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PubMed1986

Concentrations of GABA and glycine in discrete brain nuclei. Stress-induced changes in the levels of inhibitory amino acids.

Concentrations of gamma-aminobutyric acid (GABA), glycine and serine have been measured in 44 microdissected areas of the brain of the rat. All three amino acids were ubiquitously present and distributed unevenly in the brain. Very high levels of GABA were found in the anterior hypothalamic and medial preoptic nuclei and the substantia nigra; high levels were found in the interpeduncular and red nuclei in the mesencephalon and in several hypothalamic nuclei. Glycine was distributed fairly uniformly with large concentrations in certain lower brainstem nuclei. In these areas, the concentrations of glycine exceeded those of serine, while the serine-glycine ratio was 4.5:1 in the caudate nucleus, 4:1 in the cerebellum and 2.5:1 in the cerebral cortical areas. Acute stress induced with formalin (pain) resulted in a significant depletion of levels of GABA in the hypothalamus and the lower brainstem but not in the cortical areas. In the same animals, concentrations of glycine doubled in the cerebral cortex and remained unchanged elsewhere in the brain. Increased motor and behavioral activity after the acute administration of a large dose of amphetamine were associated with a 2-5-fold increase in the levels of glycine in brain, and markedly elevated the concentrations of GABA in the major biogenic amine-containing cell groups only (substantia nigra, locus coeruleus and dorsal raphe).

Animals↗

PubMed2004

Identification of the protein disulfide isomerase family member PDIp in experimental Parkinson's disease and Lewy body pathology.

Parkinson's disease (PD) is a slowly progressing neurodegenerative disorder with no clear etiology. Pathological hallmarks of the disease include the loss of dopaminergic neurons from the substantia nigra (SN) and the presence of Lewy bodies (LBs) (alpha-synuclein and ubiquitin-positive, eosinophilic, cytoplasmic inclusions) in many of the surviving neurons. Experimental modeling of PD neurodegeneration using the neurotoxins 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and 1-methyl-4-phenyl-pyridinium (MPP(+)) has identified changes in gene expression of different endoplasmic reticulum (ER) stress proteins associated with MPTP- and PD-related neurodegeneration. We show that the protein disulfide isomerase (PDI) family member pancreatic protein disulfide isomerase (PDIp), previously considered exclusively expressed in pancreatic tissue, is uniquely upregulated among PDI family members within 24 h following exposure of retinoic acid (RA)-differentiated SH-SY5Y human neuroblastoma cells to either 1 mM MPP(+) or 10 microM of the highly specific proteasome inhibitor lactacystin. RT-PCR confirms PDIp expression in brain of post-mortem human PD subjects and immunohistochemical studies demonstrate PDIp immunoreactivity in LBs. Collectively, these findings suggest that increased PDIp expression in dopaminergic (DA) neurons might contribute to LB formation and neurodegeneration, and that this increased PDIp expression may be the result of proteasome impairment.

1-Methyl-4-phenylpyridinium↗

PubMed2006

Localised reductions in gyrification in the posterior cingulate: schizophrenia and controls.

UNLABELLED: Several authors report changes in the volume and degree of cortical folding in several presumptive regions of schizophrenia patients. However, no research, to our knowledge, has looked for schizophrenia related differences in cortical volume and degree of cortical folding in post-mortem posterior cingulate cortex (PCCx). METHOD: Brain tissues from 9 people who suffered from schizophrenia (DSM-IV) and 9 controls were cut into 3 mm coronal slices. Three alternative PCCx blocks were available for research. The 3 PCCx blocks were cut into 50 microm sections. The volume and gyrification index (GI) were measured in 15 tissue sections per brain (5 sections per block). RESULTS: People who suffered with schizophrenia showed significant reductions in GI in rostral PCCx, trend reductions were seen in medial and caudal PCCx. In addition, the average volume of the rostral tissue sections was significantly lower in the schizophrenia cohort, suggesting that schizophrenia is associated with reduced volume in the rostral PCCx. However, a true volumetric assessment of the whole PCCx, rather than a limited number of sections from three alternative blocks, is needed to confirm such a hypothesis.

Adult↗

PubMed1997

Cerebral glucose transporter expression in HIV infection.

Abnormalities in cerebral glucose metabolism have been demonstrated in patients with AIDS dementia complex (ADC), with increased consumption in early disease and decreased utilization in late stages. The basis of these changes is unknown. Accordingly, a pilot study was undertaken to determine whether levels of cerebral glucose transporters GLUT1 and GLUT3 were altered by HIV disease. Frontal gray and white matter membrane preparations from patients with HIV encephalitis (HIVE), HIV infection without parenchymal neuropathology, and non-infected controls were utilized in quantitative immunoblots to measure GLUT1 and GLUT3. Results were expressed as a ratio of glucose transporter to structural protein actin. Within-group patient variability was great, precluding statistically significant differences between groups for any one brain region. However, when data for gray and white matter was pooled, results obtained statistical significance, with levels of GLUT1 increasing in HIV infection without neuropathology, and declining with HIVE. Increased GLUT1 in HIV infection without parenchymal neuropathology may be important in the biology of increased glucose consumption described with early ADC. With progression to HIVE, reduced levels of glucose transporters may contribute to late stage hypometabolism.

AIDS Dementia Complex↗

PubMed1984

The effects of post-mortem changes and calcium depletion on the ultrastructure of myocardial cells in a teleost.

The effects of post-mortem changes and calcium depletion on the ultrastructure of myocardial cells in a teleost, Gadus virens L., are described. When incubated at 4 degrees C in cacodylate buffer/Ringer's solution for 8 h some few myocardial cells appear swollen and their mitochondria contain several small (50-250 nm) flocculent densities. In tissue incubated for at least 80 h the mitochondria in all myocardial cells contain a number of such densities. Also, the size of these structures seems to increase with incubation time. Further, after being incubated for at least 150 h the myofibrils appear often twisted and broken, and the electron density of the Z and I bands gradually declines. At prolonged incubation times (about 1,000-1,300 h) the actin filaments and Z band material seem gradually to dissolve, whereas the myosin filaments still make up a distinct A band. Intercalated discs in tissue incubated in calcium-free medium for 4-28 h appear to display a nearly normal structure. The results of the present study are compared with those previously reported for mammals. The observed differences in decomposition rates within teleostean myocardial tissue are discussed.

Animals↗

PubMed1990

Changes in benzodiazepine and acetylcholine receptors in the globus pallidus in Parkinson's disease.

Experiments are described in which the benzodiazepine portion of the gamma-aminobutyric acid (GABA)/benzodiazepine receptor and the muscarinic cholinergic receptor were investigated in Parkinson's disease and control brains. Tritiated flunitrazepam and tritiated quinuclidinyl benzilate (QNB) were used to locate and quantify the receptors by autoradiographic and homogenate binding techniques. Densitometric analysis of autoradiographs of the basal ganglia allowed comparison of receptor densities in the post-mortem control and parkinsonian tissue, while homogenate binding experiments gave information concerning receptor affinity and maximum binding capacity. The results indicate that: 1) Binding of flunitrazepam to the benzodiazepine receptor is reduced in the lateral segment of the globus pallidus in Parkinson's disease. This suggest that the GABA-ergic pathway from the putamen to the lateral pallidal segment is overactive in Parkinson's disease. 2) Binding of QNB to the cholinergic receptors of the medial pallidal segment is increased in Parkinson's disease. This finding suggests underactivity of the cholinergic pathway from the pedunculopontine nucleus of the medial pallidal segment. 3) Binding of these ligands in the caudate and putamen of Parkinson's disease is not significantly different from controls. We reviewed the literature concerning the activity of these projections in parkinsonian conditions assessed by different methods and discuss here their implications for the pathogenesis of parkinsonian symptoms.

Aged↗

PubMed2006

Donor corneas for transplantation: a scanning electron microscopic study of the epithelium.

PURPOSE: Donor corneas are processed in eye banks and used for transplantation as a standard routine. The maximum time limit post-mortem for harvesting donor tissue varies greatly between eye banks. This study aimed to examine the corneal epithelium for structural changes post-mortem. METHODS: A total of 51 corneas harvested between 14 and 163 hours post-mortem were examined using scanning electron and light microscopy. RESULTS: Cell loss occurred through desquamation of flat superficial cells during the first days. In corneas with a post-mortem time of more than 2-3 days, large superficial cell sheets and deeper cells detached, starting centrally. Deep peripheral cells remained. The loss of the superficial cells revealed the 3-dimensional structure of the epithelium and the membrane characteristics of deeper cells. CONCLUSION: The longer the time post-mortem, the greater the epithelial cell loss. However, a rim of peripheral cells remained, even after 7 days. The superficial cell layer showed signs of strong lateral attachment and broke up in a sheet-like fashion. The intercellular adhesion between deeper cells and adhesion between the basal cells and the basement membrane appeared to be weak post-mortem. The cell membrane structures of the remaining cells were surprisingly well retained. The clinical implication of the study is discussed.

Adult↗

PubMed1986

Phosphorus-31 nuclear magnetic resonance study of post mortem catabolism and intracellular pH in intact excised rabbit muscle.

Phosphorus-31 nuclear magnetic resonance has been used to study the post mortem catabolism of high-energy phosphate compounds and the associated intracellular pH variation in pure fast- and slow-twitch rabbit muscles and in rabbit muscle with mixed fiber types. Comparative results from pure fiber types are reported for the first time. Large amounts of glycerophosphorylcholine (14.1 mumol/g fresh tissue) are found in the internal conoidal bundle (ICB), a pure oxidative slow twitch muscle, whereas the m. psoas major (PM), a pure glycolytic fast twitch muscle and the m. gastrocnemius caput medialis (GCM), with mixed fiber types, are devoid of the same metabolite. The total content of phosphorylated metabolites is constant among the three muscle types. The time-dependent post mortem changes in phosphorylated metabolites display the expected rapid drop in phosphocreatine and a simultaneous increase in intracellular inorganic phosphate. However, the ATP level remains constant during more than 2 h. Rate constants for metabolite breakdown and apparent ATPase activity have been determined. The comparative kinetics of intracellular acidosis at 25 degrees C yield rates of 3.3 X 10(-3) pH unit/min for PM, 2.7 X 10(-3) pH unit/min for GCM and 3.0 X 10(-3) pH unit/min for ICB. Initial intracellular pH values are 7.07, 7.20 and 7.02, respectively. Upon aging, the heterogeneity of the Pi signal reflects the existence of cellular compartments with different internal pH. The results suggest that the more intense low-pH Pi signal arises from the sarcoplasmic reticulum while the less intense resonance would reflect the sarcoplasmic higher pH. The temperature effect on post mortem catabolism in the 15-25 degrees C range has been documented. As expected, phosphocreatine and ATP breakdown increase with temperature but at a higher rate for slow-twitch ICB than for fast-twitch PM.

Adenosine Triphosphate↗

PubMed2004

Low nNOS protein in the locus coeruleus in major depression.

Disruptions of glutamatergic and noradrenergic signaling have been postulated to occur in depressive disorders. Glutamate provides excitatory input to the noradrenergic locus coeruleus (LC). In this study, the location of immunoreactivity against neuronal nitric oxide synthase (nNOS), an intracellular mediator of glutamate receptor activation, was examined in the normal human LC, and potential changes in nNOS immunoreactivity that might occur in major depression were evaluated. Tissue containing LC, and a non-limbic, LC projection area (cerebellum) was obtained from 11 to 12 matched pairs of subjects with major depression and control subjects lacking major psychiatric diagnoses. In the LC region, nNOS immunoreactivity was found in large neuromelanin-containing neurons, small neurons lacking neuromelanin, and glial cells. Levels of nNOS immunoreactivity were significantly lower in the LC (- 44%, p < 0.05), but not in the cerebellum, when comparing depressed with control subjects. nNOS levels were positively correlated with brain pH values in depressed, but not control, subjects in both brain regions. Low levels of nNOS in the LC may reflect altered excitatory input to this nucleus in major depression. However, pH appears to effect preservation of nNOS immunoreactivity in subjects with depression. This factor may contribute, in part, to low levels of nNOS in depression.

Adult↗

PubMed1985

Cortical neurons immunoreactive with antisera against neuropeptide Y are altered in Alzheimer's-type dementia.

Neurons identified by their immunoreactivity with antisera against neuropeptide Y (NPY) were studied in three selected areas of the cerebral cortex in brains from controls and in senile dementia of the Alzheimer type (ATD). Changes were more profound in temporal cortex than in parietal cortex, and more severe in parietal cortex than in frontal cortex, paralleling the severity of neuritic plaque formation and incidence of neurofibrillary tangles in these regions. NPY-i neurons became distorted, with enlarged misshapen cell somata and reduced, thickened, and gnarled dendrites. There was a sharp reduction in the extensiveness and delicacy of the axonal plexus; the reorganized axons were haphazard compared to the normal symmetry of these fibers. Besides the alteration in form and sizes, there were also appreciably fewer cells. Nevertheless, the NPY population is not eliminated. Double-label studies of NPY-i and thioflavin indicate that NPY-i fibers can participate in neuritic plaque formation although not all neuritic plaques contained NPY-i axons and not all NPY-i axons were associated with plaques. The surviving NPY cells were evident in all cortices examined, thus giving rise to the speculation that these peptide neurons may have unusual survival and reorganization potential even in terminal neurological disease.

Aged↗

PubMed1992

The role of Ca(2+)-dependent proteases (calpains) in post mortem proteolysis and meat tenderness.

This manuscript summarizes research results from our laboratory regarding the role of endogenous proteases in post mortem proteolysis resulting in meat tenderization. Proteolysis of key myofibrillar proteins is the principal reason for ultrastructural changes in skeletal muscle associated with meat tenderization. Proteases should have the following characteristics to be considered as possible candidates for bringing about post mortem changes: i) to be located within skeletal muscle cells; ii) to have access to the substrate ie, myofibrils); and iii) to be able to hydrolyze the same proteins that are degraded during post mortem storage. Of the proteases located within skeletal muscle cells and thus far characterized, only calpains have all of the above characteristics. Numerous experiments conducted in our laboratory have indicated that the calcium-dependent proteolytic system (calpains) is responsible for post mortem proteolysis. Some of this evidence includes: 1) incubation of muscle slices with buffer containing Ca2+ accelerates post mortem proteolysis; 2) incubation of muscle slices with Ca2+ chelators inhibits post mortem proteolysis; 3) infusion or injection of carcasses with a solution of calcium chloride accelerates post mortem proteolysis and the tenderization process such that post mortem storage beyond 24 h to ensure meat tenderness is no longer necessary; 4) infusion of carcasses with zinc chloride, a potent inhibitor of calpains, blocks post mortem proteolysis and the tenderization process; and 5) feeding a beta-adrenergic agonist to lambs results in a reduction of the proteolytic capacity of the calpain system, which leads to a decreased rate of post mortem proteolysis and produces tough meat.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1976

Post-mortem studies of the semistatic volume-pressure characteristics of infants' lungs.

Semistatic air volume-pressure (V-P) loops were recorded from 172 isolated lungs obtained from infants and children at necropsy. Technically unsatisfactory V-P loop behaviour and the presence of pathological changes led to the exclusion of 98 lungs. A further 10 lungs were excluded as it was decided to study the period of growth up to 90 cm crown-heel length. A total of 64 left lungs remained which were designated "normal". Control data were collected in an attempt to quantify the effects of storage and variations in inflation technique. A maximum inflation pressure of +30 cmH2O was used as a standard Pmax. The resulting maximum inflation volume (Vmax) data showed a cubic relation to the crown-heel length which deviated from the values obtained by the use of in-vivo regression equations. The extent and pattern of the deviation suggest that the technical factors are not a major contributory cause, and other explanations are discussed. The low-pressure proportional data from the deflation limb of the V-P curve are plotted against the crown-hell length, and the resulting curve is analysed. There is a sharp fall in the proportion of Vmax retained in the lung at +5 cmH2O and +2-5 cmH2O with increasing body length, but proportional volume at zero transpulmonary pressure follows the same growth-related pattern as Vmax.

Autopsy↗

PubMed1993

Cellular changes and time since death.

Based on a hypothesis that post-mortem cellular (chiefly nuclear) changes in the white blood cells could reliably be correlated with the time interval since death, (ti), serial observations were made on the counts (total, differential) and light-microscopically observable 'degenerations' of white blood cells obtained from 30 non-refrigerated cadavers (experimental group) and similar cells obtained from 200 hospital patients (control group). While neutrophils degenerated rapidly, lymphocytes did so slowly; the eosinophils and monocytes degenerated at rates between these extremes. In cadaveric blood total counts of identifiable leucocytes on average dropped to zero by 84 hours, identifiable eosinophils and monocytes were first to 'disappear' (by 60 hours), followed by neutrophils (by 66 hours), and finally lymphocytes: identifiable lymphocytes disappeared completely at or around 84 hours from the time of death. This 'differential degeneration' was surprising but useful. Based on the use of all four characteristics--total and differential white cell counts, differential degeneration and morphology of cells--a method for a reasonably exact estimation of ti is presented. The method is appropriate for ti up to 84 hrs (3 1/2 days). Zero white cell counts (total, differential) and bizarre morphology (unidentifiable white blood cells) indicate a ti > 84 hrs. Avenues for further research are indicated.

Cell Membrane↗

PubMed2004

Tau truncation during neurofibrillary tangle evolution in Alzheimer's disease.

The microtubule-associated protein, tau, is a highly soluble molecule that is nonetheless capable of self-association into filamentous deposits characteristic of a number of neurodegenerative diseases. This state change is thought to be driven by phosphorylation and/or C-terminal truncation events resulting in intracellular inclusions, such as the neurofibrillary tangles (NFTs) in Alzheimer's disease (AD). Previously, we reported the existence of a novel truncation event, cleavage at aspartic acid(421), presumably by a caspase, and also described a monoclonal antibody (Tau-C3) specific for tau cleaved at this site. Here, we report the timing of this cleavage event relative to other antibody-targeted alterations in the tau molecule during the course of NFT evolution in AD. Immunohistochemical studies indicate that cleavage at aspartic acid(421) occurs after formation of the Alz50 epitope but prior to formation of the Tau-66 epitope and truncation at glutamic acid(391) (formation of the MN423 epitope). Thus, creation of the Tau-C3 epitope appears to occur relatively early in the disease state, contemporaneous with the initial Alz50 folding event that heralds the appearance of filamentous tau in NFTs, neuropil threads, and the dystrophic neurites surrounding amyloid plaques.

Alzheimer Disease↗

PubMed2007

Mitochondrial alterations in the spinal cord of patients with sporadic amyotrophic lateral sclerosis.

Little information is available about morphologic changes of mitochondria in sporadic amyotrophic lateral sclerosis (ALS). We examined the anterior horns of the lumbar spinal cord in 14 patients with sporadic ALS and 15 age-matched controls by electron microscopy to illuminate the subject. In the controls, one patient showed occasional swollen mitochondria with markedly increased cristae and marked accumulation of mitochondria in the somata of anterior horn neurons. Another patient had periodic, stubby protrusions on the outer membrane. Among the patients with ALS, 7 showed filamentous structures in the inner compartment of the mitochondria mainly of the somata and only occasionally of the axons. The structures were composed of a stack of multilayered cristae consisting of linear structures on a longitudinal section. Other abnormal structures were periodic transverse processes like rungs of a ladder predominantly in somata and only occasionally in the axons, marked accumulation of mitochondria in the somata, dendrites or proximal axons (axon hillock and initial segment), stubby protrusions on the outer membrane, and swollen mitochondria with markedly increased cristae in the somata. The findings in this study may reflect the metabolic disturbance of mitochondria, probably associated with the pathomechanism of degenerative processes of anterior horn neurons in sporadic ALS.

Adult↗

PubMed2003

Timing of neuronal and glial ultrastructure disruption during brain slice preparation and recovery in vitro.

Hippocampal slices often have more synapses than perfusion-fixed hippocampus, but the cause of this synaptogenesis is unclear. Ultrastructural evidence for synaptogenic triggers during slice preparation was investigated in 21-day-old rats. Slices chopped under warm or chilled conditions and fixed after 0, 5, 25, 60, or 180 minutes of incubation in an interface chamber were compared with hippocampi fixed by perfusion or by immersion of the whole hippocampus. There was no significant synaptogenesis in these slices compared with perfusion-fixed hippocampus, but there were other structural changes during slice preparation and recovery in vitro. Whole hippocampus and slices prepared under warm conditions exhibited an increase in axonal coated vesicles, suggesting widespread neurotransmitter release. Glycogen granules were depleted from astrocytes and neurons in 0-min slices, began to reappear by 1 hour, and had fully recovered by 3 hours. Dendritic microtubules were initially disassembled in slices, but reassembled into normal axial arrays after 5 minutes. Microtubules were short at 5 minutes (12.3 +/- 1.1 microm) but had recovered normal lengths by 3 hours (84.6 +/- 20.0 microm) compared with perfusion-fixed hippocampus (91 +/- 22 microm). Microtubules appeared transiently in 15 +/- 3% and 9 +/- 4% of dendritic spines 5 and 25 minutes after incubation, respectively. Spine microtubules were absent from perfusion-fixed hippocampus and 3-hour slices. Ice-cold dissection and vibratomy in media that blocked activity initially produced less glycogen loss, coated vesicles, and microtubule disassembly. Submersing these slices in normal oxygenated media at 34 degrees C led to glycogen depletion, as well as increased coated vesicles and microtubule disassembly within 1 minute.

Animals↗

PubMed1993

A quantitative dendritic analysis of Wernicke's area in humans. I. Lifespan changes.

Age-related increases and decreases have been described in cortical dendritic neuropil. Here, we examine age-related changes in the basilar dendrites of supragranular pyramidal cells in human superior temporal gyrus (i.e., Wernicke's area) of left and right hemispheres. Tissue was obtained from 20 neurologically normal right-handers from 18-79 years: 10 males (Mage = 52.2 years; SDage = 17.4) and 10 females (Mage = 47.8; SDage = 20.5). In tissue prepared by a modified rapid Golgi technique, ten pyramidal cells were sampled from each hemisphere and evaluated according to the following parameters: total dendritic length, mean dendritic length, and dendritic segment count. Despite considerable interindividual variation, the data exhibited significant dendritic degeneration with aging. There was an age-related decrease in total dendritic length (r[20] = -0.44; P < 0.05) and especially in mean dendritic length (r[20] = -0.69; P < 0.001) with increasing age. Age-mean dendritic length correlations were negative for all segment orders and revealed a progressive decrease in segment length in more distal branches. The number of dendritic segments remained relatively stable across the age span sampled. The data also indicated that interhemispheric dendritic asymmetries decreased with age. Individuals under 50 years of age had significantly greater total dendritic length values in the left hemisphere. Interhemispheric dendritic differences were not significant in individuals over 50.

Adolescent↗

PubMed2001

Changes of voltage-dependent anion-selective channel proteins VDAC1 and VDAC2 brain levels in patients with Alzheimer's disease and Down syndrome.

Voltage-dependent anion-selective channel proteins (VDACs) are pore-forming proteins found in the other mitochondrial membrane of all eukaryotes and in brain postsynaptic membranes. VDACs regulate anion fluxes of a series of metabolites including ATP, thus regulating mitochondrial metabolic functions. We determined protein levels of VDACs in individual post-mortem brain regions of patients with Down Syndrome (DS) and Alzheimer's disease (AD) using two-dimensional electrophoresis (2-DE) and matrix-assisted laser desorption/ionization-mass spectroscopy (MALDI-MS). VDAC1 (SWISS-PROT accession number P21796) and VDAC2 (P45880) were unambiguously identified and quantified, but VDAC3 was not found. The spots representing VDAC1 were separated with different p/s (p/7.5, 8.5, and 10.0) probably caused by post-translational modifications as, e.g., phosphorylation. In DS cerebellum, total VDAC1 protein was elevated significantly whereas VDAC2 did not show any significant alterations. In AD brains, VDAC1 p/10.0 was significantly reduced in temporal, frontal, and occipital cortex with the p/7.5 form elevated in occipital cortex. Total VDAC1 was significantly decreased in frontal cortex and thalamus. VDAC2 was significantly elevated in temporal cortex only. The biological meaning of our results may be derangement of voltage-dependent anion-selective channel function and reflecting impaired glucose, energy, and intermediary metabolism as well as apoptotic mechanisms.

Age Factors↗