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Effects of pharmacological treatments on hippocampal NCAM1 and ERK2 expression in epileptic rats with cognitive dysfunction

View Article: PubMed Central - PubMed

ABSTRACT

The present study aimed to investigate the effects of various pharmacological agents on the hippocampal expression of neural cell adhesion molecule 1 (NCAM1) and extracellular signal-regulated kinase 2 (ERK2) in epileptic rats with cognitive dysfunction. The experiments were conducted using 120 Wistar rats: 20 controls and 100 with pilocarpine-induced status epilepticus (SE). The SE rats were randomly assigned to 5 groups (n=20/group) that received daily treatments for 1 month with one of the following: (i) saline (no effect on epilepsy); (ii) carbamazepine (an anticonvulsant); (iii) oxcarbazepine (an anticonvulsant); (iv) aniracetam (a nootropic); or (v) donepezil (an acetylcholinesterase inhibitor). Spatial learning and memory were assessed using a Morris Water Maze (MWM). Hippocampal tissue was assessed for NCAM1 and ERK2 messenger RNA (mRNA) expression by reverse transcription polymerase chain reaction, and protein expression by immunochemistry. The results revealed that SE rats had significantly poorer MWM performances compared with controls (P<0.01). Performance in SE rats was improved with donepezil treatment (P<0.01), but declined with carbamazepine (P<0.01). Compared with controls, saline-treated SE rats exhibited increased hippocampal NCAM1 mRNA expression (P<0.01). Among SE rats, NCAM1 mRNA expression was highest in those treated with donepezil, followed by aniracetam-, saline-, oxcarbazepine- and carbamazepine-treated rats. Compared to controls, saline-treated SE rats exhibited decreased hippocampal ERK2 mRNA expression (P<0.01). Among SE rats, ERK2 mRNA expression was highest in those treated with donepezil, followed by aniracetam, saline, oxcarbazepine and carbamazepine. NCAM1 and ERK2 protein expression levels were parallel to those of the mRNA. In saline-treated SE rats, hippocampal ERK2 expression was decreased and NCAM1 expression was increased; thus, these two molecules may be involved in the impairment of spatial memory. Carbamazepine augmented this impairment, whereas donepezil was found to ameliorate the dysfunction associated with epilepsy. In conclusion, ERK2 and NCAM1 have significant roles in impairment of spatial memory in SE rats. Carbamazepine may increase this impairment, while donepezil may decrease this impairment.

No MeSH data available.


Morris water maze escape times. Results are the mean escape (latency) times (in seconds) for each group per experimental day (n=20 rats/group). Each rat was tested on 5 consecutive days at the same time each day.
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f1-ol-0-0-4882: Morris water maze escape times. Results are the mean escape (latency) times (in seconds) for each group per experimental day (n=20 rats/group). Each rat was tested on 5 consecutive days at the same time each day.

Mentions: A total of 20 rats comprised a control group for normal behavioral observations, and SE was successfully established in 100 rats. Following pharmaceutical treatments, an MWM was used to test each rat for spatial navigation learning on 5 successive days. Figure 1 shows the mean escape (latency) times for each group of rats per day. As expected, the normal (control) group adapted well to this task, with the group's mean latency time decreasing each day for 5 days. By contrast, all groups of rats in which SE was established had a significantly longer mean latency time compared with the control group, even after 5 days (P=0.002 compared to control group). Thus, SE significantly altered memory associated with the spatial navigation learning task in the rats.


Effects of pharmacological treatments on hippocampal NCAM1 and ERK2 expression in epileptic rats with cognitive dysfunction
Morris water maze escape times. Results are the mean escape (latency) times (in seconds) for each group per experimental day (n=20 rats/group). Each rat was tested on 5 consecutive days at the same time each day.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4997984&req=5

f1-ol-0-0-4882: Morris water maze escape times. Results are the mean escape (latency) times (in seconds) for each group per experimental day (n=20 rats/group). Each rat was tested on 5 consecutive days at the same time each day.
Mentions: A total of 20 rats comprised a control group for normal behavioral observations, and SE was successfully established in 100 rats. Following pharmaceutical treatments, an MWM was used to test each rat for spatial navigation learning on 5 successive days. Figure 1 shows the mean escape (latency) times for each group of rats per day. As expected, the normal (control) group adapted well to this task, with the group's mean latency time decreasing each day for 5 days. By contrast, all groups of rats in which SE was established had a significantly longer mean latency time compared with the control group, even after 5 days (P=0.002 compared to control group). Thus, SE significantly altered memory associated with the spatial navigation learning task in the rats.

View Article: PubMed Central - PubMed

ABSTRACT

The present study aimed to investigate the effects of various pharmacological agents on the hippocampal expression of neural cell adhesion molecule 1 (NCAM1) and extracellular signal-regulated kinase 2 (ERK2) in epileptic rats with cognitive dysfunction. The experiments were conducted using 120 Wistar rats: 20 controls and 100 with pilocarpine-induced status epilepticus (SE). The SE rats were randomly assigned to 5 groups (n=20/group) that received daily treatments for 1 month with one of the following: (i) saline (no effect on epilepsy); (ii) carbamazepine (an anticonvulsant); (iii) oxcarbazepine (an anticonvulsant); (iv) aniracetam (a nootropic); or (v) donepezil (an acetylcholinesterase inhibitor). Spatial learning and memory were assessed using a Morris Water Maze (MWM). Hippocampal tissue was assessed for NCAM1 and ERK2 messenger RNA (mRNA) expression by reverse transcription polymerase chain reaction, and protein expression by immunochemistry. The results revealed that SE rats had significantly poorer MWM performances compared with controls (P<0.01). Performance in SE rats was improved with donepezil treatment (P<0.01), but declined with carbamazepine (P<0.01). Compared with controls, saline-treated SE rats exhibited increased hippocampal NCAM1 mRNA expression (P<0.01). Among SE rats, NCAM1 mRNA expression was highest in those treated with donepezil, followed by aniracetam-, saline-, oxcarbazepine- and carbamazepine-treated rats. Compared to controls, saline-treated SE rats exhibited decreased hippocampal ERK2 mRNA expression (P<0.01). Among SE rats, ERK2 mRNA expression was highest in those treated with donepezil, followed by aniracetam, saline, oxcarbazepine and carbamazepine. NCAM1 and ERK2 protein expression levels were parallel to those of the mRNA. In saline-treated SE rats, hippocampal ERK2 expression was decreased and NCAM1 expression was increased; thus, these two molecules may be involved in the impairment of spatial memory. Carbamazepine augmented this impairment, whereas donepezil was found to ameliorate the dysfunction associated with epilepsy. In conclusion, ERK2 and NCAM1 have significant roles in impairment of spatial memory in SE rats. Carbamazepine may increase this impairment, while donepezil may decrease this impairment.

No MeSH data available.