Upregulation of the lactate transporter monocarboxylate transporter 1 at the blood-brain barrier in a rat model of attention-deficit/hyperactivity disorder suggests hyperactivity could be a form of self-treatment.
Level 5 - mechanism / opinion, no new human data
Animal laboratory study with no human data
PubMed 30550949 · doi:10.1016/j.bbr.2018.12.023
What was done
Researchers quantified monocarboxylate transporter 1 (MCT1) expression on hippocampal brain sections from 12 spontaneously hypertensive rats (SHRs, an ADHD model) and 12 Wistar Kyoto control rats (WKYs). MCT1 levels were assessed using quantitative immunofluorescence laser scanning microscopy and postembedding immunogold electron microscopy.
What was found
Hippocampal MCT1 immunoreactivity was significantly higher in SHRs compared with WKY controls, particularly at the blood-brain barrier. The abstract does not report numerical measurements, effect sizes, or exact p-values.
Why it matters
This study provides mechanistic preclinical evidence of altered blood-brain barrier lactate transport capacity in a rodent ADHD model, supporting the hypothesis that physical hyperactivity could biologically function to supply muscle-derived lactate to the brain.
Limits
The study is limited to an animal model (SHRs) that may not fully reflect human ADHD. The sample size is modest (12 per group), only hippocampal tissue was analyzed, and actual dynamic lactate flux was not directly measured. Applying these rodent findings to clinical self-treatment concepts in humans remains theoretical.
Cited by
- supports Lactate crosses the blood-brain barrier via MCT transporters to enter the brain.