Effect of oral administration of Magnesium N-Acetyltaurinate on synaptic plasticity in rodents

We previously reported that 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced Parkinson’s disease (PD) model mice (PD mice) facilitate hippocampal memory extinction, which may be the cause of cognitive impairment in PD. Recent studies on the consumption of probiotics have reported a variety of beneficial effects on the central nervous system via the microbiota–gut–brain axis. In this study, we investigated the effects of oral administration of Bifidobacterium breve strain A1 [MCC1274] (B. breve A1) on the facilitation of hippocampal memory extinction observed in PD mice. We found that four-day consecutive oral administration of B. breve A1 restored facilitation of contextual fear extinction in PD mice. Hippocampal mRNA expression levels of postsynaptic density protein-95 and synaptophysin significantly decreased in the PD mice, but mRNA and protein expression levels of neuropsin increased. Furthermore, CA1 apical spine density was significantly reduced in PD mice. On the other hand, administration of B. breve A1 to PD mice recovered all these expression levels and the CA1 spine density to control levels. These results suggest that increased induction of neuropsin is involved in abnormal changes in hippocampal synaptic plasticity, and that B. breve A1 imposes reins on its expression, resulting in the restoration of abnormal hippocampal synaptic plasticity and the facilitation of fear extinction in PD mice.

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Abstract TP112: Role of Renexin, a Mixed Compound of Ginkgo Biloba Extract and Cilostazol, for Synaptic Plasticity in Hippocampus of Rat Model of Chronic Cerebral Hypoperfusion

Stroke ◽

10.1161/str.47.suppl_1.tp112 ◽

2016 ◽

Vol 47 (suppl_1) ◽

Author(s):

Yeon Soo Ha ◽

Jin Sung Cheong ◽

Hak-Seung Lee ◽

Hyun-Young Park ◽

Kwang Ho Cho ◽

...

Keyword(s):

Synaptic Plasticity ◽

Oral Administration ◽

Real Time ◽

Chronic Cerebral Hypoperfusion ◽

Cerebral Hypoperfusion ◽

Vehicle Group ◽

Quantitative Detection ◽

Rt Pcr ◽

Fepsp Slope ◽

Daily Oral Administration

The impairment of cognitive function such as memory and attention has been recognized in patients with chronic mild cerebral ischemia. The hippocampal memory and long-term potentiation (LTP), a cellular correlate of learning and memory, were impaired by chronic cerebral hypoperfusion induced by permanent, bilateral occlusion of the common carotid artery (2VO). Objectives: The purpose of present study was to evaluate the effects of renexin on the impaired LTP and expression of mRNA genes involving neuronal plasticity in the rat 2 VO model. Methods: Adult male Sprague-Dawley rats were randomly divide three experimental groups into:1) Sham without 2VO, 2) 2VO+vehicle, 3) 2VO+renexin. The permanent ligation of bilateral common carotid arteries was performed to elicit chronically lower blood flow to the brain. Animals were treated with oral administration of renexin(gingko biloba 20 mg/kg/day + cilostazol 25 mg/kg/day) or vehicle every day from1 day after surgery for 3 weeks. We recorded LTP induced by brief high frequency stimulation to the Schaffer collateral-CA1 pathway of the hippocampus under anesthesia in vivo. Two hours after induction of LTP, the animal was sacrificed and the hippocampus was isolated for quantitative detection of mRNA for BDNF, Arc, Egr-1 and CREB using quantitative real-time RT-PCR technique. Results: Animals of 2VO+vehicle group showed a highly significant deficit in LTP induction (15 ± 3% of control fEPSP slope; n= 7; P< 0.01) 3 weeks after 2VO. On the other hand, daily oral administration of renexin showed the marked preservation of LTP induction (98 ± 17% of control fEPSP slope; n =7; P< 0.01). On the real-time RT-PCR analysis, a significant reduction of CREB, Arc and BDNF mRNA expression was observed in the hippocampus of 2VO+vehicle group compared with that of sham group (P< 0.01). In contrast, renexin treatment increased significantly the expression of these mRNAs in the hippocampus compared with that of 2VO+vehicle group (P< 0.05). Conclusion: These results suggest that daily oral administration of renexin can ameliorate cognitive deficit through the preservation of synaptic plasticity on the level of neural circuit in rodent model of chronic cerebral hypoperfusion.

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