PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 2156406

K+ and Ca2+ channel blocking agents increase or decrease stimulus-evoked but not spontaneous quantal transmitter release in sympathetic nerve terminals.

L Stjärne·M Msghina·E Stjärne
View original source ↗Export metadata ↓

Abstract

The source did not provide an abstract. Follow the original record for more information.

Explore related subjects

4-AminopyridineAction PotentialsAdenosine TriphosphateAnimalsCadmiumCalcium Channel BlockersDrug CombinationsElectric StimulationIn Vitro TechniquesMaleMiceNerve EndingsNeuromuscular JunctionNifedipinePotassium ChannelsSympathetic Nervous SystemSynaptic TransmissionTetraethylammonium CompoundsVas DeferensComparative StudyJournal ArticleResearch Support, Non-U.S. Gov't

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

L Stjärne, M Msghina, E Stjärne. 1990. K+ and Ca2+ channel blocking agents increase or decrease stimulus-evoked but not spontaneous quantal transmitter release in sympathetic nerve terminals.. https://doi.org/10.1111/j.1748-1716.1990.tb08838.x

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2026

FGF14 (GAA) repeat expansion-associated Ataxia (SCA27B): Expanding the clinical and diagnostic spectrum from the first genetically confirmed case in Argentina.

Spinocerebellar ataxia 27B (SCA27B), caused by an FGF14 GAA repeat expansion, is an emerging cause of late-onset ataxia. We report the first genetically confirmed Argentinean case, initially misdiagnosed as alcoholic cerebellar degeneration. This case highlights diagnostic challenges, phenotypic heterogeneity, and the importance of genetic testing for this treatable disorder.

4-Aminopyridine↗
PubMed1992

K(+)-channel blockers restore synaptic plasticity in the neuromuscular junction of dunce, a Drosophila learning and memory mutant.

The effects of K(+)-channel blockers on synaptic transmission in dunce (dnc), a Drosophila learning and memory mutant, were investigated. Larvae dnc mutants lack facilitation and post-tetanic potentiation (PTP) at their motor end-plates; dnc mutants are also deficient in a form of phosphodiesterase, and exhibit abnormally high levels of cyclic adenosine 3',5'-monophosphate (cAMP). A two-microelectrode voltage-clamp was used to record end-plate currents and spontaneous end-plate currents from longitudinal ventrolateral third-instar larval muscle. The K(+)-channel blockers 3,4-diaminopyridine (3,4-DAP) and tetraethylammonium (TEA), at micromolar concentrations, caused a reversible decrease in end-plate current amplitudes both in wild-type and mutant end-plates. In the presence of blockers, a period of high-frequency stimulation (tetanus) of the nerve gave way to a transient increase in the end-plate currents of dnc mutants resembling facilitation and PTP in normal end-plates; 3,4-DAP and TEA also restored facilitation and PTP in normal end-plates after incubation with a non-hydrolysable analogue of cAMP (8Br-cAMP). It is suggested that a specific K+ conductance might be relevant to the lack of synaptic plasticity at the dnc neuromuscular synapses.

4-Aminopyridine↗
PubMed1992

Modulation by GABAB receptors of spontaneous synchronous activities induced by 4-aminopyridine in the rat hippocampus.

Field potential recordings were made in the CA3 and/or CA1 subfields of rat hippocampal slices maintained in vitro during perfusion with medium containing the convulsant drug 4-aminopyridine (4AP, 50 microM). In this experimental condition, spontaneous interictal epileptiform discharges caused by the activation of excitatory amino acid receptors and synchronous, GABA-mediated potentials occurred regularly in both areas. Interictal discharges and GABA-mediated potentials were reduced and eventually abolished in both subfields by bath application of baclofen (0.5-100 microM), which is a selective agonist for the GABAB receptor. However, interictal epileptiform events disappeared in the presence of baclofen concentrations (i.e., 4.75 +/- 0.7 microM; IC50 = 3.4 microM; n = 9) that were lower than those required for abolishing the GABA-mediated potential (i.e., 96.1 +/- 19.4 microM; IC50 = 9.8 microM; n = 12). The effects of baclofen were antagonized by the GABAB receptor antagonists saclofen (1 mM; n = 3 slices) or CGP 35348 (0.2-1 mM; IC50 = 240 microM; n = 12 slices). Our findings indicate that activation of GABAB receptors by baclofen inhibits both types of 4AP-induced activities in the rat hippocampus although epileptiform discharges appear to be more sensitive than GABA-mediated potentials to this pharmacological procedure. Although our data do not indicate whether the action of baclofen is pre- or postsynaptic, they demonstrate that this mechanism is sensitive to available GABAB receptor antagonists.

4-Aminopyridine↗