Ca2+ influx through voltage sensitive Ca2+ channels produces a rise in intracellular-free Ca2+, [Ca2+](i), that serves as a trigger for the release of neurotransmitters. We measured [Ca2+](i), in primary cultures of superior cervical ganglion (SCG) neurons of the rat using 2-(6-(bis(carboxymethyl)amino)-5-methylphenoxy)ethoxy-2-benzofuranyl) -oxazole carboxylic acids-based microfluorimetry. Recordings were obtained from either single or small bundles of neuronal processes and compared with recordings from single neuronal cell bodies. Depolarization with 50 mM K+ produced a rapid increase in [Ca2+](i) consisting of both transient and sustained components. This response pattern was seen in recordings from both the soma and processes of SCG neurons. The entire response could be reversibly blocked by 30 μM La3+. Nitrendipine, 1 μM, inhibited the response by 52 ± 7% and 49 ± 7% in the soma and processes, respectively. The dihydropyridine (HPD) agonist 1,4-dihydro-2,-dimethyl-3-nitro-4-(2-trifluoromethylphenyl)-pyridine- -carboxylic acid methyl ester enhanced depolarization-induced increases in [Ca2+](i) in both regions of the neuron. The transient component of the response was greatly reduced by predepolarization, and the remaining sustained component was inhibited 77 ± 7% by nitrendipine (1 μM). These data demonstrate that both DHP-sensitive and -insensitive Ca2+ channels are present in processes as well as cell bodies of SCG neurons. The importance of these findings is discussed in relation to the insenstivity of neurotransmitter release from sympathetic neurons to DHP antagonists.
|Original language||English (US)|
|Number of pages||8|
|State||Published - 1987|