fmrfamide and 2-5-di-tert-butylhydroquinone

fmrfamide has been researched along with 2-5-di-tert-butylhydroquinone* in 1 studies

Other Studies

1 other study(ies) available for fmrfamide and 2-5-di-tert-butylhydroquinone

Article	Year
Involvement of Ca2+ uptake by a reticulum-like store in the control of transmitter release. Neuroscience, 1992, Volume: 50, Issue:2 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. Topics: Animals; Antioxidants; Aplysia; Calcium; Egtazic Acid; Endoplasmic Reticulum; Evoked Potentials; FMRFamide; Ganglia; Hydroquinones; In Vitro Techniques; Neurons; Neuropeptides; Synapses; Synaptic Transmission	1992

Article

Year

Involvement of Ca2+ uptake by a reticulum-like store in the control of transmitter release.

Neuroscience, 1992, Volume: 50, Issue:2

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.

Topics: Animals; Antioxidants; Aplysia; Calcium; Egtazic Acid; Endoplasmic Reticulum; Evoked Potentials; FMRFamide; Ganglia; Hydroquinones; In Vitro Techniques; Neurons; Neuropeptides; Synapses; Synaptic Transmission

1992