Effects of ryanodine on the spike after-hyperpolarization in sympathetic neurones of the rat superior cervical ganglion

Abstract

Effects of ryanodine on sympathetic neurones of the rat superior cervical ganglion were investigated by means of intracellular recording. Ryanodine (1 microM) significantly shortened the after-hyperpolarization (AH) following the spike evoked by current injection or pre-ganglionic stimulation without affecting the configuration of the spikes. The shortening of AH caused by ryanodine was dose-dependent at concentrations between 0.1 and 1 microM and was slowly recovered by washing the tissue over 1 h. A partial inhibition of the apamin-sensitive slow component of AH was the maximal effect obtained at 1 microM. Although the input membrane resistance was not changed, ryanodine evoked repetitive discharges at long intervals in response to long depolarizing current pulses applied across the cell membrane. Ryanodine (5 microM) did not depress the Ca-spike but shortened the following AH in a lesser degree than that following the normal spike. Spontaneous small fluctuations of the resting membrane potential were occasionally observed under normal conditions. They were facilitated by caffeine and abolished by ryanodine. Caffeine also enhanced the slow component of the AH but did not affect it in the presence of ryanodine. These results suggest that ryanodine inhibits Ca release from intracellular store sites. The released Ca may contribute to generating the long-lasting AH and to regulating the excitability of rat sympathetic neurones.

Calcium‐dependent chloride current induced by axotomy in rat sympathetic neurons.

“…Non-axotomized rat sympathetic ganglion cells do not show ADPs (McAfee & Yarowsky, 1979;Kawai & Watanabe, 1986;Kawai & Watanabe, 1989;Sanchez-Vives & Gallego, 1993a), which is in accordance with the lack of inward tail currents in control cells bathed in 'ITX and TEA, even after increasing the current driving force by lowering the external Cl-concentration. Therefore, as discussed by Sanchez-Vives & Gallego (1993a), a new conductance appears at or near the cell body after axotomy.…”

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).…”

Mechanisms underlying intracellular signal transduction of the slow IPSP in submucous neurones of the guinea‐pig caecum.

“…However, higher concentrations of procaine decreased the amplitude of the action potential, fast EPSP and slow EPSP. Ryanodine has been shown to reduce the release of Ca2+ from the sarcoplasmic reticulum in muscle cells (Sutko, Ito & Kenyon, 1985; lino, Kobayashi & Endo, 1988) and the spike after-hyperpolarization in sympathetic neurones (Kawai & Watanabe, 1989). Ryanodine (1-10 /M) did not affect the slow IPSP or noradrenaline hyperpolarization, although it blocked the slow after-hyperpolarization following the spikes (n = 8).…”