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SHORT COMMUNICATION EFFECTS OF α 2 ‐ADRENOCEPTOR ANTAGONISTS AND IMIDAZOLINE 2 ‐RECEPTOR LIGANDS ON NEURONAL DAMAGE IN GLOBAL ISCHAEMIA IN THE RAT
Author(s) -
Craven John A.,
Conway Elizabeth L.
Publication year - 1997
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1997.tb01808.x
Subject(s) - idazoxan , neuroprotection , gliosis , imidazoline receptor , antagonist , endocrinology , medicine , receptor , pharmacology , chemistry , pathology , prazosin
SUMMARY 1. In the present study the neuroprotective effects of 3 mg/kg idazoxan, an α 2 ‐adrenoceptor antagonist and imidazolinea‐receptor (I 2 ‐receptor) ligand, 3 mg/kg methoxyidazoxan, a specific α 2 ‐adrenoceptor antagonist, and 0.6 and 3 mg/kg BU224, a selective I 2 ‐receptor ligand, were evaluated following 10 min of global ischaemia in rats. 2. Neuronal cell counts in the CA1 region of the hippocampus 8 days postischaemia indicated 46–96% cell loss compared with control ( P <0.001) and a 320% increase in [ 3 H]‐PK11195 binding ( P <0.001) used as a marker of gliosis. No significant neuroprotective effect could be detected on these markers of neuronal damage in the active treatment groups. In a subset of idazoxan‐treated rats, neuronal loss and gliosis was minimal. 3. Mean body temperature over 3 h postischaemia was lower in idazoxan‐treated rats than in the other treatment groups ( P < 0.001) and there was a correlation between mean body temperature and cell counts ( P <0.01) and mean body temperature and gliosis in this group ( P —0.057). 4. These results indicate that at the doses used neither BU224 nor methoxyidazoxan are neuroprotective in this ischaemia model and they raise the possibility that any neuroprotective effect of idazoxan may be related to hypothermic effects of the drug.