Quin2 protects against neuronal cell death due to Ca2+ overload.
Quin2-acetoxymethylester (quin2/AM) (50 microM), administered directly to the motoneuronal pool of the frog spinal cord, could be loaded into the motoneuron as well as the other cells in the lumbar region. Depolarizing responses of the ventral root to L-glutamate in the quin2-loaded side persisted even after prolonged exposure to A23187 (2.0 microM), while the responses in the unloaded side were markedly reduced. Histologically confirmed neuronal cell loss from the motoneuronal pool induced by A23187 (2.0 microM) or by a high concentration of L-glutamate (10 mM) was prevented by pretreatment with quin2/AM. A23187- and L-glutamate-induced histological and functional damage in neuronal cells and the protective effects of quin2 on them provide further evidence for cell death due to Ca2+ overloading.
Kudo
Y
Y
Department of Neuroscience, Mitsubishi Kasei Institute of Life, Tokyo, Japan.
Takeda
K
K
Yamazaki
K
K
D000634:Aminoquinolines / Q000494:pharmacology*; D000818:Animals; D000001:Calcimycin / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism*; D002470:Cell Survival / Q000187:drug effects; D002614:Chelating Agents / Q000494:pharmacology; D005971:Glutamates / Q000494:pharmacology; D018698:Glutamic Acid; D009474:Neurons / Q000187:drug effects / Q000378:metabolism*; D013116:Spinal Cord / Q000166:cytology / Q000378:metabolism
D000634:Aminoquinolines; D002614:Chelating Agents; D005971:Glutamates; D000001:Calcimycin; D018698:Glutamic Acid; C035739:Quin2; D002118:Calcium