Adrenaline depolarization in paravertebral sympathetic neurones of bullfrogs.

Responses to adrenaline (Ad) and their ionic mechanisms were analysed using intracellular recording and voltage-clamp methods in neurones of bullfrog sympathetic ganglia. Ad (5 microM-1 mM) applied directly to sympathetic neurones by pressure ejection through a micropipette produced three types of depolarizing responses (2-20 mV). Under voltage-clamp conditions, Ad (100 microM) produced fast, slow and mixed types of inward currents (AdIs) with amplitude of 2.9 +/- 1.3 nA. beta-Adrenoceptors may be responsible for the generation of these AdDs. The slow AdI which lasted for 1-5 min was associated with a decreased membrane conductance. The slow AdI decreased at hyperpolarized potential level and eventually nullified at -70 mV. No reversal of the slow AdI polarity was observed in the Ringer solution. Injection of Cs2+ into the ganglion cells produced a marked depression of the amplitude of the slow AdI. The slow AdI was blocked by bath-applied Ba2+ but not by TEA. Ad reduced the slow current relaxation, the M current, associated with voltage jumps in the membrane potential range -35 to -55 mV. The fast Ad response was associated with an increase in membrane conductance. When the membrane was depolarized, the fast AdI decreased and reversed its polarity at -36 +/- 8.3 mV. Removal of Cl ion from superfusing solution depressed the fast AdI, suggesting that activation of Cl- conductances may be involved in the generation of the fast AdI. The mixed type of Ad response exhibited characteristics of both the fast and slow Ad responses. The results suggest that Ad increases the excitability of neurones in bullfrog sympathetic ganglia.