Rhythmic hyperpolarizations and depolarization of sympathetic ganglion cells induced by caffeine

Abstract

Superfusion of the isolated sympathetic ganglion of the bullfrog with a caffeine-containing (1-6 mM) solution caused in many cells an initial slow hyperpolarization which was followed by a subliminal depolarization interruped by rhythmic hyperpolarizations. A hyperpolarization, similar to one of the rhythmic hyperpolarizations, could be triggered by an action potential in the presence of caffeine. The action potential itself was not markedly affected by caffeine except for its afterhyperpolarization which was prolonged. All these caffeine-induced hyperpolarizations were associated with a marked reduction of the membrane resistance, their amplitude was increased in a K+-free solution and decreased in a high-K+ solution, and their polarity was reversed at the same level at which the afterhyperpolarization was also inverted. This reversal level was not altered by omission of Na+ or C1- from the external medium. These hyperpolarizations were reversibly abolished by depletion of external Ca2+ or replacement of external Ca2+ by Mg2+. Excess of external Ca2+ caused a shortening of the interval between rhythmic hyperpolarizations. Furthermore, iontophoretic injection of EDTA into the cytoplasm markedly depressed the initial caffeine hyperpolarizatin and abolished both the rhythmic and evoked caffeine hyperpolarizations. The caffeine-induced depolarization was not affected by omission of external Cl-. It was decreased in a Na+-free medium, but completely eliminated by omission of both Na+ and Ca2+ from the external medium. Tetrodotoxin did not impair the production of the initial and the rhythmic hyperpolarizations. A strong depolarizing pulse could evoke a typical hyperpolarizing response in the presence of this compound. Dibutyryl cyclic AMP, d-tubocurarine, atropine, and phenoxybenzamine were without effect on the caffeine-induced hyperpolarizations and depolarization. It was concluded that each caffeine-induced hyperpolarization is the result of an increased K+ permeability, which is probably caused by a rise in the internal Ca2+ concentration. It was also concluded that the caffeine-induced depolarization is due to an increased membrane permeability to Ca2+ and Na+.

Inositol trisphosphate‐induced membrane potential oscillations in Xenopus oocytes.

“…Consistent with this model are the observations that various treatments which are likely to release calcium into the cytosol such as the addition of ACh (Kusano et al 1982;Miledi et al 1982;Oron et al 1985) or the injection of either Insl,4,5P3 (Oron et al 1985;Parker & Miledi, 1986) or calcium itself (Miledi & Parker, 1984;Dascal et al 1985;Gillo et al 1987) all induce oscillatory activity. A similar explanation may account for the observation that sympathetic ganglion cells can be induced to oscillate by the calcium-mobilizing agent caffeine (Kuba & Nishi, 1976). The frequency of this type of oscillator seems to depend upon how much calcium is introduced into the system.…”

Ca(2+)‐induced Ca2+ release and its activation in response to a single action potential in rabbit otic ganglion cells.

“…Ryanodine-sensitive AHP and spontaneous rhythmic hyperpolarizations have been reported to occur in rat superior cervical ganglion cells (Kawai & Watanabe, 1989). The AHP in the preganglionic neurones of the vagal motor nucleus in guinea-pigs has also been found to be ryanodine sensitive (Sah & Maclachlan, 1991 (Kuba & Nishi, 1976;Nohmi, Hua & Kuba, 1992a) and rabbit vesical pelvic (Nishimura et al 1988) Meissner, 1994;Kuba, 1994 ENDO, M. (1977). Calcium release from the sarcoplasmic reticulum.…”

Effects of calcium and guanosine‐3',5'‐cyclic‐monophosphoric acid on receptor potentials of toad rods.

“…The effect of increasing intracellular cGMP levels (by ionophoresis of cGMP or bathing in IBMX solutions) on the availability of Ca2+ in rods is unknown. In muscle cells, methylxanthines are able to increase Ca2+ release, and decrease the rate of uptake, by sarcoplasmic reticulum; thereby increasing the concentration of Ca2+ in and around the fibres (Weber & Herz, 1968;Endo, Tanaka & Ogawa, 1970;Kuba & Nishi, 1976). An analogous mechanism for IBMX in rod outer segments might increase the amount of Ca2+ released from the disks by light, and the increase in Ca2+ would result in the observed increased in amplitude and duration of the receptor potential.…”