Library

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Electronic Resource
    Electronic Resource
    Substance P Afferents Regulate ACTH-Corticosterone Release (1991)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 632 (1991), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1991.tb33117.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Activation of Primary Afferents in the Rabbit Ear by Noxious Heat (1991)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 632 (1991), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1991.tb33124.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Capsaicin-induced Desensitization in Rat and Rabbit (1991)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 632 (1991), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1991.tb33125.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    Time Course of Capsaicin-Evoked Release of CGRP from Rat Spinal Cord in Vitro (1992)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 657 (1992), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1992.tb22809.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 5
    Electronic Resource
    Electronic Resource
    Human and Rat Primary C-Fibre Afferents Store and Release Secretoneurin, a Novel Neuropeptide (1994)
    Oxford, UK : Blackwell Publishing Ltd
    European journal of neuroscience 6 (1994), S. 0 
    Details
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Secretoneurin is a recently discovered neuropeptide derived from secretogranin II (SgII). Since this peptide could be detected in the dorsal horn of the spinal cord we studied whether it is localized in and released from primary afferent neurons. Secretoneurin was investigated with immunocytochemistry and radioimmunoassay in spinal cord, dorsal root ganglia and peripheral organs. SgII mRNA was determined in dorsal root ganglia. Normal rats and rats pre-treated neonatally with capsaicin to destroy selectively polymodal nociceptive (C-) fibres were used. Slices of dorsal spinal cord were perfused in vitro for release experiments. Immunocytochemistry showed a distinct distribution of secretoneurin-immunoreactivity (IR) in the spinal cord and lower brainstem. A particularly high density of fibres was found in lamina I and outer lamina II of the caudal trigeminal nucleus and of the spinal cord. This distribution was qualitatively identical in rat and human post-mortem tissue. Numerous small diameter and some large dorsal root ganglia neurons were found to contain SgII mRNA. Capsaicin treatment led to a marked depletion of secretoneurin-IR in the substantia gelatinosa, but not in other immunopositive areas of the spinal cord and to a substantial loss of small (〈25 μm) SgII-mRNA-containing dorsal root ganglia neurons. Radioimmunoassay revealed a significant decrease of secretoneurin-IR in the dorsal spinal cord, the trachea, heart and urinary bladder of capsaicin-treated rats. Perfusion of spinal cord slices with capsaicin as well as with 60 mM potassium led to a release of secretoneurin-IR. In conclusion, secretoneurin is a neuropeptide which is stored in and released from capsaicin-sensitive, primary afferent (C-fibre) neurons. It may, therefore, be a novel peptidergic modulator of pain transmission or of C-fibre mediated non-nociceptive information.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1460-9568.1994.tb00996.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 6
    Electronic Resource
    Electronic Resource
    Capsaicin sensitive afferent neurons from peripheral glucose receptors mediate the insulin-induced increase in adrenaline secretion (1986)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 334 (1986), S. 71-76 
    Details
    ISSN: 1432-1912
    Keywords: Insulin ; 2-Deoxy-d-glucose ; Capsaicin ; Glucoreceptors ; Adrenaline ; Blood glucose
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. The effect of insulin and of 2-deoxy-d-glucose (2-DG) on adrenaline secretion was compared in rats pretreated as neonates with capsaicin and in rats pretreated with the drug-vehicle. 2. Capsaicin-pretreatment did not inhibit the fall in blood glucose concentrations induced by insulin or by fasting, nor did it affect the increase in blood glucose concentrations in response to 2-DG or restraint stress. 3. Capsaicin greatly reduced the rise in urinary adrenaline excretion over 24 h and the fall in the adrenaline content of the adrenal glands normally induced by insulin. 4. In contrast, capsaicin-pretreatment did not interfere with the rise in the adrenaline excretion and the fall in the adrenaline content of the adrenal glands normally induced by 2-DG. 5. Insulin-induced hypoglycaemia as well as intracellular glucopenia in the brain caused by 2-DG activate hypothalamic centres which stimulate the nervous input to the adrenal medulla and adrenaline secretion. The fact that capsaicin interfered only with the adrenal effect of insulin suggests the involvement of afferent C-fibres in this insulin effect. 6. Injection into the hepatic portal vein of a C-fibre stimulating dose of capsaicin increased arterial glucose concentrations in vehicle-pretreated rats but not in capsaicin-pretreated rats. The response was significantly diminished after bilateral vagotomy. 7. From the present results it is concluded that glucose receptors in the hepatic portal vein transmit signals via afferent, capsaicin sensitive C-fibres to the brain and that activation of this pathway is essential for the increase in adrenaline secretion elicited by insulin-induced hypoglycaemia.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00498742
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 7
    Electronic Resource
    Electronic Resource
    Effects of carbonyl cyanide p-trichloromethoxyphenylhydrazone (CCCP) and of ruthenium red (RR) on capsaicin-evoked neuropeptide release from peripheral terminals of primary afferent neurones (1990)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 341 (1990), S. 534-537 
    Details
    ISSN: 1432-1912
    Keywords: Capsaicin ; Ruthenium Red ; CCPP ; Afferent neurones
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In the superfused isolated rat urinary bladder, capsaicin as well as electrical field stimulation evoked the release of calcitonin gene-related peptide-like immunoreactivity (CGRP-IR). Carbonyl cyanide p-trichloromethoxyphenylhydrazone (CCCP, threshold 2 μM) reduced both, the capsaicin- and the electrical field stimulation-evoked release of CGRP-IR while a low concentration of Ruthenium Red (RR, 0.6 μM and 2 μM) selectively attenuated the capsaicin-evoked release of CGRP-IR but did not influence the effect of electrical field stimulation. 20 μM RR nearly abolished the capsaicin-evoked release, but also attenuated the effect of electrical field stimulation. In the isolated guinea-pig bronchus, electrical field stimulation and capsaicin induced non-cholinergic contractions which are known to be caused by tachykinin release from afferent nerve terminals. CCCP (0.6 μM) only reduced the response to field stimulation; a ten-fold higher concentration of CCCP attenuated field stimulation as well as capsaicin-induced contractions. This is in contrast to the reported selective inhibition of capsaic-ininduced contractions by RR. The present data demonstrate that CCCP generally inhibits evoked neuropeptide release, regardless of the kind of stimulation used while low concentrations of RR preferentially inhibit capsaicin-evoked neuropeptide release.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00171733
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 8
    Electronic Resource
    Electronic Resource
    Desensitization of capsaicin-evoked neuropeptide release — Influence of Ca2+ and temperature (1990)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 342 (1990), S. 671-676 
    Details
    ISSN: 1432-1912
    Keywords: Capsaicin ; Primary afferents ; Desensitization ; Temperature-dependency
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Capsaicin-induced stimulation and desensitization of neuropeptide release from primary afferent neurons was investigated in the rat urinary bladder in-vitro. The capsaicin (5 min contact time)-evoked release of calcitonin gene-related peptide-like immunoreactivity (CGRP-IR) was dose-dependent; threshold to produce detectable release was 0.1 µmol/l, the EC50 was 0.17 µmol/l. Pre-exposure of tissues to capsaicin (0.1–1.0 µmol/l, 5 min contact time) caused a dose-dependent reduction of the amount of CGRP-IR which was released by a second exposure to capsaicin. At 0.1 and 0.3 µmol/l, capsaicin was less effective to inhibit the subsequent K+-evoked release than that evoked by a second capsaicin exposure. Pre-exposure to 1 µmol/l capsaicin completely prevented subsequent K+- or capsaicin-evoked release of CGRP-IR. Exposure of the preparation to capsaicin (0.3µmol/l) in a Ca2+-free, EDTA-containing medium did not produce release of CGRP-IR. A subsequent stimulation with capsaicin in a 2.5 mmol/l Ca2+-containing superfusion solution was not less effective to release CGRP-IR than in tissues which had not been pre-exposed to capsaicin. At 18°C, the capsaicin-evoked release of CGRP-IR was reduced to 20% of the value obtained by the same dose (0.3 µmol/l for 5 min) of capsaicin at 37°C. Comparison of the desensitizing effect of 0.3 and 0.1 µmol/l capsaicin at 18°C and 37°C, respectively, showed significant inhibition of desensitization at 18°C. Inhibition of desensitization was also observed when the amount of CGRP-IR, which was released during preexposure to capsaicin (0.3 µmol/l for 10 min) at 18°C, was 3-fold higher than that produced by pre-exposure to capsaicin (0.1 µmol/l for 5 min) at 37°C. The present results show that in a narrow range of concentrations, capsaicin induces “selective” desensitization which is entirely dependent on the presence of external Ca2+ — and which is attenuated at low temperature.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00175711
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 9
    Electronic Resource
    Electronic Resource
    Release of calcitonin gene-related peptide in cardiac anaphylaxis (1997)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 355 (1997), S. 224-229 
    Details
    ISSN: 1432-1912
    Keywords: Key words Cardiac anaphylaxis ; Isolated perfused guinea-pig heart ; Eicosanoids ; Histamine ; Calcitonin gene-related peptide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We have investigated the antigen-stimulated release of calcitonin gene-related peptide (CGRP) from ovalbumin-sensitized guinea-pig isolated hearts and the interaction with other mediators of anaphylaxis released concomitantly. It was found that antigen challenge caused a significant increase of CGRP release (from basal 31.2 ± 2.9 to 51.6 ± 4.9 fmol/5 min). Anaphylactic CGRP release was significantly attenuated in the presence of the cyclooxygenase inhibitor indomethacin while the 5-lipoxygenase inhibitor Bay-X1005 ((R)-2-[4-quinolin-2-yl-methoxy)phenyl]-2-cyclopentyl acetic acid) had no significant effect. Combined treatment with the histamine receptor (H1,H2) antagonists mepyramine and cimetidine also significantly attenuated anaphylactic release of CGRP. Under control conditions antigen injection increased release of cysteinyl-leukotrienes (LT), thromboxane (TXB2) and 6-keto-prostaglandin (PG)F1α from basal values of 0.96 ± 0.09, 2.7 ± 0.7 and 3.4 ± 0.28 ng/5 min respectively, to 5.9 ± 0.9, 48.4 ± 3.4 and 6.9 ± 1.4 ng/5 min. Indomethacin abolished the release of cyclooxygenase products of arachidonate metabolism and simultaneously increased cysteinyl-LT release significantly (8.8 ± 1.4 ng/5 min). Conversely Bay-X1005 completely abolished cysteinyl-LT release and had no significant effect on anaphylactic release of TXB2 and 6-keto-PGF1α. Simultaneous blockade of H1 and H2 receptors abolished release of 6-keto-PGF1α, while release of TXB2 and cysteinyl-LT was not significantly affected. The results indicate that CGRP is not a primary mediator of the immediate hypersensitivity reaction of the heart, but is in turn released by arachidonic acid metabolites of the cyclooxygenase pathway and histamine. In contrast, LT obviously do not contribute to anaphylactic CGRP release. CGRP is a potent coronary vasodilator and could act as endogenous functional antagonist of vasoconstrictor mediators also released during cardiac anaphylaxis such as cysteinyl-LT, platelet activating factor and TXA2.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/PL00004936
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 10
    Electronic Resource
    Electronic Resource
    Studies on effects of the substance P analogues [d-Pro2, d-Trp7,9]-substance P and [d-Arg1, d-Trp7,9, l-Leu11]-substance P not related to their antagonist action (1986)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 333 (1986), S. 290-293 
    Details
    ISSN: 1432-1912
    Keywords: Tachykinin Antagonists ; Nociceptors ; Histamine release
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. Two tachykinin antagonists, [d-Pro2, d-Trp7,9]-substance P (AP-2) and [d-Arg1, d-Trp7,9, l-Leu11]-substance P (spantide) were injected or infused intraarterially into the isolated perfused rabbit ear connected to the body via the nerve only. The effects of these antagonists on venous outflow, release of histamine, and on acetylcholine-induced reflex fall in blood pressure were recorded. The effect of spantide was also investigated on cholinergic “twitch” responses to the isolated field stimulated ileum of the guineapig. 2. Bolus injections of AP-2 (6.6 nmol and 20 nmol) and spantide 20 nmol and 66 nmol) i.a. caused a dose-dependent reduction in venous outflow, which could mainly be explained by the release of histamine since the histamine H1 receptor blocker mepyramine inhibited this effect; release of histamine was also directly demonstrated. 3. Injections of AP-2 (20 nmol) and spantide (66 nmol) caused nociceptor stimulation which might in part result from the histamine release. 4. The reflex fall in blood pressure due to nociceptor stimulation by acetylcholine was reduced by less than 30% by infusion of the tachykinin antagonists in a concentration of 12 μmol l−1 but not at 2.4 μmol l−1. 5. Spantide (up to 100 μmol l−1) did not inhibit electrically evoked “twitch” responses of the guinea-pig ileum. The local anaesthetic drug procaine (4.2–42 μmol l−1) inhibited these contractions in a concentration-dependent manner. 6. It is concluded that the tachykinin antagonists might show effects which are not related to their specific tachykinin antagonistic action as indicated by the findings in the rabbit ear. However, the present results on the stimulated ileum, along with earlier data obtained at this preparation do not indicated these SP analogues having a strong general neuron suppressive action. Careful testing of specifity of tachykinin antagonists seems advisable when they are used as pharmacological tools in a new preparation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00512943
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...