Cholinergic nerve terminals contain ascorbic acid which induces Ca2+-dependent release of acetylcholine and ATP from isolated Torpedo synaptic vesicles.

نویسندگان

  • I Pinchasi
  • D M Michaelson
  • M Sokolovsky
چکیده

We have shown that a soluble, low-molecular weight, alkali-labile and oxidation-sensitive factor, prepared from the electric organ of Torpedo ocellata, induces Cap-dependent acetylcholine (ACh) release from isolated Torpedo synaptic vesicles [ 1,2]. Diverse activities of ascorbic acid in the brain have been reported [3-81. These include effects on metabolism of biogenic amines [9] and on release of neurotransmitters from isolated mammalian vesicles [lo]. We therefore tested the possibility that ascorbic acid may be the soluble factor present in Torpedo and thus a naturally-occurring mediator of ACh release in vivo.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Individual synaptic vesicles from the electroplaque of Torpedo californica, a classic cholinergic synapse, also contain transporters for glutamate and ATP

The type of neurotransmitter secreted by a neuron is a product of the vesicular transporters present on its synaptic vesicle membranes and the available transmitters in the local cytosolic environment where the synaptic vesicles reside. Synaptic vesicles isolated from electroplaques of the marine ray, Torpedo californica, have served as model vesicles for cholinergic neurotransmission. Many lin...

متن کامل

Botulinum toxin type A blocks the morphological changes induced by chemical stimulation on the presynaptic membrane of Torpedo synaptosomes.

The action of botulinum neurotoxin on acetylcholine release, and on the structural changes at the presynaptic membrane associated with the transmitter release, was studied by using a subcellular fraction of cholinergic nerve terminals (synaptosomes) isolated from the Torpedo electric organ. Acetylcholine and ATP release were continuously monitored by chemiluminescent methods. To catch the membr...

متن کامل

Transmitter release from presynaptic terminals of electric organ: inhibition by the calcium channel antagonist omega Conus toxin.

Cholinergic synaptosomes from electroplax of the ray Ommata discopyge release both ATP and ACh when depolarized with high K+ concentration in the presence of Ca2+. Others have shown that the ATP and ACh are released in the molar ratio found in isolated synaptic vesicles. Thus, it is assumed that the release of ATP reflects exocytosis of synaptic vesicles, and that transmitter release can be ind...

متن کامل

An essential role for a small synaptic vesicle-associated phosphatidylinositol 4-kinase in neurotransmitter release.

Glutamate release from nerve terminals is the consequence of Ca2+-triggered fusion of small synaptic vesicles with the presynaptic plasma membrane. ATP dependence of neurotransmitter release has been suggested to be founded, in part, on phosphorylation steps preceding membrane fusion. Here we present evidence for an essential role of phosphatidylinositol phosphorylation in stimulated release of...

متن کامل

Mefloquine selectively increases asynchronous acetylcholine release from motor nerve terminals.

Effectiveness against chloroquine-resistant Plasmodia makes mefloquine a widely used antimalarial drug. However, mefloquine's neurologic effects offset this therapeutic advantage. Cellular actions which might contribute to the neurologic effects of mefloquine are not understood. Structural similarity to tacrine suggested that mefloquine might alter cholinergic synaptic transmission. Therefore, ...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:
  • FEBS letters

دوره 108 1  شماره 

صفحات  -

تاریخ انتشار 1979