Abstract
Rationale for Pharmacotherapy of Remacemide in 4-VO Model: Studies have reported memory impairment (25) and a selective and delayed onset of CA1 pyramidal cell necrosis in man after global ischemia (18). Memory tests demonstrated anterograde amnesia in a patient (R.B.) who developed circumscribed memory impairment following an ischemic episode. Prior to death, R.B. showed no signs of cognitive impairments other than memory loss. Histological evaluations revealed selective and bilateral CA1 pyramidal cell loss (28). The 4-VO model is widely used for studying the phenomenon of “selectively vulnerable, delayed onset” pathophysiology of hippocampal CAl neurons in global ischemia (19,20). Post-ischemic pharmacological treatments may modify the functional and morphological outcome of global ischemia in the hippocampus, involving ischemically compromised but possibly still “viable” CA1 neurons (20). There is credible evidence for a critical role of the hippocampus in a specific type of spatial, representational, or episodic memory (23,24,28). Circumscribed memory impairment with selective CA1 cell necrosis has been reported in the 4-VO model (15,26). Protection of hippocampal CA1 cell damage may represent a valid “neural endpoint”, or target for drug intervention (20).
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Ordy, J.M. et al. (1992). Pharmacological Effects of Remacemide and MK-801 on Memory and Hippocampal CA1 Damage in the Rat Four-Vessel Occlusion (4-VO) Model of Global Ischemia. In: Globus, M.YT., Dietrich, W.D. (eds) The Role of Neurotransmitters in Brain Injury. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-3452-5_14
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