After traumatic brain injury (TBI), secondary
injuries develop, including neuroinflammatory processes
that contribute to long-lasting impairments. These secondary
injuries represent potential targets for treatment and
diagnostics. The translocator protein 18 kDa (TSPO) is
expressed in activated microglia cells and upregulated in
response to brain injury and therefore a potential biomarker
of the neuroinflammatory processes. Second-generation
radioligands of TSPO, such as [123I]CLINDE, have a
higher signal-to-noise ratio as the prototype ligand
PK11195. [123I]CLINDE has been employed in human
studies using single-photon emission computed tomography
to image the neuroinflammatory response after stroke.
In this study, we used the same tracer in a rat model of TBI
to determine changes in TSPO expression. Adult Sprague–
Dawley rats were subjected to moderate controlled cortical
impact injury and sacrificed at 6, 24, 72 h and 28 days post
surgery. TSPO expression was assessed in brain sections
employing [123I]CLINDE in vitro autoradiography. From
24 h to 28 days post surgery, injured animals exhibited a
marked and time-dependent increase in [123I]CLINDE
binding in the ipsilateral motor, somatosensory and parietal
cortex, as well as in the hippocampus and thalamus.
Interestingly, binding was also significantly elevated in the
contralateral M1 motor cortex following TBI. Craniotomy
without TBI caused a less marked increase in [123I]
CLINDE binding, restricted to the ipsilateral hemisphere.
Radioligand binding was consistent with an increase in
TSPO mRNA expression and CD11b immunoreactivity at
the contusion site. This study demonstrates the applicability
of [123I]CLINDE for detailed regional and quantitative
assessment of glial activity in experimental models of
TBI.