SUMMARY1. Ganglion cells of the myenteric plexus of the guinea-pig ileum have been studied with intracellular micro-electrodes.2. Three types of cell were distinguished. Type 1 cells had a high resistance (58 MQ) and had properties similar to guinea-pig sympathetic ganglion cells. Type 2 cells were also excitable but had a lower resistance (21 MO) and showed accommodation to depolarizing current pulses. Type 3 cells were inexcitable.3. Point stimulation within 150 ,m excited neurones either antidromically or orthodromically, sometimes both.4. Antidromic responses had a small all-or-nothing component which was subthreshold for the soma spike. Two or more such components sometimes occurred, and were probably due to stimulation of two or more cell processes.5. Excitatory post-synaptic potentials (e.p.s.p.s) were blocked by hexamethonium (400 /M). They progressively declined in amplitude when elicited at frequencies of 0-05 Hz or more, and this is discussed in relation to studies on acetylcholine (ACh) output. 6. Many cells often showed a slow after-hyperpolarization following a direct or antidromic spike. Its mechanism and significance are discussed.7. Spontaneous e.p.s.p.s and spikes were occasionally seen. 8. Intracellular injection of a fluorescent dye reveals that the neurones have one to seven processes, which usually arise from the poles of the oval soma.
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+.
The membrane current underlying the fast excitatory postsynaptic potential (EPSC) of bullfrog sympathetic ganglion cells was studied. The relationship between the EPSC amplitude and membrane potential was linear at negative levels of membrane potential, but deviated from the linearity toward a smaller amplitude at positive levels. The falling phase of EPSC almost followed a single exponential decay. The half-decay time (HDT) of EPSC's increased exponentially with an increase in the negativity of membrane potential. The rise time (RT) was also prolonged slightly with membrane hyperpolarization. Lowering of temperature decreased the EPSC amplitude, lengthened markedly the HDT and increased the slope relating the logarithm of the HDT to membrane potential. Neostigmine (1 x 10(-5) M) prolonged both the RT and HDT. A decrease in Ca2+ concentration caused a marked reduction in the EPSC amplitude, and a slight shortening in the RT and HDT. An increase in Ca2+ concentration significantly prolonged the RT and HDT without altering the slope of the relationship between the HDT and membrane potential, while the amplitude of EPSC was increased slightly. The HDT was independent of EPSC amplitude. It is suggested that the mechanism responsible for closing the ion channels of the nicotinic receptor at the subsynaptic membrane is regulated by membrane potential. The possible mechanisms of the action of Ca2+ on the decay phase of EPSC were discussed.
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