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M S Reid

Publications and source records attributed to M S Reid.

At least 55 records · Page 3Linked to original sources

Striatonigral GABA, dynorphin, substance P and neurokinin A modulation of nigrostriatal dopamine release: evidence for direct regulatory mechanisms.

The striatonigral pathway contains several neurotransmitters which may regulate the activity of the nigrostriatal dopamine projection in the rat. This was investigated by measuring extracellular dopamine levels in the striatum, using microdialysis, after injections of GABA (300 nmol/0.2 microliters), dynorphin A (0.5 nmol/0.2 microliters), substance P (0.07 mnol/0.2 microliters) or neurokinin A (0.09 nmol/0.2 microliters) into the ipsilateral substantia nigra, pars reticulata (SNR). Intranigral injections of GABA or dynorphin A inhibited, while intranigral injections of substance P or neurokinin A stimulated dopamine levels in the ipsilateral striatum. In rats with ibotenic acid lesions (2.5 micrograms/0.5 microliters) in the SNR, intranigral injections of GABA or dynorphin A inhibited, while intranigral injections of substance P or neurokinin A stimulated dopamine levels in the ipsilateral striatum. These responses were not significantly different than those in unlesioned rats. Analysis of the intranigral lesion with in situ hybridization revealed a heavy loss of glutamic acid decarboxylase mRNA expression in the SNR and a significant loss of tyrosine hydroxylase (TH) mRNA expression in the SNC. Immunohistochemical analysis revealed a disappearance of TH-Like immunoreactivity (LI) im dendrites in the SNR, a considerable loss of TH-LI cell bodies in the SNC and a restricted loss of neuropeptide K-LI in the SNR around the tip of the injection cannula. Furthermore, lesioned rats rotated ipsilateral to the lesion after apomorphine (1 mg/kg, s.c.), indicating that the basal ganglia output mediated via the SNR GABA neurons was impaired on the lesioned side. Analysis of the striatum revealed that a dense TH-LI fiber network could still be seen on the lesioned side. Furthermore, basal and amphetamine stimulated extracellular dopamine levels in the striatum on the lesioned side were not significantly depleted. This indicates that the ascending nigrostriatal dopamine projection was functionally intact on the lesioned side. These findings indicate that intranigral GABA, dynorphin A, substance P and neurokinin A modulation of ipsilateral striatal dopamine release is mediated via direct action on the nigrostriatal projection. Thus, it is suggested that the striatonigral pathway, which contains GABA, dynorphin, substance P and neurokinin A, exerts a direct regulatory effect on the activity of the nigrostriatal dopamine projection.

Animals↗

Effects of intranigral substance P and neurokinin A on striatal dopamine release--I. Interactions with substance P antagonists.

The functional role of striatonigral neurokinins were studied by analysing the effects of intranigral injections of substance P and neurokinin A on the extracellular level of dopamine and dihydroxyphenylacetic acid in the striatum, as measured by in vivo microdialysis in rats. Two substance P antagonists, substance P D-Pro2 D-Trp7,9 and substance P D-Arg1 D-Trp7,9 Leu11 were tested and analysed for their ability to block the neurokinin effects. Unilateral injections of substance P (0.00007-7.0 nmol injected in 0.2 microliter) as well as neurokinin A (0.009-9.0 nmol) into the substantia nigra, pars reticulata of halothane anaesthetized rats produced long-lasting increases in ipsilateral striatal dopamine and dihydroxyphenylacetic acid levels. The dose-response relationship for substance P on dopamine was biphasic, with maximal effects occurring after the middle dose (0.007-0.07 nmol). The dose-response relationship for neurokinin A was monophasic. Intranigral injections of substance P D-Pro2 D-Trp7,9 (0.07-0.7 nmol) or substance P D-Arg1 D-Trp7,9 Leu11 (0.07-0.7 nmol) produced a decrease in striatal dopamine, but an increase in striatal dihydroxyphenylacetic acid. At a low dose (0.07 nmol) substance P D-Pro2 D-Trp7,9 enhanced the dopamine increase produced by intranigral substance P (0.07 nmol) or neurokinin A (0.09), while at a high dose (0.7 nmol) it blocked both substance P and neurokinin A effects. Both doses of substance P D-Arg1 D-Trp7,9 Leu11 (0.07 and 0.7 nmol) blocked the substance P- but not the neurokinin A-induced increase in striatal dopamine. Immunohistochemical analysis revealed that high doses of substance P (7.0 nmol) and neurokinin A (0.9 and 9.0 nmol), as well as substance P D-Pro2 D-Trp7,9 and substance P D-Arg1 D-Trp7,9 Leu11 (0.07 and 0.7 nmol), induced a restricted loss of tyrosine hydroxylase in dendrites and cells, and neuropeptide K in terminals, at the site of injection. Further analysis shows that co-administration of substance P (0.07 nmol) or neurokinin A (0.09 nmol) did not modify the extent of the depletion of both immunoreactivities induced by substance P D-Arg1 D-Trp7,9 Leu11 (0.7 nmol). The extent of the effect produced by substance P D-Arg1 D-Trp7,9 Leu11 (0.7 nmol) was, however, smaller than the spread of intranigral injection of [125I]Bolton-Hunter-labelled substance P D-Arg1 D-Trp7,9 Leu11, and it is suggested that the "neurotoxic" effects of the substance P antagonists are not primarily involved in their abilities to inhibit striatal dopamine release and block the stimulation of dopamine after intranigral substance P and neurokinin A.(ABSTRACT TRUNCATED AT 400 WORDS)

3,4-Dihydroxyphenylacetic Acid↗

Effects of intranigral substance P and neurokinin A on striatal dopamine release--II. Interactions with bicuculline and naloxone.

The functional roles of striatonigral neurokinins were studied by analysing the effects of intranigral injections of substance P and neurokinin A on the extracellular levels of dopamine and dihydroxyphenylacetic acid in the striatum, as measured by in vivo microdialysis in rats. An opioid antagonist, naloxone, and a GABAergic antagonist, bicuculline, were tested and analysed for their ability to modify the neurokinin effects. Unilateral injections of substance P (0.07 nmol) or neurokinin A (0.09 nmol) into the substantia nigra, pars reticulata of halothane anaesthetized rats produced long-lasting increases in ipsilateral striatal dopamine and dihydroxyphenylacetic acid levels. Intranigral injections of naloxone (30 and 300 nmol) produced short-lasting decreases in striatal dopamine, concomitant with an increase in dihydroxyphenylacetic acid. Intranigral injections of 7.0 nmol bicuculline produced an increase, while 70 nmol produced a decrease in striatal dopamine, however, both doses produced an increase in dihydroxyphenylacetic acid. When co-administered intranigrally, the high dose of naloxone (300 nmol) completely blocked the dopamine stimulation of substance P (0.07 nmol), but only moderately inhibited that of neurokinin A (0.09 nmol). The high dose of bicuculline (70 nmol) completely blocked the dopamine stimulation of neurokinin A, but only moderately inhibited that of substance P. Naloxone (30 and 300 nmol) enhanced the dihydroxyphenylacetic acid response to substance P, while bicuculline (70 nmol) inhibited the dihydroxyphenylacetic acid response to neurokinin A. These findings complement and extend the findings in the preceding paper, demonstrating that intranigral substance P and neurokinin A stimulate striatal dopamine via different neuronal mechanisms. We suggest that opioid drugs have a greater influence over substance P while GABAergic drugs have a greater influence over neurokinin A.

Animals↗

Striatal dopamine and glutamate release: effects of intranigral injections of substance P.

The levels of extracellular striatal dopamine and glutamate were measured simultaneously in halothane-anaesthetized rats using microdialysis. Unilateral injections of substance P (0.07 nmol) into the substantia nigra, pars reticulata enhanced the levels of dopamine and glutamate in the ipsilateral striatum. Intranigral injections of neurokinin A (0.09 nmol) enhanced the levels of striatal dopamine, and intranigral injections of gamma-aminobutyric acid (300 nmol) or dynorphin A (0.5 nmol) decreased the levels of striatal dopamine, but none of these had any effect on the levels of striatal glutamate. Local perfusion with the dopamine agonists apomorphine (D1/D2), SKF 38393 (D1) or pergolide (D2) (each at 10(5) M) decreased the levels of striatal dopamine and enhanced the levels of striatal glutamate. In unilateral 6-hydroxydopamine-lesioned rats, basal striatal glutamate levels were decreased bilaterally. Furthermore, on the denervated side intranigral substance P stimulation of striatal glutamate levels was enhanced, while on the intact side intranigral substance P stimulation of striatal dopamine and glutamate levels was similar to that seen in normal rats. These findings suggest that striatonigral substance P provides a stimulatory regulation of ipsilateral striatal glutamate release. Furthermore, it is indicated that striatal glutamate release can also be regulated by dopamine terminals.

3,4-Dihydroxyphenylacetic Acid↗

The Role of Ethylene in the Inhibition of Rooting under Low Oxygen Tensions.

A 60-fold increase in ethylene content was observed in stem cuttings of chrysanthemum (Chrysanthemum x morifolium Ramat.) held in aero-hydroponics under anoxic conditions during the 8 to 12 days necessary for adventitious root formation. Ethylene, 1-aminocyclopropane-1-carboxylic acid, and 10-(malonylamino) cyclopropane-1-carboxylic acid contents were highest in the immersed portion of the cuttings, but there was substantial ethylene produced by the anoxic, misted portions of the cutting above the liquid. Application of ethylene (10 microliters per liter) to chrysanthemum cuttings stimulated root development in cuttings held in high dissolved oxygen concentrations (8.0 milligrams per liter). Since the application of ethylene did not inhibit rooting in cuttings held at low dissolved oxygen concentrations (2.0 milligrams per liter), the inhibition of rooting under low oxygen concentrations is not mediated by the observed increase in endogenous ethylene content.

Journal Article↗

Translocation and rearrangement of myeloperoxidase gene in acute promyelocytic leukemia.

Acute promyelocytic leukemia (subtype M3) is characterized by malignant promyelocytes exhibiting an abundance of abnormally large or aberrant primary granules. Myeloperoxidase (MPO) activity of these azurophilic granules, as assessed by cytochemical staining, is unusually intense. In addition, M3 is universally associated with a chromosomal translocation, t(15;17)(q22;q11.2). In this report, the MPO gene was localized to human chromosome 17 (q12-q21), the region of the breakpoint on chromosome 17 in the t(15;17), by somatic cell hybrid analysis and in situ chromosomal hybridization. By means of MPO complementary DNA clones for in situ hybridization and Southern blot analysis, the effect of this specific translocation on the MPO gene was examined. In all cases of M3 examined, MPO is translocated to chromosome 15. Genomic blot analyses indicate rearrangement of MPO in leukemia cells of two of four cases examined. These findings suggest that MPO may be pivotal in the pathogenesis of acute promyelocytic leukemia.

Bone Marrow↗

Role of carbohydrates in diurnal chilling sensitivity of tomato seedlings.

Tomato seedlings (Lycopersicon esculentum Mill.) chilled starting at different times during the light/dark cycle were most chilling-sensitive at the end of the dark period (AI King, MS Reid, BD Patterson 1982 Plant Physiol 70: 211-214). Low-temperature tolerance was regained with as little as 10 minutes of light exposure. Low light intensities were less effective than high light intensities in reducing sensitivity, and the length of exposure to light directly influenced sensitivity. Seedlings kept at low night temperatures prior to chilling were also less injured following chilling. Light also restored chilling tolerance to seedlings whose roots were removed. Supplying cut shoots with sucrose, glucose, or fructose reduced chilling sensitivity and largely eliminated the diurnal difference in sensitivity. Endogenous carbohydrate content was correlated with changes in chilling sensitivity; starch and sugar content fell markedly during the dark period. Increased concentrations of sugars were detected 15 minutes after the start of the light period. This evidence all suggests that changes in chilling sensitivity over the diurnal period are regulated by the light cycle. It also suggests that increased sensitivity at the end of the dark period could be due to carbohydrate depletion, and that chilling tolerance following light exposure is likely due to carbohydrate accumulation or closely related events.

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Transport Properties of the Tomato Fruit Tonoplast : III. Temperature Dependence of Calcium Transport.

Calcium transport into tomato (Lycopersicon esculentum Mill, cv Castlemart) fruit tonoplast vesicles was studied. Calcium uptake was stimulated approximately 10-fold by MgATP. Two ATP-dependent Ca(2+) transport activities could be resolved on the basis of sensitivity to nitrate and affinity for Ca(2+). A low affinity Ca(2+) uptake system (K(m) > 200 micromolar) was inhibited by nitrate and ionophores and is thought to represent a tonoplast localized H(+)/Ca(2+) antiport. A high affinity Ca(2+) uptake system (K(m) = 6 micromolar) was not inhibited by nitrate, had reduced sensitivity to ionophores, and appeared to be associated with a population of low density endoplasmic reticulum vesicles that contaminated the tonoplast-enriched membrane fraction. Arrhenius plots of the temperature dependence of Ca(2+) transport in tomato membrane vesicles showed a sharp increase in activation energy at temperatures below 10 to 12 degrees C that was not observed in red beet membrane vesicles. This low temperature effect on tonoplast Ca(2+)/H(+) antiport activity could only by partially ascribed to an effect of low temperature on H(+)-ATPase activity, ATP-dependent H(+) transport, passive H(+) fluxes, or passive Ca(2+) fluxes. These results suggest that low temperature directly affects Ca(2+)/H(+) exchange across the tomato fruit tonoplast, resulting in an apparent change in activation energy for the transport reaction. This could result from a direct effect of temperature on the Ca(2+)/H(+) exchange protein or by an indirect effect of temperature on lipid interactions with the Ca(2+)/H(+) exchange protein.

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cDNA cloning of human myeloperoxidase: decrease in myeloperoxidase mRNA upon induction of HL-60 cells.

Myeloperoxidase (MPO), the most abundant neutrophil protein, is a bacteriocidal component of the primary granules and a critical marker in distinguishing acute myelogenous leukemia from acute lymphoid leukemia. A cDNA clone for human MPO was isolated by immunologic screening of human hematopoietic lambda gt11 expression vector libraries with specific anti-MPO antibody. The identity of the cDNA clone was confirmed by finding that epitope-selected antibody against this clone recognizes purified MPO and MPO in human promyelocytic (HL-60) cell lysates by immunoblot analysis, and that hybrid selection of HL-60 mRNA with this cDNA clone and translation in vitro results in the synthesis of an 80-kDa protein recognized by the anti-MPO antiserum. RNA blot analysis with this MPO cDNA clone detects hybridization to two polyadenylylated transcripts of approximately 3.6 and approximately 2.9 kilobases in HL-60 cells. No hybridization is detected to human placenta mRNA. Upon induction of HL-60 cells to differentiate by incubation for 4 days with dimethyl sulfoxide, a drastic decrease in the hybridization intensity of these two bands is seen. This is consistent with previous data suggesting a decrease in MPO synthesis upon such induction of these cells. The MPO cDNA should be useful for further molecular and genetic characterization of MPO and its expression and biosynthesis in normal and leukemic granulocytic differentiation.

Cell Line↗

Changes in Cotyledon mRNA during Ethylene Inhibition of Floral Induction in Pharbitis nil Strain Violet.

Floral induction in seedlings of Pharbitis nil strain Violet, with one cotyledon removed, was manipulated by applying various ethylene treatments to the remaining cotyledon during a 16 hour inductive dark period. Exposure of cotyledons to ethylene (100 microliters per liter) for 4 hours at different times during the dark period inhibited flowering to some extent, with inhibition being greater towards the end of the dark period. RNA from cotyledons given a 16 hour dark period (induced) or exposed to 100 microliters per liter ethylene throughout the dark period, which completely inhibited flowering, was examined. The poly(A)(+)RNA was translated in vitro using a wheat germ system, and the resulting translation products were analyzed by two-dimensional sodium dodecyl sulfate-polyacrylamide gel electrophoresis. There were substantial qualitative and quantitative differences between the poly(A)(+)RNA extracted from induced cotyledons and that from those exposed to ethylene throughout the dark period. Some of these changes are similar to those observed when flowering was inhibited by photoperiodic treatments (M Lay-Yee, RM Sachs, MS Reid 1987 Planta. In press). The significance of these findings to our understanding of the molecular control of flower induction is discussed.

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Light stimulates the rapid formation of inositol trisphosphate in squid retinas.

To test the hypothesis that inositol trisphosphate (InsP3) mediates adaptation and excitation in invertebrate photoreceptors, we measured its formation on a rapid time scale in squid retinas. For squid, excitation and adaption occurs within 0.1 and 1-2 s respectively. We could detect an elevation in InsP3 within 200 ms of a bright flash. This increase is about 240% over dark basal levels and is maintained for at least 2 min after a flash. The increase probably occurs in the photoreceptors, which are the only neurons in squid retinas. Analysis by h.p.l.c. indicates that the light-regulated isomer is Ins(1,4,5)P3, which is formed by the hydrolysis of phosphatidylinositol bisphosphate (PtdInsP2).

Animals↗

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Disease Outbreaks↗

Effects of low temperature and respiratory inhibitors on calcium flux in plant mitochondria.

The effects of low temperature on uptake and release of (45)Ca(2+) were studied with sound, well-coupled mitochondria extracted at room temperature from avocado (Persea americana Mill, cv Fuerte) fruits. Low Ca(2+) concentrations (10 micromolar) were employed to simulate physiological conditions. At 25 degrees C, the rate of Ca(2+) uptake decreased with time, whereas at 5 degrees C the initial rate, though lower, remained linear. As a consequence total uptake at 5 degrees C was substantially greater than at 25 degrees C for periods greater than 5 min. Preincubation of mitochondria at 5 degrees C enhanced subsequent Ca(2+) uptake at 25 degrees C. Ca(2+) uptake was inhibited by carbonyl cyanide-m-chlorophenyl hydrazone (CCCP) and by ruthenium red, but neither KCN nor salicylhydroxamic acid separately or together had any major inhibitory effect. Preloaded mitochondria held for 60 min in a Ca-free medium lost little Ca(2+) at 25 degrees C and none at 5 degrees C, except in the presence of ruthenium red or CCCP.

Journal Article↗

Diurnal changes in the chilling sensitivity of seedlings.

Seedlings of tomato (Lycopersicon esculentum, Mill.) varied diurnally in their sensitivity to chilling temperatures. If chilled near the end of the dark period when they were most sensitive, the time taken to kill half of the seedlings was approximately 3 days, whereas in samples taken 4 hours after the onset of dark, a period of 6 days of chilling was required. Sensitivity dropped rapidly after the onset of the light period. This rhythm was exogenously controlled by the diurnal changes in light, rather than in the temperature. The susceptibility of predawn seedlings could be reduced by exposure to light, by water stress, or by abscisic acid applied to the leaves. However, the subsequent changes in sensitivity to chilling did not correlate with stomatal aperture. Six other chilling-sensitive species showed similar diurnal changes in their chilling sensitivity.

Journal Article↗

Epinasty of Poinsettias-the Role of Auxin and Ethylene.

Upward physical restraint of the normally horizontal bracts of poinsettia (Euphorbia pulcherrima Willd.) resulted in increased ethylene production and epinastic curvature of the petioles after 5 days. Downward restraint caused little change in ethylene production or epinasty, indicating that the enhanced ethylene production observed in petioles bent upwards is not due to the bending stress alone. Epinasty, measured upon removal of upward physical restraint, was not affected by spraying plants with aminoxyacetic acid to reduce ethylene production or with silver thiosulfate to prevent ethylene action. Removal of the bract blades prevented the epinastic response of the petiole, and the response was restored by applying indoleacetic acid to the cut petiole end. Redistribution of auxin appears to be responsible for both the epinasty and the increased ethylene production of reoriented poinsettia bracts.

Journal Article↗

Effects of pH and Ethephon on Betacyanin Leakage from Beet Root Discs.

Betacyanin leakage from beet root discs was found to increase with decreasing pH of the incubation medium. Although 10 millimolar Ca(2+) reduced pigment leakage at pH 3.5, it was ineffective at pH 2.3. Leakage was also stimulated by 100 micrograms per milliliter (2-chloroethyl)-phosphonic acid (pH 3.1), but when the solution was neutralized, this leakage was eliminated. Bubbling C(2)H(4) through a neutral medium containing beet discs had no effect on pigment leakage; it appears that the effect of Ethephon solutions on this process is a function of their low pH.

Journal Article↗