Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2021 Feb 8;9(2):167. doi: 10.3390/biomedicines9020167

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© 2021 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

PMC Copyright notice

Living B. breve A1 in the gut lumen leads to the restoration of PD-induced aberrant higher induction of neuropsin, the mechanism of which is caused by a still unknown signal via the gut–brain axis. Neuropsin-mediated signaling plays an important role in synaptic plasticity; physiologically activated neuropsin cleaves extracellular proteins in the synaptic cleft such as fibronectin, vitronectin, L1cam, EphB2 (the cleavage of EphB2 reduces EphB2-NMDA binding), and mNRG-1(the released moiety cleaved from mNRG-1 binds ErbB4 and triggers its phosphorylation), and modifies pre- and postsynaptic interactions and synaptic signal transmission [22,34]. However, an aberrant higher induction of neuropsin observed in PD mice causes abnormal changes in hippocampal synaptic plasticity and function. Oral administration of B. breve A1 restored the facilitation of contextual fear extinction and the decreased hippocampal dendritic spine density in PD mice via normalization of an aberrant higher induction of neuropsin. Abbreviations: EphB2, EPH receptor B2; ErbB4, NRG-1 receptor p185; L1cam, L1 cell adhesion molecule; mNRG-1, mature neuregulin-1; NMDAR, N-methyl-d-aspartic acid receptor.