Marked and variable inhibition by chemical fixation of cytochrome oxidase and succinate dehydrogenase in single motoneurons.

Chalmers, Gordon; Edgerton, V. Reggie

doi:10.1177/37.6.2542395

Cited by 49 publications

(19 citation statements)

References 9 publications

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“…The tissue sections were air dried for 30 min and subsequently stained for SDH activity for 10 min at room temperature. 9,10 The activity of SDH, an oxidative marker enzyme, was rendered visible by incubating the sections in 0.1M phosphate buffer (pH 7.6) containing 0.9 mM sodium azide, 0.9 mM 1-methoxyphenazine methylsulfate, 1.5 mM nitroblue tetrazolium, 5.6 mM EDTA-disodium salt, and 48 mM succinate disodium salt. The reaction was terminated by multiple rinses in distilled water, dehydrating in graded alcohols, and passing through xylene.…”

Section: Enzyme Histochemical Procedures and Analysesmentioning

confidence: 99%

Comparison of the response of motoneurons innervating perineal and hind limb muscles to spaceflight and recovery

et al. 2000

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Section: Enzyme Histochemical Procedures and Analysesmentioning

confidence: 99%

Comparison of the response of motoneurons innervating perineal and hind limb muscles to spaceflight and recovery

et al. 2000

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“…A series of sections was processed for C O quantitative histochemistry using previously described procedures (Gonzalez-Lima and Jones, 1994;C ada, 1994, 1998;Gonzalez-Lima et al, 1997). Fresh-frozen tissue was used, and preincubation fixation was restricted to 5 min because of its detrimental effects on C O activity (Chalmers and Edgerton, 1989;Gonzalez-Lima and C ada, 1998). Briefly, slides were first treated in 10% sucrose phosphate buffer (0.1 M, pH 7.6) containing 0.5% glutaraldehyde (Grade II) for 5 min.…”

Section: Methodsmentioning

confidence: 99%

Energy Hypometabolism in Posterior Cingulate Cortex of Alzheimer's Patients: Superficial Laminar Cytochrome Oxidase Associated with Disease Duration

2001

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Among brain regions affected in Alzheimer's disease (AD), the posterior cingulate shows the earliest and largest decrement in energy metabolism. Positron emission tomography (PET) studies have shown that these decrements appear before the onset of memory deficits or other symptoms in persons at genetic risk for AD. This study compares in vivo imaging results and in situ postmortem analyses by examining the posterior cingulate (area 23) in 15 AD patients and 13 age-matched nondemented controls using quantitative cytochrome oxidase histochemistry as an intracellular measure of oxidative energy metabolic capacity. Each of the six layers of the posterior cingulate demonstrated a decline in cytochrome oxidase activity in AD relative to controls, whereas adjacent motor cortex showed no significant differences. This decrement did not appear to be mainly secondary to nonspecific decrement in mitochondrial enzymes, oxidative stress, cell loss, or histopathology. The cytochrome oxidase decrement was most severe in the superficial layer I (Ϫ39%), which demonstrated a correlation to disease duration. Covariance analyses suggest that superficial laminas undergo a functional uncoupling from the deeper layers of posterior cingulate cortex in AD, whereas no such effects are found in motor cortex or controls. These findings expand on previous results from PET studies by illuminating the layer-specific cytochrome oxidase contributions to energy hypometabolism. The findings suggest a decrement of cytochrome oxidase in posterior cingulate cortex, with progressive reduction within the superficial laminas linked to disease duration. Such decrement could contribute to some of the behavioral symptoms displayed by AD patients. This decrement appeared greater in women.Key words: cytochrome oxidase; energy metabolism; posterior cingulate cortex; Alzheimer's disease; brain mapping; gender Decrements in energy metabolism are one of the earliest detectable abnormalities in Alzheimer's disease (AD). Positron emission tomography (PET) studies on subjects homozygotic for the ⑀4 allele of the apolipoprotein E (APOE) gene, with no symptoms of AD, demonstrate metabolic reductions in posterior cingulate, parietal, temporal, and prefrontal cortices (Reiman et al., 1996;Small et al., 2000). Their largest decrement was in the posterior cingulate cortex (PCC) (Reiman et al., 1996), as in the case of AD (Minoshima et al., 1994). Another PET study (Minoshima et al., 1997) confirmed that although normal subjects show intense PCC metabolic activity, early-stage AD patients suffered a PCC decrement (21-22%) that was significantly greater than that seen in other cortical regions. This greater hypometabolism determined by PET is not merely an artifact of generalized atrophy (Ibanez et al., 1998) or AD histopathology that is lower in PCC than the other regions (Braak and Braak, 1998), although degeneration of PCC occurs in AD (Brun and Gustafson, 1976). Severity of AD symptoms is correlated with hypoactivity in PCC but not temporal regions, as measured with PE...

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“…The sections were stained for SDH activity, an indicator of mitochondrial oxidative potential, for 10 min at room temperature [5,6]. The SDH activity was determined in an incubation medium containing 100 mM phosphate buffer (pH 7.5), 0.9 mM sodium azide, 0.9 mM 1-methoxyphenazine methylsulphate, 1.5 mM nitroblue tetrazolium, 5.6 mM EDTA-disodium salt, and 48 mM succinate disodium salt.…”

Section: Succinate Dehydrogenase (Sdh) Activitymentioning

confidence: 99%

Growth-Related Changes in Skeletal Muscle Fiber Type and Insulin Resistance in Diabetic Otsuka Long-Evans Tokushima Fatty Rats.

Yasuda

Ishihara

Adachi

et al. 2001

Acta Histochem. Cytochem

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We investigated whether a relationship exists between the fiber type distribution in skeletal muscles and the insulin resistance of different ages of diabetic rats. The fiber type distributions of the slow soleus and fast plantaris muscles in 5-, 9-, and 21-week-old male Otsuka LongEvans Tokushima Fatty (OLETF) rats as an animal model of spontaneous type 2 diabetes mellitus were examined and compared with those in age-matched nondiabetic Long-Evans Tokushima Otsuka (LETO) rats. In the soleus muscle, a higher percentage of type I fibers was observed in the 9-and 21-week-old OLETF rats compared with the age-matched LETO rats, and there were no type IIA fibers remaining in the soleus muscle of the OLETF rats. In the plantaris muscle, a lower percentage of type IIA fibers and a higher percentage of type IIB fibers were observed in the 9-and 21-week-old OLETF rats compared with the agematched LETO rats. In addition, a lower percentage of type I fibers in the plantaris muscle was observed in the 9-weekold OLETF rats compared with the agematched LETO rats, and there were no type I fibers in the plantaris muscle of the 21-week-old OLETF rats. All 20-weekold OLETF rats showed serum insulin concentrations of more than 20 ng/ml. The present study suggests that insulin resistance and impaired glucose tolerance from altered muscle fiber type are linked to the cause of diabetes.

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Marked and variable inhibition by chemical fixation of cytochrome oxidase and succinate dehydrogenase in single motoneurons.

Cited by 49 publications

References 9 publications

Comparison of the response of motoneurons innervating perineal and hind limb muscles to spaceflight and recovery

Comparison of the response of motoneurons innervating perineal and hind limb muscles to spaceflight and recovery

Energy Hypometabolism in Posterior Cingulate Cortex of Alzheimer's Patients: Superficial Laminar Cytochrome Oxidase Associated with Disease Duration

Growth-Related Changes in Skeletal Muscle Fiber Type and Insulin Resistance in Diabetic Otsuka Long-Evans Tokushima Fatty Rats.

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