The effects of soman on the electrical properties and excitability of bullfrog sympathetic ganglion neurones

Abstract

1. The effects of soman (0.1-10 microM), an irreversible inhibitor of acetylcholinesterase (AChE), were examined on the electrical properties of ganglion neurones of the paravertebral sympathetic chain of the bullfrog, Rana catesbeiana. 2. Soman (10 microM) depolarized 29 of 35 (83%) ganglion neurones studied by 6.4 +/- 0.65 mV within 10 min of application and reduced the cell input resistance in 9 of 11 neurones examined (82%) to 55 +/- 5.3% of control. 3. Soman (10 microM) significantly reduced the maximum amplitude and the maximum rate of rise of the action potential and the duration, but not the amplitude, of the after-hyperpolarization (AHP) following the action potential elicited by either direct or antidromic stimulation. The maximum rate of fall and the duration of the action potential were not significantly affected by soman. These actions of soman were independent of the agent-induced depolarization. When examined by a single microelectrode voltage clamp, soman reduced the amplitude and the time constant of the current underlying the slow AHP, IAHs. 4. Soman (1-10 microM) produced an increase in neuronal excitability which was evidenced as either an increase in the number of action potentials or a decrease in the interspike interval in response to constant-current depolarizing pulses. The soman-induced increase in excitability occurred independently of both the agent-induced depolarization and the decrease in input resistance, was reversible with washing, was not caused by an inhibition of the M-current and was also recorded in dissociated sympathetic ganglion neurones.5. The effects of soman on the membrane potential, input resistance and the duration of the AHP but not cell excitability were blocked by pretreatment with atropine (10 microM). Pretreatment with dihydro-/J-erythroidine (DHbetalE) (10 microM) was ineffective in blocking or reversing the effects of soman. These results suggest that the direct actions of soman on the electrical properties of these neurones are mediated by activation of muscarinic receptors.