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THE EFFECTS OF PIPERAZINE ON RAT SYMPATHETIC NEURONES
Author(s) -
CONNOR J.D.,
CONSTANTI A.,
DUNN P.M.,
FORWARD ANNE,
NISTRI A.
Publication year - 1981
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1981.tb09990.x
Subject(s) - piperazine , neuroscience , sympathetic nervous system , pharmacology , medicine , chemistry , biology , endocrinology , blood pressure
1 The neuronal effects of the anthelmintic piperazine (Pip) on rat sympathetic ganglia were studied in vitro by means of intracellular and extracellular recording techniques 2 Surface potential recordings indicated that Pip (0.1–10 mM as citrate, 1–30 mM as hexahydrate) produced a sustained depolarization (reversible on washing) of rat ganglia. γ‐Aminobutyric acid (GABA, 1–100 μM) also evoked reversible depolarizations but, unlike Pip, responses to the higher doses of GABA declined during a 2 min exposure. Depolarizations produced by Pip or carbachol (but not GABA) were markedly depressed by hexamethonium bùt only slightly by bicuculline or picrotoxin 3 Intracellular recordings revealed that Pip‐induced depolarizations were accompanied by an increase in membrane conductance and a broadening and depression of the directly‐evoked spike 4 In the presence of hexamethonium (1 mM), the responses to Pip hexahydrate and to cholinoceptor agonists were abolished, but Pip citrate still changed the spike configuration and induced membrane hyperpolarization with a small conductance increase. These residual effects were mimicked by superfusing with Na citrate or Ca 2+ ‐free medium, suggesting that significant Ca 2+ binding by the citrate anion of the Pip salt was probably responsible for the observed activity of Pip citrate in the presence of hexamethonium 5 It is concluded that on rat ganglia Pip is a nicotinic agonist, with no detectable GABA‐mimetic activity.