Further probes into the molecular sites of damage to cerebral adenylate cyclase following postischemic reperfusion

Gene C. Palmer, David J. Jones, S. Jo Palmer, Barbara C. Christie-Pope, Lawrence Poulakos

Research output: Contribution to journalArticlepeer-review

3 Scopus citations

Abstract

A variety of pharmacological agents were used as experimental probes to determine with greater precision the site(s) of damage to cerebral adenylate cyclase as a consequence of postischemic reperfusion in the gerbil. A paradigm of 60-min bilateral ischemia followed by 40-min reperfusion results in a decreased sensitivity of the catalytic site of adenylate cyclase to Mn2+. Likewise, the GTP-transducer site (guanine nucleotide regulatory or G protein) revealed depressed responses to GTP in the absence or presence of norepinephrine, dopamine agonists, substance P, yohimbine, and cholera and pertussis toxins. Moreover, a crude preparation of GTPase disclosed that damage elicited by postischemic reperfusion was directed to the higher-affinity form of this enzyme, which is associated with the overall function of the guanine nucleotide regulatory protein. Injury to adenylate cyclase was unrelated either to the ability of adrenergic ligands to bind to associated receptor sites or to the capacity of the brain to generate visual evoked potentials in response to visual stimuli.

Original languageEnglish (US)
Pages (from-to)1-23
Number of pages23
JournalNeurochemical Pathology
Volume5
Issue number1
DOIs
StatePublished - Aug 1 1986

Keywords

  • Cerebral ischemia
  • GTPase
  • adenylate cyclase, cerebral, damage to following postischemic reperfusion
  • adrenergic ligands
  • cholera toxin
  • dopamine
  • gerbil
  • guanine nucleotide regulatory protein
  • pertussis toxin
  • substance P
  • yohimbine

ASJC Scopus subject areas

  • Neuroscience(all)
  • Molecular Biology
  • Clinical Neurology

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