WIDESPREAD METABOLIC DEPRESSION AND REDUCED SOMATOSENSORY CIRCUIT ACTIVATION FOLLOWING TRAUMATIC BRAIN INJURY IN RATS

The effects of fluid percussion brain injury on the basal metabolic st ate and responsiveness of a somatosensory circuit to physiologic activ ation were investigated with [C-14]2-deoxyglucose autoradiography. Und er controlled physiologic conditions and normothermic brain temperatur e (37 degrees C), rats were injured with a moderate fluid percussion p ulse ranging from 1.7 to 2.1 atm. At 4 or 24 h after traumatic brain i njury (TBI), unilateral vibrissae stimulation was carried out, resulti ng in the metabolic activation of the whisker-barrel circuit. In sham- operated control animals, whisker stimulation resulted in the metaboli c activation of the ipsilateral trigeminal medullary complex (177% of control), contralateral ventrobasal thalamus (143% control), and prima ry somatosensory cortex (153% control). At 4 h after injury, local cer ebral metabolic rates of glucose (ICMRglu) were significantly depresse d throughout the traumatized hemisphere. Although depressed ICMRglu wa s most pronounced in cortical regions adjacent to the evolving contusi on (53% of control), significant decreases were also seen in more remo te areas, including the frontal cortex (75% of control), hippocampus ( 79% control), and lateral thalamus (68% of control). At 24 h following TBI, ICMRglu remained significantly reduced at the impact site, withi n the ipsilateral somatosensory cortex and lateral thalamus. Stimulus- evoked increases in ICMRglu were depressed within all three relay stat ions of the vibrissae-barrel-field circuit at 4 and 24 h after TBI. Th ese results demonstrate both focal and diffuse metabolic depression af ter moderate TBI. Although the most severe and longer lasting metaboli c consequences occurred in cortical and thalamic regions destined to e xhibit histopathologic damage, milder abnormalities, most prominent in the early posttraumatic period, were also seen in noninjured areas. T he inability to activate the somatosensory circuit metabolically indic ates that circuit dysfunction is an acute consequence of TBI. Widespre ad circuit or synaptic dysfunction would be expected to participate in the functional and behavioral consequences of TBI.