ATP closes a potassium and opens a cationic conductance through different receptors in neurons of guinea pig submucous plexus.

Intracellular recordings were made to study the actions of ATP and related nucleotides on neurons from the guinea pig submucous plexus. Local application of ATP, by pressure, induced a depolarization in most AH-type neurons, which had a latency of several milliseconds, lasted for about 5 sec, appeared to reverse at about +4 mV and occurred concomitantly with a reduction in input resistance. Pressure application of ATP also depolarized the S-type neurons. In most of these cells the depolarization had two phases: the first component resembled the depolarization observed in AH cells and the second component was much slower in onset and was longer lasting (30-90 sec). The slower component was associated with an increase in input resistance, reversed polarity near the potassium equilibrium potential and was observed in isolation in 30% of S neurons. Superfusion of ATP or other analogs (0.03-10 microns) induced a slow depolarization in most of S neurons with the following rank order of potency: 2-methylthio-ATP > ATP > adenosine-5'-o-3-thiotriphosphate = ADP; alpha, beta-methylene ATP and beta, gamma-methylene ATP were inactive (10-100 microM). When whole-cell recordings were used, fast superfusion with ATP or other analogs (3-1000 microM) evoked, at negative membrane potentials, a rapidly desensitizing inward current. This current reversed polarity at about 0 mV and was much reduced in low extracellular sodium concentration. The rank order of potency of the used agonists was: ATP = adenosine-5'-o-3-thiotriphosphate = 2-methylthio-ATP > > alpha,beta-methylene ATP = beta,gamma-methylene ATP; adenosine, AMP or ADP (1 mM) were inactive.(ABSTRACT TRUNCATED AT 250 WORDS)

• Publication year

  1994

• Venue

  Journal of Pharmacology and Experimental Therapeutics

• Publication date

  1994-03-01

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1016/s0022-3565(25)38588-5PMID 7511165
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

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