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 26;15:652494. doi: 10.3389/fnbeh.2021.652494

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

Copyright © 2021 Crews, Fisher, Deason and Vetreno.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

PMC Copyright notice

Adult galantamine treatment reversed the adolescent intermittent ethanol (AIE)-induced increase of proinflammatory neuroimmune signaling molecules in the adult basal forebrain. (A) Modified unbiased stereological assessment revealed a 20% (±5%) increase of high-mobility group box 1 immunoreactive (HMGB1 + IR) cells in the adult (P73) basal forebrain of AIE-treated subjects, relative to CONs. Adult galantamine treatment from P57 to P73 did not affect HMGB1 + IR in CONs, but reversed the AIE-induced increase of HMGB1 + IR cells in adulthood, relative to vehicle-treated AIE subjects. (B) Modified unbiased stereological assessment revealed a 46% (±5%) increase of Toll-like receptor 4 immunoreactive (TLR4 + IR) cells in the adult (P73) basal forebrain of AIE-treated subjects, relative to CONs. Adult galantamine treatment alone did not affect expression of TLR4 + IR cells in CONs, but reversed the AIE-induced increase of TLR4 + IR cells in adulthood, relative to vehicle-treated AIE subjects. Representative photomicrographs of TLR4 + IR cells in the adult basal forebrain of CON- and AIE-treated subjects. Scale bar = 50 μm. (C) Immunofluorescent co-labeling revealed TLR4 (red) colocalization with choline acetyltransferase immunoreactive (ChAT + IR) neurons in the adult basal forebrain. Closed arrowheads = TLR4 + IR colocalization with ChAT + IR neurons (yellow). Scale bar = 50 μm. (D) Modified unbiased stereological assessment revealed a 28% (±5%) increase of receptor for advanced glycation end-products immunoreactive (RAGE + IR) cells in the adult (P73) basal forebrain of AIE-treated subjects, relative to CONs. Adult galantamine treatment alone did not affect RAGE + IR in CONs, but reversed the AIE-induced increase of RAGE + IR cells in adulthood, relative to vehicle-treated AIE subjects. Representative photomicrographs of RAGE + IR cells in the adult basal forebrain of CON- and AIE-treated subjects. Scale bar = 50 μm. (E) Immunofluorescent co-labeling revealed RAGE (red) colocalization with ChAT + IR neurons in the adult basal forebrain. Closed arrowheads = RAGE + IR colocalization with ChAT + IR neurons (yellow). Scale bar = 50 μm. (F) Modified unbiased stereological assessment revealed a 15% (±4%) increase of phosphorylated nuclear factor kappa-light-chain-enhancer of activated B cells p65 immunoreactive (pNF-κB p65 + IR) cells in the adult (P73) basal forebrain of AIE-treated subjects, relative to CONs. Adult galantamine treatment alone did not affect pNF-κB p65 + IR cells in CONs, but reversed the AIE-induced increase of pNF-κB p65 + IR cells in adulthood, relative to vehicle-treated AIE subjects. Data are presented as mean ± SEM (n = 8/group). ^∗p < 0.05, ^∗∗p < 0.01.