Block of neuronal Ca++ influx by the anti-ischemic agent TA3090

D. Bleakman, P. S. Chard, S. Foucart, R. J. Miller

Research output: Contribution to journalArticlepeer-review


We examined the effect of the novel anti-ischemic drug, TA3090 on Ca++ entry into peripheral and central neurons. TA3090 inhibited voltage-dependent Ca++ entry into rat dorsal root ganglion (DRG) and sympathetic neurons. The degree of inhibition produced by the drug was voltage-dependent. TA3090 also inhibited Ca++ entry into DRG cells elicited by trains of action potentials. TA3090 inhibited Ca++ influx into neurons from the hippocampus. As in peripheral neurons, TA3090 blocked Ca++ influx associated with a Ca++ current in voltage-clamped cells or elicited by trains of action potentials. Furthermore, TA3090 blocked Ca++ influx stimulated by glutamate or N-methyl-D-aspartate. In addition, TA3090 blocked excitatory glutamate-mediated synaptic transmission between hippocampal pyramidal neurons. These data indicate that the protective effects of TA3090 in the brain under ischemic conditions may be partly or completely due to its ability to inhibit neuronal Ca++ influx.

Original languageEnglish (US)
Pages (from-to)430-438
Number of pages9
JournalJournal of Pharmacology and Experimental Therapeutics
Issue number1
StatePublished - 1991

ASJC Scopus subject areas

  • Molecular Medicine
  • Pharmacology


Dive into the research topics of 'Block of neuronal Ca++ influx by the anti-ischemic agent TA3090'. Together they form a unique fingerprint.

Cite this