Involvement of Ca2+ uptake by a reticulum-like store in the control of transmitter release.
At an identified neuro-neuronal synapse of Aplysia, 2,5-diterbutyl 1,4-benzohydroquinone, a selective blocker of the reticulum Ca2+ pump, was found to potentiate evoked quantal release of acetylcholine through an increased accumulation of Ca2+ in the presynaptic neuron during depolarization without any accompanying changes in the presynaptic Ca2+ current. We conclude that a rapid Ca2+ buffering system, similar to that associated with the endoplasmic reticulum, must be present in the nerve terminal and play a role in the control of Ca2+ which reaches the release system.
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Laboratoire de Neurobiologie Cellulaire et Moléculaire, C.N.R.S., Gif-sur-Yvette, France.
Baux
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Trudeau
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Tauc
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D000818:Animals; D000975:Antioxidants / Q000494:pharmacology; D001048:Aplysia; D002118:Calcium / Q000378:metabolism*; D004533:Egtazic Acid / Q000494:pharmacology; D004721:Endoplasmic Reticulum / Q000378:metabolism*; D005071:Evoked Potentials / Q000187:drug effects; D019835:FMRFamide; D005724:Ganglia / Q000502:physiology; D006873:Hydroquinones / Q000494:pharmacology*; D066298:In Vitro Techniques; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D009479:Neuropeptides / Q000494:pharmacology; D013569:Synapses / Q000187:drug effects / Q000502:physiology*; D009435:Synaptic Transmission / Q000187:drug effects*
D000975:Antioxidants; D006873:Hydroquinones; D009479:Neuropeptides; C019359:2,5-di-tert-butylhydroquinone; D004533:Egtazic Acid; D019835:FMRFamide; D002118:Calcium