TY - JOUR
T1 - Neuropathology in sensory, but not motor, brainstem nuclei of the rat whisker circuit after diffuse brain injury
AU - Miremami, Jahan D.
AU - Talauliker, Pooja M.
AU - Harrison, Jordan L.
AU - Lifshitz, Jonathan
N1 - Funding Information:
The authors certify that they have no affiliations with any organization or entity with any financial interest in the subject matter discussed in this paper. This study was supported by the University of Kentucky College of Medicine, KSCHIRT #7-11, R01 NS-065052, the Appalachian and Minority Science, Technology, Engineering and Mathematics Majors (AMSTEMM) grant NSF-0431552, and the Bucks for Brains Presidential Funds for undergraduate research.
PY - 2014/9
Y1 - 2014/9
N2 - Neurological dysfunction after traumatic brain injury (TBI) is associated with pathology in cortical, subcortical, and brainstem nuclei. Our laboratory has reported neuropathology and microglial activation in the somatosensory barrel cortex (S1BF) and ventral posterior medial thalamus (VPM) after diffuse TBI in the rat, which correlated with post-injury whisker sensory sensitivity. The present study extends our previous work by evaluating pathology in whisking-associated sensory and motor brainstem nuclei. Brains from adult, male rats were recovered over 1 month after midline fluid percussion or sham injury. The principal trigeminal nucleus (PrV, sensory nucleus) and facial nucleus (VIIN, motor nucleus) were examined for neuropathology (silver histochemistry) and microglial activation (Iba1). Significant neuropathology in PrV was evident at 2 and 7 days post-injury compared to sham. Iba1-labeled microglia showed swollen somata and thickened processes over 1 month post-injury. In contrast, the VIIN showed non-significant neuropathology and reduced labeling of activated Iba1 microglia over 1 month post-injury. Together with our previous data, neuropathology and neuroinflammation in the whisker somatosensory pathway may contribute to post-injury sensory sensitivity more than the motor pathway. Whether these findings are direct results of the mechanical injury or consequences of progressive degeneration remains to be determined.
AB - Neurological dysfunction after traumatic brain injury (TBI) is associated with pathology in cortical, subcortical, and brainstem nuclei. Our laboratory has reported neuropathology and microglial activation in the somatosensory barrel cortex (S1BF) and ventral posterior medial thalamus (VPM) after diffuse TBI in the rat, which correlated with post-injury whisker sensory sensitivity. The present study extends our previous work by evaluating pathology in whisking-associated sensory and motor brainstem nuclei. Brains from adult, male rats were recovered over 1 month after midline fluid percussion or sham injury. The principal trigeminal nucleus (PrV, sensory nucleus) and facial nucleus (VIIN, motor nucleus) were examined for neuropathology (silver histochemistry) and microglial activation (Iba1). Significant neuropathology in PrV was evident at 2 and 7 days post-injury compared to sham. Iba1-labeled microglia showed swollen somata and thickened processes over 1 month post-injury. In contrast, the VIIN showed non-significant neuropathology and reduced labeling of activated Iba1 microglia over 1 month post-injury. Together with our previous data, neuropathology and neuroinflammation in the whisker somatosensory pathway may contribute to post-injury sensory sensitivity more than the motor pathway. Whether these findings are direct results of the mechanical injury or consequences of progressive degeneration remains to be determined.
KW - Microglial activation
KW - Neuropathology
KW - Rat
KW - Traumatic brain injury
KW - Vibrissal circuitry
UR - http://www.scopus.com/inward/record.url?scp=84906273085&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84906273085&partnerID=8YFLogxK
U2 - 10.3109/08990220.2014.897602
DO - 10.3109/08990220.2014.897602
M3 - Article
C2 - 24702476
AN - SCOPUS:84906273085
VL - 31
SP - 127
EP - 135
JO - Somatosensory Research
JF - Somatosensory Research
SN - 0899-0220
IS - 3
ER -