{'fraction_non_alphanumeric': 0.05007473841554559, 'fraction_numerical': 0.03961136023916293, 'mean_word_length': 4.510288065843621, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
[mRNA expression alteration of two-pore potassium channels in the brain of beta-amyloid peptide25-35-induced memory impaired rats].

AIM
To study mRNA expression alteration of two-pore potassium channels in the brain of beta-amyloid peptide25-35 (beta-AP25-35)-induced memory impaired rats.


METHODS
Memory impairments induced in rats by single icv injection of beta-AP25-35 (2 mmol.L-1) 5 microL were assessed in the Morris water maze test. The mRNA expression levels of three two-pore potassium channels TREK-1, TREK-2 and TRAAK were detected in rat cerebral cortex and hippocampus by reverse transcription-polymerase chain reaction (RT-PCR).


RESULTS
In the Morris water maze test, the escape latencies of the beta-AP25-35-treated rats were longer than those of the control group in 1st, 2nd and 4th training day, suggesting that the memory of beta-AP25-35-treated rats was obviously impaired. Compared with the control group, the mRNA levels of TREK-1, TREK-2 and TRAAK in the hippocampus of the beta-AP25-35-treated rats were increased by 40.0%, 27.9% and 18.9%, respectively; while no significant change of TREK-1, TREK-2 and TRAAK mRNA levels was observed in the cortex.


CONCLUSION
The mRNA expression levels of two-pore potassium channels were increased significantly in the brain of beta-AP25-35-induced memory impaired rats.