Correlation between behavioral status and cerebral glucose utilization in rats following freezing lesion

Colle, Lois M.; Holmes, Larry J.; Pappius, Hanna M.

doi:10.1016/0006-8993(86)91366-1

Cited by 48 publications

(23 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…As reported in the current study, 6 h following a lateral F-P injury, the cerebral cortex and underly ing hippocampus ipsilateral to the site of insult ex hibited a marked decrease in LCMR g lc • This repli cates our previous work and agrees with several other studies exhibiting a dif fuse metabolic depression following cerebral isch emia (Kushner et al, 1984;Shiraishi et al, 1989), cortical freezing lesions (Pappius, 1981(Pappius, , 1982(Pappius, , 1988Papius and Wolfe, 1983;Colle et al, 1986), and sen sorimotor cortex ablations (Feeney et a1., 1985). Al though this metabolic diaschisis appears to be a rel atively common phenomenon following injury, the mechanisms behind its expression are not well un derstood.…”

Section: Hypometabolismsupporting

confidence: 92%

Hippocampal CA₃Lesion Prevents Postconcussive Metabolic Dysfunction in CA₁

Yoshino¹,

Hovda²,

Katayama³

et al. 1992

J Cereb Blood Flow Metab

View full text Add to dashboard Cite

Summary: Immediately following fluid-percussion (F-P) brain injury, the hippocampus exhibits a marked increase in its local CMR g lc (LCMR g l c ; ILmol/lOO g/min) as deter mined using [14C]2-deoxY-D-glucose autoradiography. This injury-induced increase in metabolism is followed in 6 h by a subsequent decrease in LCMR g lc' These two postinjury metabolic states may be the result of ionic dis ruptions following trauma via stimulation of glutamate gated ion channels. To determine if endogenous gluta mate innervation to the CAl region of the hippocampus can provide an anatomical basis for this proposed mech anism, it was removed by kainic-acid-induced destruc tion of CA3, and the effect on CAl metabolism following concussive injury was studied. Five days before a lateral F-P injury (3.5-4.5 atm), kainic acid (0.5 ILg) or vehicle was stereotaxically injected into the left ventricle of 65 rats. Histological inspection indicated that kainic acid produced severe cell loss primarily in the CA3 region of the hippocampus ipsilateral to the injection. The meta bolic results indicated that immediately following injury, animals with an intact hippocampus exhibited an increase Following cerebral concussion in the rat, as pro duced using fluid-percussion (F-P) , the cerebral cortex and hippocampus exhibit pronounced changes in glucose metabolism. During the acute period, these regions exhibit a marked increase in this metabolism as determined by e 4 C]2-deoxY-D-

show abstract

Section: Hypometabolismsupporting

confidence: 92%

Hippocampal CA₃Lesion Prevents Postconcussive Metabolic Dysfunction in CA₁

Yoshino¹,

Hovda²,

Katayama³

et al. 1992

J Cereb Blood Flow Metab

View full text Add to dashboard Cite

show abstract

“…This distinguishes the present studies from other investigations of brain injury, where acute insults to the brain were shown to result in widespread metabolic deficits that improved with time [4,11,30,46]. In brain lesion models, the period of post-injury metabolic depression has been shown to correlate with the duration of behavioral deficits [11,20,45].…”

Section: Discussionmentioning

confidence: 49%

“…Three way ANOVA for percent asymmetry with factors of Group, Brain Region and Time revealed a significant main effect for Group (F [1,264] = 154.96, P < 0.001) and Region (F [10,264] = 7.46, P < 0.001) but no main effect for Time (F [1,264] = 0.19, P = 0.657). A significant interaction occurred between Group and Brain Region (F [1,11] = 11.96, P < 0.001), where the most impacted regions were the primary motor cortex followed by the primary sensory and frontal cortices (F [3,11] =45.1, P<0.001). Two-way repeated measures analysis of percent asymmetry data from only cannulated animals that completed both scans were performed for each region, where factors were Group and Time.…”

Section: [ 18 F]fdg Micropet Resultsmentioning

confidence: 99%

Metabolic and behavioral deficits following a routine surgical procedure in rats

et al. 2007

View full text Add to dashboard Cite

To test the hypothesis that functional metabolic deficits observed following surgical brain injury are associated with changes in cognitive performance in rodents, we performed serial imaging studies in parallel with behavioral measures in control animals and in animals with surgical implants. Memory function was assessed using the novel object recognition (NOR) test, administered 3 days prior to and 3, 7, 14, and 56 days after surgery. At each time point, general locomotion was also measured. Metabolic imaging with 18 F-fluorodeoxyglucose ([ 18 F]FDG) occurred 28 and 58 days after surgery. Animals with surgical implants performed significantly worse on tests of object recognition, while general locomotion was unaffected by the implant. There was a significant decrease in glucose uptake after surgery in most of the hemisphere ipsilateral to the implant relative to the contralateral hemisphere. At both time points, the most significant metabolic deficits occurred in the primary motor cortex (-25%; p<0.001), sensory cortex (-15%, p<0.001) and frontal cortex (-12%; p<0.001). Ipsilateral areas further from the site of insertion became progressively worse, including the sensory cortex, dorsal striatum and thalamus. This data was supported by a voxel-based analysis of the PET data, which revealed again a unilateral decrease in [ 18 F]FDG uptake that extended throughout the ipsilateral cortex and persisted for the duration of the 58-day study. Probe implantation in the striatum results in a widespread and long lasting decline in cortical glucose metabolism together with a persistent, injury-related deficit in the performance of a cognitive (object recognition) task in rats.

show abstract

“…In other words, the energy needs of cortical areas in injured brain were thought to be diminished because of a functional depression. Such an interpretation is supported by the demonstration in this model of in jury of somatosensory deficits that were signifi cantly correlated with the extent of the depression of glucose utilization in the cortical areas of the le sioned hemisphere (Colle et aL, 1986).…”

mentioning

confidence: 55%

The Effect of p-Chlorophenylalanine on Cerebral Metabolism and Biogenic Amine Content of Traumatized Brain

Pappius

Dadoun

McHugh

1988

J Cereb Blood Flow Metab

View full text Add to dashboard Cite

Summary: It was shown previously that focal cortical freezing lesions in rats cause widespread decrease in local cerebral glucose utilization (LCGU) in cortical areas of the lesioned hemisphere. This was interpreted as reflecting a depression of cortical activity. It was then demonstrated that cortical serotonin (5-HT) metabolism was increased throughout the lesioned hemisphere of a focally injured brain. To find out if the changes in the serotonergic system are of functional importance and me diate the observed changes in LCG U, the effects of the inhibition of 5-HT synthesis with p-chlorophenylalanine (PCP A) on cerebral metabolism and biogenic amine con tent in injured brain were studied. PCPA in doses up to 300 mg/kg had little, if any, effect on LCG U in intact brain and in doses up to 100 mg/kg did not modify the depressed LCGU in injured brain. In doses of 200 and 300 mg/kg, PCP A selectively increased cortical glucose utilization in the lesioned hemisphere where it was de pressed following injury. PCPA decreased 5-HT levels in U sing focal cortical freezing in the rat as a model of cerebral injury and the deoxyglucose (DG) method as developed and described by Sokoloff et al. (1977) to assess the functional state of trauma tized brain, earlier studies (Pappius, 1981) showed that a widespread, but not uniformly distributed, depression of local cerebral glucose utilization Abbreviations used: DG, deoxyglucose; DHBA, dihydroxy benzylamine; 5-HIAA, 5-hydroxyindoleacetic acid; 5-HT, sero tonin; LCGU, local cerebral glucose utilization; NE, norepi nephrine; PCPA, p-chlorophenylalanine . 324the cortical and raphe areas of both intact and injured brain in a dose-dependent manner. However, at doses of PCPA ineffective on LCGU (50 and 100 mg/kg), traumati zation still resulted in increased 5-HT metabolism. Doses of PCPA that ameliorated the depression of LCGU in in jured brain completely prevented increases in both 5-HT and its metabolite 5-hydroxyindoleacetic acid seen fol lowing traumatization in untreated animals. These results provide evidence that decreased LCGU in lesioned brain is due to an activation of the serotonergic system by trau matization. The data are in agreement with the postulated inhibitory role of serotonin in the cortex and its involve ment in functional alterations associated with injury. They suggest that blockage of this neurotransmitter system may have a potential in the development of novel therapeutic approaches to brain injury. Key Words: Brain injury-p-Chlorophenylalanine-Local cerebral glucose utilization -Norepinephrine -Serotonin.(LCGU ) developed with time after lesioning. The effects were not related to the location of the le sion, which was regularly placed in the parietal cortex, but could be made more frontally or cau dally with the same results (Colle et aI., 1986). The most severe metabolic depression occurred in all the cortical regions of the lesioned hemisphere were 3 days after the lesion LCGU was -50% of normal from frontal to visual cortex (Pappius, 198 1). Thus, the ...

show abstract

Correlation between behavioral status and cerebral glucose utilization in rats following freezing lesion

Cited by 48 publications

References 20 publications

Hippocampal CA₃Lesion Prevents Postconcussive Metabolic Dysfunction in CA₁

Hippocampal CA₃Lesion Prevents Postconcussive Metabolic Dysfunction in CA₁

Metabolic and behavioral deficits following a routine surgical procedure in rats

The Effect of p-Chlorophenylalanine on Cerebral Metabolism and Biogenic Amine Content of Traumatized Brain

Contact Info

Product

Resources

About

Correlation between behavioral status and cerebral glucose utilization in rats following freezing lesion

Cited by 48 publications

References 20 publications

Hippocampal CA3Lesion Prevents Postconcussive Metabolic Dysfunction in CA1

Hippocampal CA3Lesion Prevents Postconcussive Metabolic Dysfunction in CA1

Metabolic and behavioral deficits following a routine surgical procedure in rats

The Effect of p-Chlorophenylalanine on Cerebral Metabolism and Biogenic Amine Content of Traumatized Brain

Contact Info

Product

Resources

About

Hippocampal CA₃Lesion Prevents Postconcussive Metabolic Dysfunction in CA₁

Hippocampal CA₃Lesion Prevents Postconcussive Metabolic Dysfunction in CA₁