Marco Capogna

Presynaptic inhibition of calcium-dependent and -independent release elicited with ionomycin, gadolinium, and alpha-latrotoxin in the hippocampus

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Presynaptic inhibition of calcium-dependent and -independent release elicited with ionomycin, gadolinium, and alpha-latrotoxin in the hippocampus. / Capogna, M; Gähwiler, B H; Thompson, S M.

In: Journal of Neurophysiology, Vol. 75, No. 5, 05.1996, p. 2017-28.

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Capogna, M ; Gähwiler, B H ; Thompson, S M. / Presynaptic inhibition of calcium-dependent and -independent release elicited with ionomycin, gadolinium, and alpha-latrotoxin in the hippocampus. In: Journal of Neurophysiology. 1996 ; Vol. 75, No. 5. pp. 2017-28.

Bibtex

@article{a27d00a637f64341b0081da255ee3ea0,
title = "Presynaptic inhibition of calcium-dependent and -independent release elicited with ionomycin, gadolinium, and alpha-latrotoxin in the hippocampus",
abstract = "1. Presynaptic inhibition of synaptic transmission in the hippocampus was investigated by comparing the effects of several agonists on miniature excitatory and inhibitory postsynaptic currents (mEPSCs and mIPSCs). 2. The Ca2+ ionophore ionomycin increased the frequency of mEPSCs and mIPSCs but did not affect their amplitude. Ionomycin-induced release required extracellular Ca2+ and was prevented by pretreatment with botulinum neurotoxin serotype F, like evoked synaptic transmission. Unlike evoked transmission, however, this increase did not involve activation of voltage-dependent Ca2+ channels because it was insensitive to Cd2+. 3. Both the lanthanide gadolinium and alpha-latrotoxin produced increases in the frequency of mEPSCs and mIPSCs, but their actions were independent of extracellular Ca2+. 4. Adenosine, the gamma-aminobutyric acid-B (GABAB) receptor agonist baclofen, and a mu-opioid receptor agonist strongly reduced the frequency of synaptic currents triggered by all three secretagogues. 5. We conclude that activation of these presynaptic receptors can reduce high frequencies of vesicular glutamate and GABA release by directly impairing transmitter exocytosis. Presynaptic inhibition of gadolinium- and alpha-latrotoxin-induced release indicates that this impairment occurs without changes in intraterminal Ca2+ homeostasis and when vesicle fusion is rendered Ca2+ independent, respectively. 6. The inhibition of ionomycin-induced release provides additional evidence for a direct, neurotransmitter receptor-mediated modulation of the proteins underlying vesicular docking or fusion as an important component of presynaptic inhibition of evoked synaptic transmission.",
keywords = "Adenosine/pharmacology, Animals, Baclofen/pharmacology, Botulinum Toxins/pharmacology, Calcium/physiology, Calcium Channels/drug effects, Cardiovascular Agents/pharmacology, D-Ala(2),MePhe(4),Met(0)-ol-enkephalin/pharmacology, Depression, Chemical, Extracellular Space/drug effects, GABA Agonists/pharmacology, Gadolinium/pharmacology, Hippocampus/drug effects, In Vitro Techniques, Ionomycin/pharmacology, Ionophores/pharmacology, Neurotransmitter Agents/metabolism, Patch-Clamp Techniques, Rats, Receptors, Presynaptic/agonists, Spider Venoms/pharmacology, Synaptic Transmission/drug effects",
author = "M Capogna and G{\"a}hwiler, {B H} and Thompson, {S M}",
year = "1996",
month = may,
doi = "10.1152/jn.1996.75.5.2017",
language = "English",
volume = "75",
pages = "2017--28",
journal = "Journal of Neurophysiology",
issn = "0022-3077",
publisher = "American Physiological Society",
number = "5",

}

RIS

TY - JOUR

T1 - Presynaptic inhibition of calcium-dependent and -independent release elicited with ionomycin, gadolinium, and alpha-latrotoxin in the hippocampus

AU - Capogna, M

AU - Gähwiler, B H

AU - Thompson, S M

PY - 1996/5

Y1 - 1996/5

N2 - 1. Presynaptic inhibition of synaptic transmission in the hippocampus was investigated by comparing the effects of several agonists on miniature excitatory and inhibitory postsynaptic currents (mEPSCs and mIPSCs). 2. The Ca2+ ionophore ionomycin increased the frequency of mEPSCs and mIPSCs but did not affect their amplitude. Ionomycin-induced release required extracellular Ca2+ and was prevented by pretreatment with botulinum neurotoxin serotype F, like evoked synaptic transmission. Unlike evoked transmission, however, this increase did not involve activation of voltage-dependent Ca2+ channels because it was insensitive to Cd2+. 3. Both the lanthanide gadolinium and alpha-latrotoxin produced increases in the frequency of mEPSCs and mIPSCs, but their actions were independent of extracellular Ca2+. 4. Adenosine, the gamma-aminobutyric acid-B (GABAB) receptor agonist baclofen, and a mu-opioid receptor agonist strongly reduced the frequency of synaptic currents triggered by all three secretagogues. 5. We conclude that activation of these presynaptic receptors can reduce high frequencies of vesicular glutamate and GABA release by directly impairing transmitter exocytosis. Presynaptic inhibition of gadolinium- and alpha-latrotoxin-induced release indicates that this impairment occurs without changes in intraterminal Ca2+ homeostasis and when vesicle fusion is rendered Ca2+ independent, respectively. 6. The inhibition of ionomycin-induced release provides additional evidence for a direct, neurotransmitter receptor-mediated modulation of the proteins underlying vesicular docking or fusion as an important component of presynaptic inhibition of evoked synaptic transmission.

AB - 1. Presynaptic inhibition of synaptic transmission in the hippocampus was investigated by comparing the effects of several agonists on miniature excitatory and inhibitory postsynaptic currents (mEPSCs and mIPSCs). 2. The Ca2+ ionophore ionomycin increased the frequency of mEPSCs and mIPSCs but did not affect their amplitude. Ionomycin-induced release required extracellular Ca2+ and was prevented by pretreatment with botulinum neurotoxin serotype F, like evoked synaptic transmission. Unlike evoked transmission, however, this increase did not involve activation of voltage-dependent Ca2+ channels because it was insensitive to Cd2+. 3. Both the lanthanide gadolinium and alpha-latrotoxin produced increases in the frequency of mEPSCs and mIPSCs, but their actions were independent of extracellular Ca2+. 4. Adenosine, the gamma-aminobutyric acid-B (GABAB) receptor agonist baclofen, and a mu-opioid receptor agonist strongly reduced the frequency of synaptic currents triggered by all three secretagogues. 5. We conclude that activation of these presynaptic receptors can reduce high frequencies of vesicular glutamate and GABA release by directly impairing transmitter exocytosis. Presynaptic inhibition of gadolinium- and alpha-latrotoxin-induced release indicates that this impairment occurs without changes in intraterminal Ca2+ homeostasis and when vesicle fusion is rendered Ca2+ independent, respectively. 6. The inhibition of ionomycin-induced release provides additional evidence for a direct, neurotransmitter receptor-mediated modulation of the proteins underlying vesicular docking or fusion as an important component of presynaptic inhibition of evoked synaptic transmission.

KW - Adenosine/pharmacology

KW - Animals

KW - Baclofen/pharmacology

KW - Botulinum Toxins/pharmacology

KW - Calcium/physiology

KW - Calcium Channels/drug effects

KW - Cardiovascular Agents/pharmacology

KW - D-Ala(2),MePhe(4),Met(0)-ol-enkephalin/pharmacology

KW - Depression, Chemical

KW - Extracellular Space/drug effects

KW - GABA Agonists/pharmacology

KW - Gadolinium/pharmacology

KW - Hippocampus/drug effects

KW - In Vitro Techniques

KW - Ionomycin/pharmacology

KW - Ionophores/pharmacology

KW - Neurotransmitter Agents/metabolism

KW - Patch-Clamp Techniques

KW - Rats

KW - Receptors, Presynaptic/agonists

KW - Spider Venoms/pharmacology

KW - Synaptic Transmission/drug effects

U2 - 10.1152/jn.1996.75.5.2017

DO - 10.1152/jn.1996.75.5.2017

M3 - Journal article

C2 - 8734600

VL - 75

SP - 2017

EP - 2028

JO - Journal of Neurophysiology

JF - Journal of Neurophysiology

SN - 0022-3077

IS - 5

ER -