NEURON MEMBRANE DEPOLARIZATION BY CYCLIC 3'5'-ADENOSINE MONOPHOSPHATE AND ITS POSSIBLE ROLE IN NEURON MOLECULAR CELL COMPUTER (MCC) ACTION

  • 1 January 1978
    • journal article
    • research article
    • Vol. 23  (2) , 305-311
Abstract
The separate 4th intracellular microelectrode was used for controlling the conditions of cyclic nucleotide injection in neurons of Helix pomatia. Iontophoretic increase in intracellular cyclic[c] AMP concentration elicits membrane depolarization in many neurons. Phosphodiesterase inhibitors 3-isobutyl-1-methylxanthine and SQ-20009 [1-ethyl-4-(isopropylidene-hydrazino)- 1H-pyrazolo-[3,4-b] pyridine-5-carboxylic acid ethyl ether hydrochloride] prolong this depolarization and elevate its level. In cell F-1 of Helix brain sometimes cAMP induces weak hyperpolarization, but this response turns to usual depolarization after 3-isobutyl-l-methylxanthine application. Cell molecular computer probably has an analog input, where diffusion of cAMP, cGMP and Ca2+ being a modelling process. Adenylate cyclase and guanylate cyclase and ionic channels of membrane are regulated sources. Phosphodiesterases with Ca2+-binding activator proteins are molecular outflows and protein kinases, detectors that transform the data about the concentrations of cAMP and cGMP into codes for MCC. Protein kinases control over the activity of proteins directly. The depolarization effect on neuron membrane seems associated with protein kinase activation or with direct action of cAMP on phospholipase.