Prosencephalic mechanisms of ECoG desynchronization in cerveau isolé cats.
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Biomedical subjects
F Belardetti
Publications and source records attributed to F Belardetti.
Neuronal inhibition by the peptide FMRFamide involves opening of S K+ channels.
Neurotransmitters modulate the activity of ion channels through a variety of second messengers, including cyclic AMP, cyclic GMP and the products of phosphatidylinositol breakdown. Little is known about how different transmitters acting through different second-messenger systems interact within a cell to regulate single ion channels. We here describe the reciprocal actions of serotonin and the molluscan neuropeptide, FMRFamide, on individual K+ channels in Aplysia sensory neurons. In these cells, serotonin causes prolonged all-or-none closure of a class of background conductance K+ channels (the S channels) through cAMP-dependent protein phosphorylation. Using single-channel recording, we have found that FMRFamide produces two actions on the S channels; it increases the probability of opening of the S channels via a cAMP-independent second-messenger system and it reverses the closures of S channels produced by serotonin or cAMP.
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Lipoxygenase metabolites of arachidonic acid as second messengers for presynaptic inhibition of Aplysia sensory cells.
Biochemical and biophysical studies on Aplysia sensory neurons indicate that inhibitory responses to the molluscan peptide FMRFamide are mediated by lipoxygenase metabolites of arachidonic acid. These compounds are a new class of second messengers in neurons.
Animals↗
[Desynchronizing prosencephalic mechanisms in the chronic "brain isolated" cat].
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[Desynchronizing prosencephalic mechanisms in the acute "isolated brain" preparation].
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