Lesions to Schaffer collaterals prevent ischemic death of CA1 pyramidal cells.
The contribution of excitatory inputs to CA1 pyramidal cell death after ischemia was examined using rats with unilateral destruction of CA3 pyramidal cells. Intracerebroventricular injection of L-alpha-kainic acid (KA) was performed before the induction of transient forebrain ischemia. Five days after ischemic insult, pyramidal cells and L-glutamate binding sites in the CA1 region ipsilateral to the KA injection were preserved in spite of neuronal necrosis and a significant decrease in L-glutamate receptor density in the contralateral CA1 region, indicating the critical role of Schaffer collaterals in delayed neuronal death.
D000818:Animals; D001665:Binding Sites; D002545:Brain Ischemia / Q000473:pathology / Q000503:physiopathology*; D005971:Glutamates / Q000378:metabolism; D018698:Glutamic Acid; D006624:Hippocampus / Q000098:blood supply* / Q000378:metabolism / Q000473:pathology; D007608:Kainic Acid / Q000494:pharmacology; D008297:Male; D009434:Neural Pathways / Q000503:physiopathology; D051381:Rats; D011919:Rats, Inbred Strains
D005971:Glutamates; D018698:Glutamic Acid; D007608:Kainic Acid