1986
DOI: 10.1016/0006-8993(86)90878-4
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Ischemic CA-1 pyramidal cell loss is prevented by preischemic colchicine destruction of dentate gyrus granule cells

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Cited by 121 publications
(28 citation statements)
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“…Since the major excitatory input to the hippocampus is from the entorhinal cortex, it can be assumed that ritanserin exerts its neuroprotective effects by depression of the entorhinal output. This hypothesis is supported by studies demonstrating that both lesions of the entorhinal afferent 46 -47 and destruction of the entorhinal cortex 48 protect CA1 pyramidal neurons from ischemic degeneration. Therefore, 5-HT 2 antagonists may protect by depressing CA1 neuronal hyperexcitation by inhibiting the action of neurons in the dentate gyrus and/or entorhinal cortex.…”
supporting
confidence: 68%
“…Since the major excitatory input to the hippocampus is from the entorhinal cortex, it can be assumed that ritanserin exerts its neuroprotective effects by depression of the entorhinal output. This hypothesis is supported by studies demonstrating that both lesions of the entorhinal afferent 46 -47 and destruction of the entorhinal cortex 48 protect CA1 pyramidal neurons from ischemic degeneration. Therefore, 5-HT 2 antagonists may protect by depressing CA1 neuronal hyperexcitation by inhibiting the action of neurons in the dentate gyrus and/or entorhinal cortex.…”
supporting
confidence: 68%
“…A number of observations are consistent with the suggestion that increased excitatory activity in spe cific neuronal pathways may play a significant role in postischemic neuronal injury (Suzuki et al, 1983;Benveniste et al, 1984;Wieloch et al, 1985;Roth man and Olney, 1986;Johansen et al, 1986;J�rgensen et al, 1987;Chang et al, 1989). The an ticonvulsant, MK-801, is a potent noncompetitive antagonist of the N-methyl-D-aspartate (NMDA) glutamate receptor subtype (Wong et al, 1986) with demonstrated protective effects against glutamate toxicity and hypoxic/ischemic injury in vitro (Gold berg et al, 1987;Hahn et al, 1988).…”
supporting
confidence: 66%
“…This may seem surprising, as pre vious lesion studies indicate that deafferentation of hippocampal neurons may alleviate ischemic cell death (Wieloch et al, 1985;Johansen et al, 1986;J�rgensen et al, 1987;Benveniste et al, 1989;Kaplan et al, 1989;Buchan and Pulsinelli, 1990). It should be noted in this regard that the average level of Glu-LI in the terminals predominantly reflects the size of the vesicular pool (Ji et al, 1991).…”
Section: Redistribution Of Glutamatementioning
confidence: 99%