EFFECTS OF INTRACEREBRAL ILOPROST INJECTIONS ON MOTOR-ACTIVITY AND CHEMICALLY-INDUCED SEIZURES IN RATS

AKARSU E. S., AYHAN I.

METHODS AND FINDINGS IN EXPERIMENTAL AND CLINICAL PHARMACOLOGY, cilt.14, sa.7, ss.517-522, 1992 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 14 Sayı: 7
  • Basım Tarihi: 1992
  • Dergi Adı: METHODS AND FINDINGS IN EXPERIMENTAL AND CLINICAL PHARMACOLOGY
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED)
  • Sayfa Sayıları: ss.517-522
  • Anahtar Kelimeler: PROSTACYCLIN, ILOPROST, PENTYLENETETRAZOL, SEIZURE, MOTOR ACTIVITY, GABA, SUBSTANTIA-NIGRA PARS-RETICULATA, RAT, SUBSTANTIA NIGRA, PROSTAGLANDIN FORMATION, INDUCED CONVULSIONS, BRAIN, PROSTACYCLIN, MICE, GABA, PROPAGATION, STIMULATION, BLOOD
  • Ankara Üniversitesi Adresli: Evet

Özet

The effects of iloprost, a chemically stable analog of prostacyclin, on motor activity, pentylenetetrazol (PTZ)- and strychnine (ST)-induced seizures were studied in rats. Depression on motor activity was observed after a 500 ng/icv dose. Thus, both spontaneous locomotor activity and exploratory behavior were significantly reduced. While iloprost was ineffective against ST-induced seizures, it produced dose-dependent inhibition of PTZ-induced seizures. ED50 (95% confidence limits) value of iloprost for the suppression of clonic convulsions induced by PTZ was 224.96 (100.43-504.00) ng/icv. Anticonvulsive effect of iloprost was significantly potentiated by clonazepam pretreatment. In this case ED50 of iloprost was 39.40 (23.88-65.01) ng/icv. Unilateral iloprost injections into substantia nigra pars reticulata in a relatively lower dose range (0.5-2.0 ng/ic) also dose-dependently inhibited PTZ-induced seizures. In comparison to other prostanoids iloprost seems to have more potent and selective anticonvulsive activity against PTZ- induced seizures without marked motor depressant action in rats. It is further suggested that antiseizure effect of iloprost might be mediated by GABAergic inhibitory mechanisms.