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Biomedical subjects

M E Morris

Publications and source records attributed to M E Morris.

At least 19 recordsLinked to original sources
PubMed1995

Correlation of anoxic neuronal responses and calbindin-D28k localization in stratum pyramidale of rat hippocampus.

Immunohistochemical staining for the calcium-binding protein calbindin-D28k (CaBP) was combined with Lucifer Yellow (LY) identification and intracellular recording of changes in membrane parameters of pyramidal neurons in CA2, CA1, and the subiculum of rat hippocampal slices during brief exposure (4.0 +/- 0.19 min) to N2. Anoxia evoked either a depolarization or hyperpolarization of membrane potential (VM) (+21.5 +/- 2.79 mV above VM = -70.5 +/- 1.50 mV, n = 30 and -7.2 +/- 0.72 mV below VM = -68.2 +/- 1.34 mV, n = 24, respectively) and a fall in membrane resistance of approximately 20%. Differences in the response could be correlated with the presence or absence of CaBP and the localization of neurons in different layers of stratum pyramidale and sectors of the hippocampus. For neurons immunopositive for calbindin (CaBP(+)), depolarization was observed more frequently (83%) than hyperpolarization (17%); in contrast, 44% of responses of calbindin-negative (CaBP(-)) neurons were depolarizing and 56% were hyperpolarizing. Depolarizations of CaBP(+) neurons were more gradual in slope, and more rapidly reached a plateau in comparison with those recorded in CaBP(-) neurons. Responses of neurons in the superficial layer of stratum pyramidale (in which 79% of CaBP(+) pyramidal neurons were situated) were mainly depolarizing (91%), while for those in the deep layer (which contained 89% of the CaBP(-) cells) such responses were observed less often (45%). Depolarization was also more common than hyperpolarization for cells located in CA2/CA1c/CA1b (63%) than in the CA1a/subicular region (37%). The depolarizing response of the majority of pyramidal neurons which are CaBP(+), superficial, and closer to CA3 may reflect an efficient buffering of intracellular Ca2+, which maintains a low [Ca2+]i, steep gradient for Ca2+ influx and may facilitate the movement of Ca2+ away from points of entry. The neurons which are CaBP(-), deep, and closer to subiculum and in which N2 evokes hyperpolarization, on the other hand, may have a sustained elevation/accumulation of cytosolic Ca2+ which could activate K+ conductance, inhibit Ca2+ influx, and stabilize the membrane potential. These experiments provide a functional correlate for CaBP and suggest that it may have a significant role in Ca2+ homeostasis and the determination of selective neuronal vulnerability.

Animals↗
PubMed1995

Effects of acute caffeine ingestion and menopause on sulfate homeostasis in women.

Inorganic sulfate is a physiological anion which is utilized in the metabolism of both endogenous compounds and xenobiotics. Its homeostasis is maintained predominantly by facilitated reabsorptive processes in the kidneys. The objectives of the present investigation were to evaluate the effects of menopausal status and caffeine ingestion on the serum concentrations and clearance of inorganic sulfate. Thirty-nine women who were classified as premenopausal, postmenopausal with or without estrogen treatment, and postmenopausal with osteoporosis participated in the study. The women were studied on two separate occasions following the ingestion of a decaffeinated beverage to which 6 mg caffeine/kg lean body mass or no caffeine was added. All women were habitual caffeine users (mean ingestion of 588 mg caffeine per day) but abstained from all caffeine sources for 2 weeks prior to the control study day. Postmenopausal women with estrogen supplementation exhibited significantly lower sulfate serum concentrations (0.24 +/- 0.02 mM vs. 0.32 +/- 0.04 mM in premenopausal women, mean +/- SD, p < 0.05) and a decreased renal reabsorption of sulfate for the control (no caffeine) period. There was no difference in serum sulfate or sulfate reabsorption in estrogen supplemented postmenopausal women, compared with women not taking estrogen. Postmenopausal women with osteoporosis had significantly lower creatinine and sulfate clearances than postmenopausal women with estrogen supplementation which may be related to their older age, or factors related to the disease process. The 6 mg/kg dose of caffeine caused a diuresis, but no change in GFR, as indicated by urine volume and creatinine clearance values, respectively. Caffeine administration resulted in an increase in the sulfate excretion rate; there was no change in sulfate serum concentrations. The results of this investigation indicate that menopause results in decreased sulfate serum concentrations that may be the consequence of a decreased renal reabsorption of sulfate. Secondly, this investigation demonstrated that caffeine ingestion increases the urinary excretion of sulfate, an effect that may be related to the diuretic effect of caffeine or due to a caffeine-induced alteration in the renal reabsorption of sulfate.

Adult↗
PubMed1995

Renal adaptation to altered dietary sulfate in rats.

Proximal tubular reabsorption is of primary importance in the regulation of the homeostasis of inorganic sulfate, an electrolyte that is necessary for biosynthetic and detoxification reactions. The objective of the present investigation was to determine the effect of dietary sulfate deprivation, produced by a diet low in methionine, on the renal transport of sulfate. Female Lewis rats were fed a diet containing negligible amounts of sulfate and cystine and low in methionine (0.37%) or a control diet (methionine 1.12%, cystine 0.07%) for 8 days to examine the urinary excretion rate and renal clearance of sulfate. The sulfate excretion rate was decreased by day 4 of the low methionine diet and remained low. Both the urinary excretion rates and renal clearance values were significantly decreased on day 8 (144 +/- 71 vs. 517 +/- 264 mumol/12 hr in controls, mean +/- S.D., n = 7, P < .005 and 0.38 +/- 0.19 vs. 1.07 +/- 0.61 ml min-1 kg-1 in controls, n = 5-6, P < .05, respectively), although the serum sulfate concentrations were unchanged. In vitro transport studies were performed in kidney cortex brush border membrane (BBM) and basolateral membrane vesicles isolated from rats fed either the low methionine or control diet for 7 to 9 days. The Vmax for BBM sodium/sulfate cotransport was increased in kidneys from animals that received the low methionine diet (1.1 +/- 0.10 vs. 0.75 +/- 0.08 nmol mg of protein-1 10 sec-1 in controls, n = 5, P < .001); there were no significant differences in the Km.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Influence of temperature on anoxic responses of neocortical pyramidal neurons.

Intracellular recordings were made in pyramidal neurons of layers II-III of rat fronto-parietal neocortical slices. The membrane and synaptic properties and effects of brief (4-6 min) anoxia-anoxic depolarization and synaptic depression--were recorded at temperatures between 26 and 37.5 degrees C. In normoxic conditions, both warming (> or = 35 degrees C) and cooling (< or = 32 degrees C) induced a reduction in the amplitude of early and late excitatory postsynaptic potentials and abolished inhibitory postsynaptic potentials. Excitatory postsynaptic potential latency decreased with warming and increased with cooling. Warming also induced spontaneous brief depolarizations, had a general slow depolarizing effect on resting membrane potential, and decreased input resistance. During oxygen deprivation, the steepness of the rising phase of the anoxic depolarization and the duration of the repolarization phase were augmented by warming above 36.5 degrees C (3.7 +/- 0.1 vs 1.9 +/- 0.1 mV/min and 8.75 +/- 0.98 vs 4.16 +/- 0.28 min, respectively). The peak amplitude of the anoxic depolarization increased in only one-third of trials (6.6 +/- 0.6 vs 4.3 +/- 0.4 mV). Warming potentiated the depressant effect of anoxia: at 36.5 degrees C early excitatory postsynaptic potential amplitude decreased to 32.3 +/- 5.2% of control compared with 58.3 +/- 1.2% at 33.5 degrees C, the late excitatory postsynaptic potential was abolished in < 2 min, and the recovery of the compound excitatory postsynaptic potential was prolonged (12.8 +/- 0.8 vs 7.8 +/- 0.3 min). Cooling reduced the amplitude of the anoxic depolarization and increased the input resistance.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Ability to modulate walking cadence remains intact in Parkinson's disease.

Gait hypokinesia (slowness) is a characteristic feature of Parkinson's disease. It is not clear, however, whether the slowness is due to a problem in regulation of the timing of consecutive steps or the control of stride size. Examination of cadence control for slow to medium walking speeds has shown an increase in step frequency that was a compensation for reduced stride length. In this investigation the ability of Parkinsonian patients to modulate their cadence (steps per minute) at the fast walking speeds exhibited by age and height matched controls was examined. The findings indicated that cadence control remains unaffected throughout its entire range in Parkinson's disease and that gait hypokinesia is directly attributable to an inability to internally generate sufficiently large steps.

Adaptation, Physiological↗
PubMed1992

Processing procedures for recovering enteric viruses from wastewater sludges.

A powdered beef extract specially formulated for recovering viruses from environmental samples and designated as beef extract V was evaluated using indigenous and viral seeded wastewater sludge samples. When beef extract V was used to process activated and aerobically digested sludge solids, virus recoveries were shown to be similar to other methods that used commercially available supplemented beef extract. When used to process other sludge solids (primary and activated without primary clarification), cytotoxicity resulted in the BGM cell line used for virus assay. When these sludge solids were processed with the supplemented commercially marketed beef extract cell toxicity did not occur. Metal concentrations in the processed sewage sludge eluates were analyzed, but based on the levels observed they could not be shown as the source of the cytotoxicity. This did not exclude possible synergistic cytotoxic effects or organometal complexes. The commercially marketed beef extract was supplemented with either a floccing aid (FeCl3), a filter aid (Celite) or a floc prepared from paste beef extract. The paste beef floc supplement proved to be the most useful and reliable method for processing for viruses from wastewater sludge solids.

Animals↗
PubMed1992

Influence of NSAID-induced inhibition of renal prostaglandin synthesis on inorganic sulfate clearance in rats.

The objective of the present investigation was to examine the influence of inhibition of renal prostaglandin synthesis on the renal clearance of inorganic sulfate, an electrolyte involved in the biotransformation of both exogenous and endogenous substrates. Homeostasis of inorganic sulfate is maintained predominantly by renal reabsorption in the proximal tubule. Using a crossover study design, the renal clearance of sulfate was assessed in conscious female Lewis rats during control periods and following the infusion of two structurally dissimilar nonsteroidal anti-inflammatory drugs, ibuprofen (IBU) and indomethacin (INDO). Animals were infused with IBU or INDO to achieve steady state concentrations of 59 +/- 8 micrograms/ml (mean +/- SD) of IBU and 22 +/- 3 micrograms/ml of INDO. At these serum concentrations, IBU and INDO produced greater than 80% decrease in the urinary excretion of prostaglandin (PG) E2. Treatment with either IBU or INDO significantly increased the renal clearance of sulfate, but did not alter the glomerular filtration rate as assessed by creatinine clearance. The role of prostaglandins in the effects of IBU and INDO on sulfate homeostasis was investigated by examining the influence of concomitant intraarterial PGE2 administration (infusion of 0.1 micrograms/min) on nonsteroidal anti-inflammatory drug-induced alterations in sulfate renal clearance. Although PGE2 alone did not significantly alter the renal clearance of inorganic sulfate or that of creatinine, the PGE2 infusion abolished the effects of IBU on sulfate renal clearance. Concomitant PGE2 administration also significantly increased the sulfate reabsorption rate in INDO-treated animals; other parameters were not significantly changed, although the fractional reabsorption of sulfate tended to increase (P = 0.17). The reason for the less pronounced effect on PGE2 on the INDO-sulfate interaction is as yet unknown, but may be partly due to additional mechanisms involved in the INDO-induced alterations in sulfate clearance. The results of these studies suggest that prostaglandin inhibition represents one mechanism whereby IBU can alter the renal clearance of inorganic sulfate.

Animals↗
PubMed1992

Brain and CSF magnesium concentrations during magnesium deficit in animals and humans: neurological symptoms.

Magnesium is an essential cofactor for many enzymatic reactions, especially those involved in energy metabolism. Deficits of magnesium are prevalent due to inadequate intake or malabsorption and due to the renal loss of magnesium that occurs in certain disease states (alcoholism, diabetes) and with drug therapy (diuretics, aminoglycosides, cisplatin, digoxin, cyclosporin, amphotericin B). Protracted deficits of magnesium in humans and animals result in neurological disturbances, including hyperexcitability, convulsions and various psychiatric symptoms ranging from apathy to psychosis, some of which can be reversed with magnesium supplementation, others requiring correction of the dysregulation mechanism. Although the role of magnesium in neuronal function is not completely understood, a lowering of CSF or brain magnesium can induce epileptiform activity and there is an association between decreased CSF magnesium and the development of seizures. CSF concentrations of magnesium are normally higher than magnesium plasma ultrafiltrate (diffusible) concentrations due to the active transport of magnesium across the blood-brain barrier. Under conditions of magnesium deficiency, CSF concentrations decline, although this decline lags behind and is less pronounced than the changes observed in plasma magnesium concentrations. Decreases in CSF magnesium concentrations correlate with the alterations observed in extracellular brain magnesium concentrations in animals following the dietary deprivation of magnesium. CSF magnesium concentrations can readily be repleted following magnesium supplementation, although high dose magnesium therapy, such as that used in the treatment of convulsions in eclampsia, will only increase CSF magnesium concentrations to a very limited degree (approximately 11-18 per cent) above physiological concentrations. Greater increases in CSF magnesium may occur in neonates since neonatal swine, following treatment with magnesium, have CSF magnesium concentrations that are similar to their plasma concentrations. There has been a recent resurgence of interest in magnesium deficiency and its neurological consequences due to the finding that magnesium, at physiological concentrations, blocks N-methyl-D-aspartate (NMDA) receptors in neurones. NMDA receptors are normally activated by glutamate and/or aspartate which represent the principal neurotransmitters for excitatory synaptic transmission in vertebrate CNS. Magnesium deficiency produces epileptiform activity in the CNS which can be blocked by NMDA receptor antagonists. Other mechanisms, including alterations in Na+/K(+)-ATPase activity, cAMP/cGMP concentrations and calcium currents in pre- and postsynaptic membranes, may also be at least partially responsible for the neuronal effects associated with low brain magnesium. Further studies are necessary to increase our understanding of the neurological implications of magnesium deficit in the central nervous system.

Animals↗
PubMed1992

Electrogoniometric feedback: its effect on genu recurvatum in stroke.

The purpose of this study was to determine the effect of combining electrogoniometric feedback with contemporary physical therapy procedures for treatment of genu recurvatum following stroke. Twenty-six patients suffering knee hyperextension resulting from cerebrovascular disorders were allocated to either a control group or an experimental group. Both groups received treatment for knee hyperextension during two consecutive phases. During phase I the control group received physical therapy and the experimental group received electrogoniometric feedback as an adjunct to physical therapy. In phase II both groups received physical therapy alone. Each phase lasted four weeks, during which time patients were treated 45 minutes daily, five days every week. Subjects in the experimental group showed greater reduction in knee hyperextension. This was particularly evident in phase II when the difference between groups for reduction in knee hyperextension reached statistical significance (U = 40, p = 0.011). These results suggest that the addition of electrogoniometric feedback to standard physical therapy enhanced the effectiveness of treatment for genu recurvatum in stroke.

Adult↗
PubMed1991

Depolarizing effects of anoxia on pyramidal cells of rat neocortex.

The response of rat neocortical pyramidal neurons (layers II III) in vitro to brief periods of anoxia is a reversible depolarization of 3.8 +/- 1.01 mV (mean +/- S.E.M.; n = 114), which is accompanied by a moderate decrease in input resistance and significant depression of evoked synaptic activity. This effect is mimicked by ouabain, and is partially attenuated by the excitatory amino acid (EAA) antagonist, kynurenic acid. The estimated reversal potential (Vrev) for the anoxic depolarization (AD) is between -35 and -40 mV; in the presence of TTX a Vrev of -65 mV is obtained. Although a partial failure of Na(+)-K(+) pump activity and release of EAAs may contribute the generation of the AD, other processes are likely to be involved.

Animals↗
PubMed1991

Nucleotide sequence of the LYS2 gene of Saccharomyces cerevisiae: homology to Bacillus brevis tyrocidine synthetase 1.

The Saccharomyces cerevisiae LYS2 gene, which encodes alpha-aminoadipate reductase, an essential enzyme in the yeast lysine biosynthetic pathway, has been sequenced. A large open reading frame (ORF) has been identified which can specify a 1392-amino acid protein with a deduced Mr of 155,344. A DNA database search using the translated LYS2 ORF as a probe has revealed significant aa sequence homology to the Bacillus brevis enzyme tyrocidine synthetase 1.

Aldehyde Oxidoreductases↗
PubMed1991

Changes in extracellular K+ evoked by GABA, THIP and baclofen in the guinea-pig hippocampal slice.

Changes in [K+]0 evoked by the inhibitory amino acid transmitter, GABA (gamma-aminobutyric acid) and its agonists were recorded with ion-selective microelectrodes in the CA1 stratum pyramidale of guinea-pig hippocampal slices. Bath applications of GABA (0.1-10 mM) produced dose-dependent increases in [K+]0 (EC50 = 4 mM, Rmax = 1.6 mM), with a peak and decline during exposure, followed by undershoot during recovery. In contrast the selective GABAA agonist, THIP (4,5,6,7-tetrahydroisoxazolo-(5,4-c)-pyridin-3-ol) (0.01-1 mM) showed approximately ten-fold greater potency and evoked only increases in [K+]0 (EC50 = 0.5 mM, Rmax = 2 mM). Reduction of temperature from 34 degrees to 22 degrees C caused a more than two-fold augmentation of the K+0 accumulation evoked by GABA, but no change in that due to THIP. The GABAA antagonist, BMI (bicuculline methiodide) (100 microM) completely blocked responses to THIP and partially antagonized those to GABA. Responses to GABA were synergistically enhanced by pentobarbital (100 microM). Only small, delayed and inconsistent changes could be evoked by relatively high concentrations of the GABAB agonist, DL-baclofen (0.01-1 mM). The K+ changes evoked by GABA appear to be mediated by the activation of GABAA receptors with low affinity and to be related to their depolarizing action. Although the response includes an electrogenic component which suggests the involvement of Na-dependent transmitter uptake/transport, the increase in K+0 probably reflects an outward counter/co-transport of K+ with Cl/HCO3 anion shifts and/or activation of a voltage-dependent K+ conductance.

Animals↗
PubMed1991

Sulfate homeostasis. IV. Probenecid-induced alterations of inorganic sulfate in rats.

Homeostasis of inorganic sulfate is maintained by the capacity-limited renal reabsorption of sulfate in the proximal tubule. The purpose of the present investigation was to determine if probenecid, the classical inhibitor of renal organic anion secretion, may affect sulfate renal clearance. Two groups of rats were administered in a randomized crossover design, an i.v. bolus dose (20.6 or 92.4 mg/kg) and 4-hr infusion (0.28 or 0.59 mg/min/kg) of probenecid or vehicle, and blood and urine samples were collected. At a steady-state serum concentration of 0.45 mM, probenecid had no significant effect on the serum concentrations or renal clearance of inorganic sulfate, whereas at a serum concentration of 1.4 mM, probenecid treatment caused a significant decrease in serum sulfate concentrations (0.57 +/- 0.11 vs 0.96 +/- 0.19 mM in controls, mean +/- SD, n = 6, P less than 0.001) due to an increase in the renal clearance of sulfate (3.88 +/- 1.18 vs 2.13 +/- 0.84 ml/min/kg in controls, P less than 0.01). The fraction of the filtered sulfate that was reabsorbed was significantly decreased (0.38 +/- 0.23, vs 0.74 +/- 0.09 in controls, P less than 0.01). Therefore, probenecid treatment results in the inhibition of the renal reabsorption of inorganic sulfate in rats in vivo.

Animals↗
PubMed1991

Evaluation of "true" creatinine clearance in rats reveals extensive renal secretion.

The renal clearance of endogenous creatinine is widely used to assess glomerular filtration rate (GFR) and renal function in animal investigations. The objective of the present investigation was to evaluate the extent of renal secretion of endogenous creatinine in rats and the effect of probenecid, the classical inhibitor of organic anion transport, on creatinine clearance. Ten female Lewis rats received 3H-inulin (5-muCi i.v. bolus followed by 5 muCi/hr) throughout a 6-hr period. Three hours after initiation of the inulin infusion, probenecid was administered (92.4-mg/kg i.v. bolus followed by 0.59 mg/min/kg). Steady-state serum concentrations of about 500 micrograms/ml probenecid were achieved. Renal clearance was assessed between 1 and 3 hr (control) and between 4 and 6 hr (probenecid treatment). A preliminary study in seven rats demonstrated no time-dependent change in inulin or creatinine clearance between these two study intervals. Creatinine clearances were determined by an alkaline picrate assay which incorporated Fuller's earth (Lloyd reagent) to remove interfering noncreatinine chromogens from serum samples and these values were compared with those using a nonspecific picrate assay. "True" clearance ratios of creatinine to inulin (Clcr/CLin) were greater than unity (2.33 +/- 0.83, mean +/- SD) and were significantly decreased after probenecid treatment (1.26 +/- 0.28, P less than 0.01). Probenecid had no effect on GFR, as assessed by inulin clearance. Using the nonspecific picrate assay, CLcr/CLin was 1.12 +/- 0.41, which was not significantly different from unity and which decreased to 0.53 +/- 0.12 after probenecid treatment. Therefore, creatinine undergoes extensive renal secretion in female Lewis rats.

Animals↗
PubMed1991

Sulfate homeostasis. III. Effect of chronic naproxen or sulindac treatment on inorganic sulfate disposition in arthritic patients with renal impairment.

The purpose of the present investigation was to examine the influence of chronic naproxen (500 mg twice daily) or sulindac (200 mg twice daily) therapy on the disposition of inorganic sulfate in arthritic subjects with impaired renal function. Subjects were studied during a control period (after a 7-day NSAID washout) and after 14 days of treatment with either naproxen or sulindac. During the control period subjects in this investigation exhibited higher serum sulfate concentrations and lower sulfate renal clearance values than reported for younger subjects with normal renal function. Treatment with either sulindac or naproxen significantly decreased creatinine clearance. Sulindac therapy also increased the serum sulfate concentration and decreased the clearance of sulfate; a similar trend was observed after naproxen therapy but the average change was smaller and not statistically significant. There were significant correlations between the creatinine and the sulfate clearances or serum concentrations. The glomerular filtration rate of inorganic sulfate was not altered by drug treatment and there was no impairment of reabsorption. The serum concentrations and renal clearance of other electrolytes (sodium, potassium, magnesium, calcium, phosphorus) were largely unaffected. Therefore, chronic treatment with naproxen or sulindac decreases the renal clearance of endogenous sulfate in humans: this appears to be a consequence of the decrement in renal function observed in subjects with preexisting mild renal impairment.

Aged↗