- 1.
The isolated, intact heart of the marine arachnid Limulus polyphemus continues to beat in vitro for many hours. Application of γaminobutyric acid (GABA) decreased the heart beat frequency with a threshold of 3xlO−7 moll−1 and an EC50 of 2.0±0.6xlO−5 moll−1 (mean±s.D., N = 8). At lO−4moll−1 and above the heart beat was completely and reversibly inhibited.
- 2.
The agonist potency profile of the Limulus heart chronotropic GABA receptor was very similar to that of the vertebrate GABAA receptor: muscimol > ZAPA>GABA=⋍TACA>isoguvacine>THIP>3-aminopropane sulphonic acid> imidazole-4-acetic acid ⋍ß-guanidino proprionic acid ⋍5-aminovalerate. In contrast, the antagonist profile differed dramatically: bicuculline, pitrazepin and SR 95103, as well as the channel blocker picrotoxin, were without effect at concentrations up to 10−4moll−1.
- 3.
The benzodiazepines clorazepate, flunitrazepam, flurazepam and diazepam, as well as the barbiturate sodium pentobarbital, were without effect on the GABA response, suggesting that the Limulus heart GABA receptor is not complexed with the benzodiazepine and barbiturate modulatory subunits that characterize vertebrate GABAA receptor.
- 4.
The GABAB ligands baclofen, phaclophen and kojic amine were inactive on the heart. However, 3-aminopropyl-phosphonous acid (CGA147 823), a potent and highly selective GABAb agonist, was the most active of the compounds tested. It inhibited the heart beat with a threshold of about SnmolP1, an EC50 of 4.0±2.7×10−7 mol1−1, and produced total inhibition of the heart at 10−5moll−1. CGA 147 823 was inactive on the locust thoracic somal GABA receptors.
- 5.
cis-4-aminocrotonic acid (CACA), the ligand defining a proposed GAB Actype receptor, was inactive on the heart.
- 6.
The GABA-induced inhibition of the heart beat was enhanced by pretreatment with the GABA uptake inhibitor nipecotic acid but not with sodium valproate or ß-alanine.
- 7.
The Limulus heart chronotropic GABA receptor appears to be of a hitherto undescribed type that differs in pharmacology from the vertebrate GABAA and GABAB receptors as well as from the well-defined GABA receptors on the somata of locust neurones and the muscle fibres of insects and the nematode Ascaris.
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