presynaptic mechanisms of action. Kinase-induced potentiation of spontaneous release does not require modulation of axon terminal Ca2+ channels. This mechanism may also contribute substantially to the potentiation of evoked release.

KW - Animals

KW - Cadmium/pharmacology

KW - Colforsin/pharmacology

KW - Cyclic AMP-Dependent Protein Kinases/physiology

KW - Drug Synergism

KW - Electrophysiology

KW - Hippocampus/physiology

KW - In Vitro Techniques

KW - Kinetics

KW - Neural Inhibition/physiology

KW - Phorbol 12,13-Dibutyrate/pharmacology

KW - Presynaptic Terminals/physiology

KW - Protein Kinase C/physiology

KW - Rats

KW - Synaptic Transmission/physiology

M3 - Journal article

C2 - 7869096

VL - 15

SP - 1249

EP - 1260

JO - The Journal of neuroscience : the official journal of the Society for Neuroscience

JF - The Journal of neuroscience : the official journal of the Society for Neuroscience

SN - 0270-6474

IS - 2

ER -