Increased inter-spike intervals and fast after-hyperpolarization of action potentials in rat hippocampal pyramidal cells accompanied with altered calbindin immunoreactivity 10-12 months after global forebrain ischemia.
In vivo electrophysiological recordings of CA1/CA2 pyramidal cells were performed 10-12 months after global forebrain ischemia (four-vessel occlusion, 15 mm) and were compared to levels of calbindin expression. Ischemic animals were subdivided in non-sclerotic ischemic (NSI) and sclerotic ischemic (SI) groups depending on the absence or presence of hippocampal sclerosis. A decreased excitability was observed in neurons from both groups, as shown by significant prolongation of inter-spike intervals (ISI) of evoked action potentials and by increased amplitude of fast after-hyperpolarization (fAHP). The ratio of calbindin-positive CA1/CA2 pyramidal cells decreased from 59% in control to 33% and 8% in NSI and SI animals, respectively. These results suggest that decreased excitability of CA1/CA2 pyramidal cells represents a protective mechanism against ischemia-induced neurodegeneration and might be related to decreased calbindin expression.
D000818:Animals; D064026:Calbindins; D004594:Electrophysiology; D005071:Evoked Potentials / Q000502:physiology; D020925:Hypoxia-Ischemia, Brain / Q000378:metabolism* / Q000473:pathology; D008297:Male; D017966:Pyramidal Cells / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D064030:S100 Calcium Binding Protein G / Q000096:biosynthesis*; D012598:Sclerosis; D013997:Time Factors
D064026:Calbindins; D064030:S100 Calcium Binding Protein G