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  • 1
    Online Resource
    Online Resource
    Excitation-Contraction Coupling in Skeletal, Cardiac, and Smooth Muscle. (1992)
    New York, NY :Springer,
    Details
    Keywords: Muscle, Smooth-Physiology. ; Electronic books.
    Type of Medium: Online Resource
    Pages: 1 online resource (450 pages)
    Edition: 1st ed.
    ISBN: 9781461533627
    Series Statement: Advances in Experimental Medicine and Biology Series ; v.311
    URL: https://ebookcentral.proquest.com/lib/geomar/detail.action?docID=6493071
    DDC: 591.1852
    Language: English
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    GEOMAR EBL
  • 2
    Electronic Resource
    Electronic Resource
    Clonidine Inhibition of Norepinephrine Release from Normal and Morphine-Tolerant Guinea Pig Cortical Slices (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 58 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Endogenous norepinephrine (NE) release in cerebral cortex slices taken from normal and morphine-tolerant guinea pigs was measured by HPLC. In normal slices, a linear relationship was found between electrically evoked NE release and the log of the frequency of stimulation in the range of 1–20 Hz. The efficiency of the α2-mediated autofeedback was tested by adding the α2 agonist clonidine and the α2 antagonist idazoxan. NE release was dose-dependently reduced by clonidine (1 nmol/L–1 μmol/L) and increased by idazoxan (10–100 nmol/L). The inhibition by clonidine was significantly greater at 1 Hz than at 3 Hz, whereas the absolute increase in NE release induced by idazoxan was greater at 3 Hz than at 1 Hz. Morphine at 1 μmol/L (a concentration per se ineffective) shifted to the left the clonidine concentrations able to inhibit NE release at 3 and 1 Hz (1–10 nmol/L), but at both frequencies, the opiate reduced the maximal inhibition induced by clonidine at 1 μmol/L. In slices taken from morphine-tolerant guinea pigs (in the presence of morphine at 1 μmol/L), clonidine (1 nmol/L–1 μmol/L) was ineffective at the stimulation rate of 3 Hz, but it was more active than in normal slices at 1 Hz. Such a response pattern suggests a reduced availability of α2 receptors and an increase in their sensitivity to clonidine. However, chronic morphine treatment did not influence the physiological autoinhibition because the increase in NE release elicited by idazoxan (10–100 nmol/L) at 1 and 3 Hz was the same in normal and in “morphine-tolerant”slices. Therefore, morphine tolerance affects only the clonidine responsiveness of some α2 receptors, possibly located far from the hot spots of NE release. In contrast, the autofeedback exerted by synaptically released transmitter, as evaluated by testing idazoxan, remains unchanged.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb11361.x
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  • 3
    Electronic Resource
    Electronic Resource
    Comparison of [3H]Choline and d-[3H]Aspartate Efflux from Guinea Pig and Human Neocortex (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 58 (1992), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The outflow of [3H]choline ([3H]Ch) evoked by electrical field stimulation and the efflux of d-[3H]Asp induced by 35 mM KCl and 1–10 μM ouabain were studied in human and guinea pig cortical slices, kept under identical experimental conditions. [3H]Ch outflow was significantly lower whereas d-[3H]Asp efflux was significantly higher in humans than in guinea pigs. This suggests a different proportion of the two neuronal systems in these two species. Blockade of muscarinic autoreceptors with atropine increased, whereas stimulation of α2 receptors with norepinephrine (NE) reduced, the evoked [3H]Ch outflow to the same extent in human and guinea pig cortical slices. Conversely, NE did not affect ouabain-induced d-[3H]Asp efflux, suggesting that an α2-mediated control is not operative in the glutamatergic cortical structures. Desmethylimipramine, 2–5 μM, was able to increase [3H]Ch outflow through atropine-like mechanisms only in the human. This drug at 20–50 μM inhibited [3H]Ch and d-[3H]Asp efflux in both species, through mechanisms unrelated to its monoamine reuptake blocking properties. Thus, similarities and differences can be detected between humans and guinea pigs with regard to (a) the relative potency of the cholinergic and acidic amino acidergic signals and (b) the modulation of neurotransmitter outflow by drugs acting on auto- and heteroreceptors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1992.tb11363.x
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  • 4
    Electronic Resource
    Electronic Resource
    α1Adrenoreceptpr-Mediated Increase in Acetylcholine Release in Braip Slices During Morphine Tolerance (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 53 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Norepinephrine, clonidine, and phenylephrine increased the electrically evoked release of endogenous acetylcholine in cortical slices taken from morphine-tolerant guinea pigs. This effect was α1adrenoreceptor mediated and was opposite to the α2-adrenoreceptor-mediated inhibition of acetylcholine release, normally elicited by norepinephrine and clonidine. In the presence of prazosin, clonidine recovered its normal inhibitory properties, suggesting that morphine tolerance induced the appearance of an α1adrenoreceptor-mediated response that overshadowed, but did not cancel, the still present α2-adrenoreceptor inhibitory control. The attempt to prove the presence of α-adrenoreceptors on the nerve endings by testing the effect of norepinephrine in synaptosomal preparations (preloaded with [3H]choline and de-polarized with KCL and veratridine) was unsuccessful. Therefore the problem of the exact location of this excitatory input remains to be solved. These results confirm previous findings reporting the increase in cortical acetylcholine release induced by the α-adrenoreceptor agonists in morphine-tolerant, freely moving guinea pigs and demonstrate that opiate tolerance inverts the direction of the noradrenergic modulation even in the isolated intracortical cholinergic structures.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb07397.x
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  • 5
    Electronic Resource
    Electronic Resource
    STEADY STATE MAINTENANCE OF ELECTROLYTES IN THE SPINAL CORD OF THE FROG (1979)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 32 (1979), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Isolated frog spinal cords equilibrated from 3 to 24 h in Ringer's solution maintained steady state conditions with regard to electrolyte composition. Total sodium and chloride contents measured on the same spinal cords were found to be nearly equivalent (Na = 46.6 ± 1.4μmol/g wet wt vs Cl = 46.2 ± 1.2μmol/g wet wt). Calcium and magnesium contents were 3.0 ± 0.5 and 4.8 ± 0.2pμol/g wet wt respectively for fresh spinal cords and 2.1 ± 0.4 and 5.5 ± 0.9pmol/g wet wt respectively for spinal cords equilibrated for 24 h. Zinc content was 0.29 ± 0.01 μmol/g wet wt. Insulin space was found to be smaller than sucrose space (0.24 ml/g vs 0.37 ml/g). Sodium and chloride spaces were slightly higher than sucrose space. Sodium and chloride in the non-sucrose space was 4.8 and 9.5 μmol/g wet wt. Residual radioactive sodium, or sodium content of spinal cords washed out for 180 min in non-radioactive Ringer's solution or in choline or lithium Ringer's solution, was 4.2 ± 0.4μmol/g wet wt (n = 9). The agreement between residual sodium content and sodium in the non-sucrose space suggests that the mean intracellular sodium content of the spinal cord neurons is low.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1979.tb02278.x
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  • 6
    Electronic Resource
    Electronic Resource
    The Release of γ-Aminobutyric Acid, Glutamate, and Acetylcholine from Striatal Slices: A Mass Fragmentographic Study (1981)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 36 (1981), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The release processes of endogenous Acetylcholine (ACh), γ-aminobutyric acid (GABA), glutamate (Glu) and glutamine (GLN) were studied in superfused guinea-pig caudatal slices. Basal ACh release remained constant for up to 2 h, while the basal release of GABA, Glu and GLN declined to half or less of its initial values after 1 h of superfusion. Electrical stimulation increased the ACh release by 700–800% and that of GABA by 80% whereas it decreased the output of Glu by 50% and failed to modify the GLN efflux. KCl (25 mM) increased the output of ACh by 400%, that of GABA by approximately 500% and decreased that of Glu by 40%. Substituting of CaCl2 by MgCl2 in the superfusion medium reduced the basal ACh release by 70% whereas no differences were observed in the basal efflux of GABA, Glu and GLN. Under these conditions, no evoked release of ACh or of GABA was detected, following electrical or KCl stimulation. Tetrodotoxin 5 × 10-7 M decreased the basal ACh release by 60% and increased the GABA efflux by 40%. The toxin abolished the stimulus-evoked ACh efflux but scarcely affected that of GABA. These results are consistent with a possible neurotransmitter role of ACh and GABA in the striatum and show some differences in the ionic mechanisms underlying GABA and ACh release.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1981.tb00420.x
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  • 7
    Electronic Resource
    Electronic Resource
    THE EFFECTS OF PSYCHOACTIVE AGENTS ON CALCIUM UPTAKE BY PREPARATIONS OF RAT BRAIN MITOCHONDRIA (1971)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 18 (1971), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The effects of chlorpromazine and other psychoactive agents on the uptake of calcium by partially purified preparations of mitochondria from rat brain were studied in vitro. Chlorpromazine at concentrations of about 0-1 ITIM caused a marked inhibition of mitochondrial calcium transport. Perphenazine also exhibited this action and was slightly more potent than chlorpromazine. Imipramine inhibited mitochondrial calcium uptake but higher concentrations were necessary than in experiments with chlorpromazine. The sulph-oxide of chlorpromazine did not inhibit calcium transport when tested at concentrations similar to those used with chlorpromazine. Up to concentrations of 20 mM, lithium ions did not influence mitochondrial calcium uptake.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1971.tb05075.x
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  • 8
    Electronic Resource
    Electronic Resource
    ELECTROLYTE DISTRIBUTION IN RABBIT SUPERIOR CERVICAL GANGLION (1969)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 16 (1969), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract— Superior cervical ganglia of the rabbit were removed and analysed for Na+, K+, Ca2+, Mg2+ and Cl−. The mean electrolyte content in μmole/g wet wt. was as follows: Na+, 64.7 ± 1.3; K+, 65.1 ± 2.7; Ca2+, 3.71 ± 0.28; Mg2+, 3.70 ± 0.50; and Cl−, 50.15 ± 2.26. Water content was 0.76 ± 0.01 ml/g wet wt. Extracellular space was 0.37 ± 0.01 ml/g, and the vascular space 0.0238 ± 0.0002. The mean resting potential of the rabbit superior cervical ganglion was – 68.6 mv. After correction for extracellular electrolyte content, the potential differences, ENa, EK and Ecl, were estimated to be +33.6 mv, –96.9 mv and -41.1 mv, respectively, in the ganglia.Permeability coefficients for K+, Na+, and Cl− were estimated to be 1:0.06:0.02. Replacement of sodium in physiological saline solution by lithium results in a displacement of 94 per cent of the sodium content of the ganglion and 69 per cent of the potassium after 30 min of equilibration.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1969.tb10367.x
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  • 9
    Electronic Resource
    Electronic Resource
    CALCIUM UPTAKE AND EXCHANGE IN LEG NERVES OF THE CRAB ‘LIBINIA EMARGINATA’ (1978)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 30 (1978), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The kinetics of washout of radioactive calcium (45Ca) from nerves of the larger legs of Libinia emarginata equilibrated in various solutions of artificial sea water (ASW) containing 1, 11, 22 or 44 mM-Ca was followed. In every case two components were found when the period of washout was not more than 30 min. The washout of 14C labelled inulin and sucrose gave one and two components respectively; these substances were considered to exist in the extracellular regions of nerve fibers. Comparison of the total calcium of the nerves determined spectrophotometrically and by measurement of radioactivity indicated that the exchangeability of calcium in the nerves in ASW containing 44 and 22 mM-Ca was 100%. In the case of nerves equilibrated in 11 mM-CaASW, two groups of nerves, one (group A) containing a high concentration of Ca (13.6 μmol/g) and the other (group B) containing a low concentration (7.3 μmol/g), were detected Several factors which could account for the accumulation of Ca in nerve fibers in group A were considered. The electrolyte data relating to group A nerve fibers indicated that Ca accumulation may be due to the presence of a high concentration of sodium in those fibers. However, the exchangeability of Ca for group A was about 47%; and in group B fibers, it was 61%. The exchangeability was less than 41% in the case of nerves equilibrated in 1 mM-CaASW. The kinetic parameters of 45Ca washout from the nerve fibers have been used to develop a model for the distribution of calcium among the different compartments of the nerve fibers.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1978.tb07031.x
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  • 10
    Electronic Resource
    Electronic Resource
    In Vitro Evidence for Increased Facilitation of Striatal Acetylcholine Release via Pre- and Postsynaptic NMDA Receptotors in Hemiparkinsonian Rats (1999)
    Oxford UK : Blackwell Science Ltd
    Journal of neurochemistry 72 (1999), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract : The NMDA-evoked acetylcholine release from striatalslices and synaptosomes was investigated in rats subjected to unilateralinjection of 6-hydroxydopamine into the substantia nigra. In slices preparedfrom the striatum contralateral to the lesion, the NMDA-evoked endogenousacetylcholine release was not significant at 10 μM NMDA andmaximal at 100 μM NMDA (124 ± 19%). Conversely, in slicestaken from the dopamine-depleted striatum, NMDA was effective even at 10μM (41 ± 4%), and at 100 μM (196 ± 24%)efficacy was nearly doubled. In synaptosomes prepared from the contralateralstriatum, NMDA maximally stimulated 20 mM KCl-induced endogenousacetylcholine release at 1 μM (66 ± 5.1%), with lowerconcentrations (0.01-0.1 μM) being ineffective. Conversely, insynaptosomes prepared from the dopamine-depleted striatum, NMDA maximallyenhanced the K+-evoked acetylcholine release at 0.1 μM (118 ± 12.4%). Concentration-response curves of NMDA-evoked acetylcholine release in sham-operated rats could be superimposed on those observed in the contralateral striatum of the 6-hydroxydopamine-lesioned animals. The present data support the view of an increased glutamatergic regulation of striatal acetylcholine release via pre- and postsynaptic NMDA receptors during Parkinson's disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.1999.720875.x
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