Ceftriaxone has a similar effect on astrocytic and neuronal GLT-1 distribution after mild traumatic brain injury.

Traumatic brain injury (TBI) is a significant health problem around the world. Even mild TBI (mTBI) can cause long-term neurodegenerative consequences such as Alzheimer's disease. Excitotoxicity plays a vital role in neuronal death after TBI, and Glutamate Transporter 1 (GLT-1) may be a therapeutic target for reducing TBI outcomes. It has been found that ceftriaxone (a beta-lactam antibiotic) can reduce TBI symptoms, including astrocyte reactivity and inflammation, and may also affect GLT-1 expression. The primary objective of this study is to investigate how ceftriaxone affects GLT-1 in neurons and astrocytes. mTBI was modelled in male albino mice using a modified Marmarou's weight-drop method. Ceftriaxone (250 mg/kg) was administered intraperitoneally for 3 and 5 days after injury. We immunolabeled coronal brain slices to detect GLT-1 expression and distribution, using antibodies to Glial Fibrillary Acidic Protein (GFAP - astrocytic marker), NeuN (neuronal marker), and GLT-1. The presence of fluorescently labelled areas and the ratio of fluorophores within each area were examined using an image processing plugin that identifies regions with substantial staining in confocal microscopy images. In this article, we address the dynamics of changes in fluorescence intensity and area for the regions we describe as GFAP, NeuN, and GLT-1. We found that GLT-1 dynamics change in both neurons and astrocytes following mTBI, but ceftriaxone affects these changes. In our opinion, due to the displacement of glutamate transporter clusters in cells, they cannot properly fulfil their function of limiting excitability produced by trauma.