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Interactions of N-ethylmaleimide and aluminium fluoride with GABA B receptor function in rat neocortical slices

Tipo de material: TextoTextoSeries ; European Journal of Pharmacology, 287(2), p.197-200, 1995Trabajos contenidos:
  • Ong, J
  • Kerr, D.I.B
Tema(s): Recursos en línea: Resumen: Interactions of N-ethylmaleimide and aluminium fluoride (AlF 4)with GABA B receptors have been examined using spontaneously discharging rat neocortical slices. The suppression of discharges by the GABA B receptor agonist baclofen (5-10 /zM)was irreversibly prevented by N-ethylmaleimide (10-50 tzM)and its analog N-phenylmaleimide (10-50 /zM), whilst superfusion of slices with NaF (10 mM)and A1C13 (100 ~M)to form a fluoroaluminate (AIF4-)complex markedly potentiated the action of baclofen. The lipoxygenase inhibitors, nordihydroguaiaretic acid (10-50/~M)and eicosatetraynoic acid (10-50/~M)or the phospholipase A 2 inhibitor bromophenacylbromide (50-100/~M)did not affect the response to baclofen. The depressant action of baclofen is evidently mediated through G-proteins, but is not dependent on arachidonic acid metabolites
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Interactions of N-ethylmaleimide and aluminium fluoride (AlF 4)with GABA B receptors have been examined using spontaneously discharging rat neocortical slices. The suppression of discharges by the GABA B receptor agonist baclofen (5-10 /zM)was irreversibly prevented by N-ethylmaleimide (10-50 tzM)and its analog N-phenylmaleimide (10-50 /zM), whilst superfusion of slices with NaF (10 mM)and A1C13 (100 ~M)to form a fluoroaluminate (AIF4-)complex markedly potentiated the action of baclofen. The lipoxygenase inhibitors, nordihydroguaiaretic acid (10-50/~M)and eicosatetraynoic acid (10-50/~M)or the phospholipase A 2 inhibitor bromophenacylbromide (50-100/~M)did not affect the response to baclofen. The depressant action of baclofen is evidently mediated through G-proteins, but is not dependent on arachidonic acid metabolites

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