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The mechanism of action of local anesthetics on synaptic transmission and their effects on synaptic components and on electrophysiologic properties of the nerve cell body are not clear. Therefore, the effects of lidocaine and bupivacaine on pre- and postsynaptic mechanisms underlying synaptic transmission in sympathetic ganglia were studied utilizing the techniques of intracellular recording and stimulation on isolated superfused superior cervical ganglia of rats. Lidocaine and bupivacaine either depressed or completely blocked synaptic transmission in sympathetic ganglia in a dose-dependent manner. Blockade of axonal conduction in presynaptic fibers was preceded by increased latency (the latency increased from 11.2 +/- 0.9 to 16.5 +/- 1.4 ms, mean +/- SEM, P less than 0.01) when the drugs were applied to the presynaptic nerves. Application of the drugs directly to the ganglion produced alterations in postsynaptic membrane properties consisting of decreased membrane resistance (from 40 +/- 3 to 32 +/- 3 M omega, P less than 0.01), increased firing threshold (from 14 +/- 0.5 to 18 +/- 0.5 mV, P less than 0.01), and decreased action potential amplitude (P less than 0.01) and/or blockade of action potential generation. Resting postsynaptic membrane potential did not change significantly. These changes were reversible. However, even after the excitatory postsynaptic potential resulting from presynaptic nerve stimulation had fully recovered during washout of the local anesthetic, the threshold for evoking the spike potential (firing level) still remained elevated for both presynaptic and intracellular stimulation of the ganglion cell, suggesting prolonged cell depression.(ABSTRACT TRUNCATED AT 250 WORDS)

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While the effects of local anaesthetics on axonal conduction and axonal membrane have been extensively studied, there is little information about the actions of these agents on nerve cell soma. Therefore, the effects of the amide local anaesthetic bupivacaine on the electrophysiologic properties of the nerve cell soma were studied on isolated superfused superior cervical ganglia of rats. Administration of 100-200 nM of bupivacaine to the preparation produced marked changes in membrane properties of the cell soma. The resting membrane potential did not change, but the membrane resistance decreased 20% (P less than 0.01). The firing threshold, the action potential duration at 50% of maximal amplitude, and the intracellular current threshold for firing the cells increased significantly (P less than 0.01), while the action potential amplitude decreased significantly (P less than 0.01), before its complete blockade. The results show that the cell soma is a major site of action of local anaesthetics. The implication of the results is that when local anaesthetics are applied to areas where cell bodies and processes (axons and dendrites) are present together, such as during celiac plexus block, lumbar sympathetic block, stellate ganglion block, etc., they will all be effectively depressed and/or blocked.

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Neuronal activity has been recorded extracellularly from the medulla of anesthetized rats. Units whose discharge frequency varied in phase with respiratory airflow were located bilaterally between 1.5 and 2 mm lateral to midline, extending from 1 mm caudal to 1.5 mm rostral to the obex, in the ventral two-thirds of the medulla. Expiratory units predominated and were intermingled with inspiratory units. Ten different patterns of discharge were distinguished, varying from a short burst at the beginning of expiration to a resting discharge which increased in frequency during either inspiration or expiration. Evidence was also obtained that fiber tracts from other areas of the brain cross midline just caudally to the obex and pass to the respiratory centers on which they apparently exert and excitatory action.