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  • Sensory fibres  (2)
  • Acetylcholine  (1)
  • Axoplasmic transport  (1)
  • Horseradish peroxydase (HRP)  (1)
  • 1
    Electronic Resource
    Electronic Resource
    The site of action of capsaicin on the guinea-pig isolated ileum (1978)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 305 (1978), S. 75-81 
    Details
    ISSN: 1432-1912
    Keywords: Capsaicin ; Cholinergic mechanism ; Periarterial mesenteric nerves ; Sensory fibres ; Ileum innervation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The site and mode of action of capsaicin were analysed on the guinea-pig isolated ileum. 1. Capsaicin produced longitudinal contraction (EC50 4.2×10−8 g/ml) followed by a specific, rapid and irreversible tachyphylaxis (IC50 2.8×10−7 g/ml). 2. Capsaicin was ineffective in the presence of tetrodotoxin (2×10−7 g/ml) or on ilea kept for 24–48 h at 4°C, without an oxygen supply. 3. On ileal segments, the perivascular mesenteric nerves of which were transsected 5–8 days before the experiment, practically no response to capsaicin was obtained. Chronic abdominal bilateral vagotomy was without any effect. 4. Hyoscine (1×10−8–1×10−6 g/ml) or morphine (2×10−6 g/ml) strongly inhibited contractions produced by capsaicin. Neither mecamylamine (1×10−5 g/ml), nor nicotine (5×10−5 g/ml) and dimethylphenylpiperazinium (5×10−6 g/ml) caused any change, while an increased response to capsaicin was obtained in the presence of hexamethonium (1×10−4 g/ml). 5. Unaltered contractions were produced by capsaicin on ileal segments made tachyphylactic to 5-HT, bradykinin or substance P. Histamine antagonists at H1 and H2 receptors (chloropyramine, burimamide), the prostaglandin synthesis inhibitor indomethacin, pretreatment with the adrenergic neuron blocking agent guanethidine, as well as in vivo reserpine pretreatment were also ineffective in this respect. 6. It is concluded that in the guinea-pig ileum capsaicin causes predominantly cholinergic contraction by stimulating terminals of extrinsic, non-parasympathetic nerves.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00497008
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    New type of nerve-mediated cholinergic contractions of the guinea-pig small intestine and its selective blockade by capsaicin (1978)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 305 (1978), S. 83-90 
    Details
    ISSN: 1432-1912
    Keywords: Capsaicin ; Cholinergic mechanism ; Periarterial mesenteric nerves ; Sensory fibres ; Ileum innervation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. Electrical stimulation (2–50Hz) of mesenteric nerves of the guinea-pig isolated ileum resulted in contraction of preparations pretreated with adrenergic neuron blocking agents (guanethidine, bretylium), or on preparations obtained from animals pretreated with reserpine. Stimulation at low frequencies (2–10 Hz) also caused contraction in untreated preparations. 2. The response was abolished by hyoscine (1 ×10−7–1×10−6 g/ml) or morphine (2×10−7 g/ml). However, previous bilateral vagotomy, hexamethonium (1×10−4 g/ml), mecamylamine (1×10−5 g/ml), or desensitization of the gut to 5-HT caused practically no inhibition. 3. Capsaicin inhibited or abolished (IC50 1.5 ×10−8 g/ml) the contraction elicited by stimulation of mesenteric nerves in an irreversible manner. The drug did not inhibit the contraction to field stimulation of the postganglionic cholinergic fibres. 4. Neither the contraction of the duodenum to stimulation of the preganglionic vagal fibres, nor the adrenergic inhibition elicited by periarterial nerve stimulation were influenced by capsaicin. 5. It is concluded that the cholinergic response described above is neither parasympathetic in origin nor can it explained on the basis of a cholinergic mechanism in adrenergic neurotransmission (Burn's theory). A hypothesis is put forward that nerve fibres characterized by their specific sensitivity to capsaicin, presumably originating from sensory neurons excite cholinergic neurons of the myenteric plexus.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00497009
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Peripheral effects of opioid drugs on capsaicin-sensitive neurones of the guinea-pig bronchus and rabbit ear (1987)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 336 (1987), S. 316-320 
    Details
    ISSN: 1432-1912
    Keywords: Acetylcholine ; [d-Met2, Pro5]-enkephalin-amide ; Prostaglandin E2 ; Capsaicin ; Sensory nerves
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of a potent opioid agonist, [d-Met2, Pro5]-enkephalinamide was investigated on two responses involving capsaicin-sensitive afferent neurones, namely, atropine-resistant contractions of the guinea-pig bronchus evoked by electrical field stimulation and the nociceptor stimulation to intraarterial injections of acetylcholine or capsaicin into the vascularly isolated rabbit ear. The hypotheses to be tested were whether (a) opioid receptor activation may inhibit mediator release from primary afferent neurones and (b) the opioid could exert an analgesic effect at a peripheral site of action. Non-cholinergic contractions of the guinea-pig isolated main bronchi due to electrical stimulation were concentration-dependently inhibited by [d-Met2, Pro5]-enkephalinamide (10 nM–1 μM). This effect was abolished by naloxone (1 μM). Naloxone alone induced no change in the stimulation-evoked contractions of the bronchus, indicating that no endogenous opioid control was present. Substance P and neurokinin A induced bronchial contractions that were not influenced by [d-Met2, Pro5]-enkephalinamide. This indicates that [d-Met2, Pro5]-enkephalinamide inhibits electrically-evoked bronchial contractions by reduced mediator release from capsaicin-sensitive sensory nerve endings, since these contractions are most probably brought about by tachykinins, released from afferent neurones. Capsaicin-induced bronchial contractions were in contrast to electrical stimulation not influenced by [d-Met2, Pro5]-enkephalinamide which suggests a different site of action. The activation of sensory neurones in the rabbit ear by i. a. injection of acetylcholine and capsaicin was not reduced under infusion of [d-Met2, Pro5]-enkephalinamide (1 and 10 μM) or lofentanil (1 and 10 μM). The enhancement of the effect of acetylcholine by infusion of prostaglandin E2 (0.15 μM) also remained unchanged under infusion of 10 μM [d-Met2, Pro5]-enkephalinamide. A peripheral analgesic action of the two opioid agonists studied is therefore not indicated.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00172684
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Capsaicin-induced inhibition of axoplasmic transport is prevented by nerve growth factor (1985)
    Springer
    Cell & tissue research 240 (1985), S. 569-573 
    Details
    ISSN: 1432-0878
    Keywords: Capsaicin ; Horseradish peroxydase (HRP) ; Nerve growth factor (NGF) ; Dorsal root ganglion ; Neurones ; Axoplasmic transport
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Capsaicin injected into the scrotal skin of rats was observed to induce a decrease in the amount of horseradish peroxidase (HRP) transported in the pudendal nerve to the sixth lumbar dorsal root ganglion on the pretreated side. This was seen as a decrease in the number of HRP-labelled neurones compared to the control side. A morphometric study confirmed that the effect of capsaicin was exerted predominantly on the small neurones. Injection of nerve growth factor (NGF) into the pudendal nerve prevented the deleterious effects of capsaicin, thereby suggesting a possible site of action and mechanism for the effect of capsaicin on peripheral nerves.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00216346
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    Paper (German National Licenses)
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