Histamine activates chloride conductance in motor neurons of the lobster cardiac ganglion.
1. Individual motor neurons of the lobster cardiac ganglion were voltage clamped with two microelectrodes. Superfusion of histamine evoked a concentration-dependent membrane current. The mean effective concentration (EC50) for the concentration-effect relationship was 28 microM. 2. The amplitude and polarity of the histamine-activated current depended on intracellular and extracellular Cl- concentration. The membrane potential at which the current polarity reversed was a function of the Cl- equilibrium potential. 3. The histamine-activated Cl- conductance was voltage dependent, increasing with depolarization. As a consequence, the histamine-evoked current showed outward rectification. 4. We conclude that histamine activates a Cl- conductance with biophysical properties similar to the crustacean Cl- conductance activated by gamma-aminobutyric acid (GABA) and to the histamine responses described in lobster olfactory and stomatogastric neurons. 5. The response to histamine was competitively inhibited (IC50 = 7 microM) by cimetidine, an H2 subtype inhibitor in mammals. Ranitidine, pyrilamine, chlorpheniramine, diphenhydramine, and cyproheptadine were 50-100 times less potent than cimetidine. Tubocurarine, a Cl- channel blocker, blocked with an IC50 of 20 microM, but picrotoxin did not begin to inhibit the histamine response until concentrations exceeded 0.1 mM. 6. These results suggest that the response cannot easily be classified with the use of the pharmacological categories developed in mammals. Like the Cl(-)-dependent responses to various neurotransmitters in a number of invertebrates, the histamine response in the lobster cardiac ganglion was inhibited by tubocurarine. 7. Both GABA and histamine had similar effects on the motor neurons, but only GABA inhibited pacemaker bursts. In this respect, GABA more resembles the endogenous inhibitory postsynaptic potential.(ABSTRACT TRUNCATED AT 250 WORDS)
Hashemzadeh-Gargari
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Department of Neurology, Emory University School of Medicine, Atlanta, Georgia 30322.
Freschi
J E
JE
D000818:Animals; D002712:Chlorides / Q000378:metabolism*; D003712:Dendrites / Q000187:drug effects / Q000378:metabolism; D005724:Ganglia / Q000187:drug effects / Q000378:metabolism*; D006321:Heart / Q000294:innervation; D006632:Histamine / Q000494:pharmacology*; D006635:Histamine H2 Antagonists / Q000494:pharmacology; D066298:In Vitro Techniques; D007473:Ion Channels / Q000187:drug effects; D008564:Membrane Potentials / Q000187:drug effects; D009046:Motor Neurons / Q000187:drug effects / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism; D008121:Nephropidae / Q000378:metabolism*; D009474:Neurons / Q000187:drug effects / Q000378:metabolism*; D011189:Potassium Chloride / Q000494:pharmacology
D002712:Chlorides; D006635:Histamine H2 Antagonists; D007473:Ion Channels; D011189:Potassium Chloride; D006632:Histamine