Improved HCN channels in pyramidal neurons and their new expression levels in pericytes and astrocytes in the gerbil hippocampal CA1 subfield following transient ischemia

Abstract

Hyperpolarization-activated cyclic nucleotide-gated (HcN) channels have been known to participate in the regulation of neuronal excitability, synaptic transmission and long-term potentiation in the hippocampus. The present study investigated transient ischemia-induced changes of HcN1 and HcN2 expressions in the Cornu Ammonis 1 (CA1) subfield of the hippocampus in gerbils subjected to 5 min transient global cerebral ischemia (tgcI). Neuronal death was exhibited in pyramidal neurons of the striatum pyramidale in the cA1 subfield 4 days after tgCI. HCN1 and HCN2 immunoreactivities were demonstrated in intact cA1 pyramidal neurons, and were transiently and markedly increased in the cA pyramidal neurons at 6 h after ischemia. Thereafter, they gradually decreased in a time-dependent manner. A total of 4 days after ischemia, HcN1 and HcN2 immunoreactivities were barely detected in the cA1 pyramidal neurons; however, HcN1 and HcN2 were began to be expressed in pericytes and astrocytes at 4 days after ischemia. The results indicated that HcN1 and HcN2 expression levels were apparently changed in the gerbil hippocampal CA1 subfield following tgCI and suggested that ischemia-induced alterations in HcN1 and HcN2 expression levels may be closely associated with the death of cA1 pyramidal neurons following 5 min of tgcI.

CD200 Change Is Involved in Neuronal Death in Gerbil Hippocampal CA1 Field Following Transient Forebrain Ischemia and Postischemic Treatment with Risperidone Displays Neuroprotection without CD200 Change

“…In the CA2/3 field after tFI, there was no significant alteration of NeuN immunoreactivity until 5 days post-tFI between the sham group and ischemia group ( Figure 2 Da,Dc). This finding means that DND does not occur in the CA2/3 field, and this finding is consistent with previous results observed by us [ 4 , 24 , 25 ].…”

“…As previously described in our published papers [ 4 , 24 , 25 ], the surgical procedure of tFI in the gerbils was performed. Briefly, the gerbils were anesthetized with a mixture of 2.5% isoflurane (Baxtor, Deerfield, IL, USA) in 67% nitrous oxide and 33% oxygen.…”

“…Brain sections containing the hippocampus were prepared as previously described in our studies [ 4 , 24 , 25 ]. In brief, the gerbils in the sham ( n = 5 at each point in time) and tFI ( n = 7 at each point in time) group were deeply anesthetized for euthanasia with 70 mg/kg of pentobarbital sodium at 6 h, 12 h, 24 h, 2 days, and 5 days after sham and tFI operation ( Figure 9 ).…”

Pycnogenol® Supplementation Attenuates Memory Deficits and Protects Hippocampal CA1 Pyramidal Neurons via Antioxidative Role in a Gerbil Model of Transient Forebrain Ischemia

“…Namely, transient focal brain ischemia induced by OMCA in a rat is induced for at least 1 h, and the ischemic damage represents infarction (necrosis of tissue), showing that the damage evokes motor dysfunction due to ischemic damage in the striatum and cerebral cortex [ 25 , 38 ]. In contrast, 5-min TFI evokes selective neuronal loss/death in the CA1 region of gerbil hippocampus and develops memory deficits [ 17 , 18 , 19 , 20 ]. Namely, 5-min TFI in the gerbil brings death or loss of pyramidal neurons located in the CA1 area from 4–5 days after TFI [ 39 , 40 ].…”

“…To the best of our knowledge, few research studies on neuroprotective effect of PYC against transient forebrain ischemia (TFI) and its protective mechanisms have been reported. TFI can be induced in gerbils by occlusion of common carotid arteries (OCCA) in gerbils and evokes death (loss) of pyramidal cells, which are principal neurons in the cornu ammonis (CA1) region of gerbil hippocampus, and memory deficits [ 17 , 18 , 19 , 20 ]. Therefore, the aim of this research was to examine neuroprotective effect of PYC and its protective mechanisms in gerbils with TFI.…”