| Research Abstract |
Two groups of neurons were identified in the ganglion of Aplysia by their responses to various transmitters. The first group of neurons responded with a K^+-dependent hyperpolarization to either dopamine (DA), acetylcholine (ACh), histamine (HA), or Phe-Met-Arg-Phe-NH (FMRFamide). The second group of neurons responded with a Na^+, Ca^<2+>-dependent slow depolarization to either DA, serotonin (5HT), or FMRFamide. Inhmllular injection of pertussis toxin (PTX) into these ems of cells selectively depressed all K^+-dependent responses without affecting Na^+, Ca^<2+>-dependent responses. The depressing effect was irreversible in all cells irrespective of their agonists and receptors. Application of cholera toxin (CTX) selectively depressed all Na^+, Ca^<2+>-dependent responses without affecting K^+-dependent responses. The depressing effect was irreversible in all cells irrespective of their agonists and receptors. Intracellular application of guanosinethiodiphosphate (GDPbetaS) depressed no
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t only K^+-dependent responses but also Na^+, Ca^<2+>-dependent responses irrespective of their agonists and receptors. However, GDPbetaS had no effect on either Cl^--dependent responses or nicotinic responses of the same cell. Neither a phospholipase C inhibitor (NCDC) nor a phosphohpase A_2 inhibitor (Mepacrine) exhibited significant depressing effect on the K^+-dependent responses of all cells with various agonist-receptor systems. Neither an adenylate cyclase inhibitor (3'deoxyadenosine) nor A-kinase inhibitor (H-8) exhibited significant depressing effect on the Na^+, Ca^<2+>-dependent responses of all cells with various agonist-receptor systems.
These results strongly suggested that the opening of receptor operated K^+-channels are all regulated by PTX-sensitive G-protein, and that the slow, Na^+, Ca^<2+>-dependent responses to various transmitters are all mediated by CTX-sensitive G-protein. However, it is, unlikely that K^+-dependent responses are due to the activations of phosphohpase C or phospholipase A_2, and that Na^+, Ca^<2+>-dependent responses are due to the activations of adenylate cyclm and subsequent A-kinase. Less
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