Abstract
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.
Highlights
Parkinson’s disease (PD) is the neurodegenerative disease caused by the selective and progressive loss of dopaminergic (DAergic) neurons in the substantia nigra pars compacta (SNpc), which leads to a reduction in DAergic fibers in the striatum from the nucleus and results in extrapyramidal motor dysfunctions in patients with PD [1]
We examined the effects of daily oral administration of B. breve A1 for 4 days on the facilitation of fear extinction in PD mice
The results of this study demonstrated that oral administration of B. breve A1 restores the facilitation of contextual fear extinction in PD mice via the prevention of abnormal changes in hippocampal synaptic plasticity, the mechanism of which is probably due to the normalizing of an aberrant higher induction of neuropsin without stimulating the cyclic adenosine monophosphate (cAMP)/cAMP response element-binding protein (CREB) pathway in the hippocampus
Summary
Parkinson’s disease (PD) is the neurodegenerative disease caused by the selective and progressive loss of dopaminergic (DAergic) neurons in the substantia nigra pars compacta (SNpc), which leads to a reduction in DAergic fibers in the striatum from the nucleus and results in extrapyramidal motor dysfunctions in patients with PD [1]. Non-motor symptoms sometimes appear in patients with PD before the onset of motor dysfunction [2,3]. The probability of onset of cognitive impairment is relatively high, appearing in about 40% of PD patients [4]. It recently became widely known that probiotics are good for health through the daily intake of adequate amounts of living microorganisms [5]. Several species of probiotics have been reported to maintain a suitable intestinal environment [6], reduce the risk of infectious disease via normalization of the immune system [7,8], and help prevent the onset of obesity [9] and cancer [10] through improving the intestinal bacterial flora.
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