Answers are grounded in this paper and cite their sources.
In many neurons, transmitter release from presynaptic terminals is triggered by Ca2+ entry via dihydropyridine-insensitive Ca2+ channels. We have looked for cDNAs for such channels in the nervous system of the marine ray Discopyge ommata. One cDNA (doe-2) is similar to dihydropyridine-sensitive L-type channels, and two cDNAs (doe-1 and doe-4) are similar to the subfamily of dihydropyridine-insensitive non-L-type channels. doe-4, which encodes a protein of 2326 aa, most closely resembles a previously cloned N-type channel. doe-1, which encodes a protein of 2223 aa, is a member of a separate branch of the non-L-type channels. Northern blot analysis reveals that doe-1 is abundant in the forebrain. doe-4 is more plentiful in the electric lobe and, therefore, may control neurotransmitter release in motor nerve terminals. These results show that the familial pattern of Ca(2+)-channel genes has been preserved from a stage in evolution before the divergence of higher and lower vertebrates > 400 million years ago. The cloning of these channels may be a useful starting point for elucidating the role of the Ca2+ channels in excitation-secretion coupling in nerve terminals.
No takes yet. Share an insight, caveat, or question.
Horne et al. (1993) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: