Effects of haloperidol and phentolamine on the crustacean cardiac ganglion.
Haloperidol (a dopamine D2 blocker in vertebrates) and phentolamine (an alpha-adrenergic blocker) alter the pattern of bursting by the isolated cardiac ganglion of the lobster when perfused at concentrations of 10(-6)-10(-5) mol/l. Both drugs decrease the frequency of bursting and increase burst duration. They are most effective in slowing the ganglion when applied selectively to the anterior ganglionic trunk, the same region of the ganglion where dopamine (DA) and 5-hydroxytryptamine (5HT) are most effective in speeding up bursting. When exogenous monoamine transmitters are applied in the presence of 3x10(-6) mol/l haloperidol, the effect of 5HT, but not of DA, is significantly reduced. At the same concentration, phentolamine does not suppress the actions of DA, 5HT or noradrenaline (NA). Both haloperidol and phentolamine significantly alter the properties of endogenous burst-organizing potentials (driver potentials) generated by motorneurons in the ganglion. It is possible that the effects of these drugs on bursting reflect alteration of endogenous electrical properties of the constituent neurons, rather than receptor antagonism.
Berlind
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Biology Department, Wesleyan University, Middletown, CT 06457, USA. aberlind@wesleyan.edu
D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000818:Animals; D018492:Dopamine Antagonists / Q000494:pharmacology; D004594:Electrophysiology; D006220:Haloperidol / Q000494:pharmacology*; D006321:Heart / Q000187:drug effects* / Q000502:physiology; D009046:Motor Neurons / Q000187:drug effects* / Q000502:physiology; D008121:Nephropidae; D010646:Phentolamine / Q000494:pharmacology*
D000317:Adrenergic alpha-Antagonists; D018492:Dopamine Antagonists; D006220:Haloperidol; D010646:Phentolamine