Pharmacological dissection of receptor-associated and voltage-sensitive ionic channels involved in catecholamine release

P-type Ca2+ channels mediate excitatory and inhibitory synaptic transmitter release in crayfish muscle.

“…While at reptilian, amphibian, and avian synapses the sensitivity of transmitter release to w-CgTX suggests the involvement of the N-type VDCC (9)(10)(11)(12)(13)(14), hormone release from rat neurohypophysis (18) and bovine chromaffm cells (16) and substance P release from rat dorsal root ganglia neurons (15) involved in transmitter release at both invertebrate (3) and mammalian neuromuscular synapses (22) and at mammalian central synapses (22,26), since they are insensitive to co-CgTX or DHP (19-21, 24, 25) and are inhibited by FTX or co-Aga-IVA. Our results indicate that invertebrate excitatory neuromuscular transmission is mediated by P-type VDCCs and provide original evidence indicating that these channels are also involved in invertebrate inhibitory neuromuscular transmission.…”

“…It has also been proposed that norepinephrine release from rat sympathetic neurons is mediated by the N-type VDCC (15). In contrast, both catecholamine and substance P released from bovine chromaffm cells and rat dorsal root ganglia neurons, respectively, are strongly inhibited by DHPs (16)(17)(18), suggesting a major participation of the L-type VDCC. However, while mammalian neuromuscular transmission is insensitive to either w-CgTX or DHPs (19)(20)(21), evoked synaptic transmission in squid giant synapse (3) and mammalian neuromuscular system (22) has been found to be inhibited by FTX and by its synthetic arginine-polyamine (spermidine) analogue (sFTX) (22,23), consistent with a key involvement of the P-type VDCC.…”

Modulation of secretion by dopamine involves decreases in calcium and nicotinic currents in bovine chromaffin cells.

“…In bovine chromaffin cells, it is well known that cholinergic agonists induce opening of ion channels associated with nicotinic receptors, giving rise to Na+ influx (Kilpatrick et al 1981 b;Fenwick et al 1982 a;Amy & Kirshner, 1982;Cena et al 1983;Corcoran & Kirshner, 1983;Wada et al 1984), depolarization and the firing of Ca2+ and Na+-dependent action potentials (Kidokoro, 1985). Na+ entry through voltage-dependent channels plays a facilitatory but not obligatory role in stimulation of secretion by cholinergic agonists and is observed only when stimulation is induced by low levels of agonists (Kidokoro, 1985;Kirshner, 1987).…”

“…Apomorphine at concentrations up to 100 /tM had no detectable effect on basal Depolarizing agents like KCl and veratridine stimulate Ca2+ uptake and catecholamine secretion and Ca2+ channel antagonists abolish these processes (Aguirre, Pinto & Trifaro, 1977;Schneider, Cline, Rosenheck & Sonenberg, 1981;Holz, Senter & Frye. 1982;Cena, Nicolas, Sanchez-Garcia, Kirpekar & Garcia, 1983;Artalejo et al 1987;Kirshner, 1987), indicating a key role for voltage-sensitive Ca2+ channels during secretion from chromaffin cells. Thus, a potential target for the inhibitory action of apomorphine on catecholamine release may be voltagedependent Ca2+ channels.…”

“…The main difference between nicotine-and high-K+-induced secretion resides in the activation pathway for Ca2+ entry Amy & Kirshner, 1982;Cena et al 1983;Wada et al 1984;Artalejo et al 1987;Kirshner, 1987). Nicotine binds to its receptor and opens the associated ionophore, allowing mainly Na+ entry (Fenwick, Marty & Neher, 1982a; Kidokoro, 1985) and local depolarization.…”