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Intracellular recording from neurones of the guinea‐pig gall‐bladder.
Author(s) -
Mawe G M
Publication year - 1990
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1990.sp018259
Subject(s) - apamin , hyperpolarization (physics) , tetraethylammonium , membrane potential , tetrodotoxin , depolarization , biophysics , chemistry , excitatory postsynaptic potential , reversal potential , stimulation , electrophysiology , calcium , resting potential , biology , endocrinology , neuroscience , potassium , potassium channel , biochemistry , patch clamp , stereochemistry , receptor , organic chemistry , nuclear magnetic resonance spectroscopy
1. Intracellular recordings were made from neurones of the guinea‐pig gall‐bladder in vitro. Intracellular injection of horseradish peroxidase revealed a simple structure, consisting of a soma and a single process, but no discernible dendritic arborization. 2. The resting membrane potential was ‐50.5 +/‐ 0.4 mV and the input resistance was 80 M omega. 3. Gall‐bladder neurones spiked only once at the onset of depolarizing current pulses. Action potentials were blocked by tetrodotoxin, but a Ca2(+)‐dependent spike could be elicited in the presence of tetrodotoxin and tetraethylammonium. 4. Action potential after‐hyperpolarizations had a duration of 172 +/‐ 3.7 ms and reversed at a membrane potential of ‐93 mV; this reversal potential was linearly related to the logarithm of the external potassium concentration. The initial phase of the after‐hyperpolarization was inhibited by tetraethylammonium (1‐10 mM) and was not affected by 3,4‐diaminopyridine. The late phase of the after‐hyperpolarization was blocked by apamin (10 nM) or curare (500 microM). Both the early and late phases of the after‐hyperpolarization were inhibited when the preparation was perfused with a calcium‐free, high‐magnesium solution. The calcium‐free, high‐magnesium solution had no effect on the membrane potential or input resistance of these cells. 5. Fast excitatory synaptic responses and antidromic responses were elicited in gall‐bladder neurones by focal stimulation of fibre tracts. High‐frequency fibre tract stimulation often resulted in prolonged, calcium‐dependent, depolarizations that were associated with a decrease in input resistance. 6. 5‐Hydroxytryptamine and substance P caused depolarizations that were associated with a decrease in input resistance. Bethanechol caused hyperpolarizations that were associated with a decrease in input resistance and which were blocked by atropine.