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R Amann

Publications and source records attributed to R Amann.

172 records · Page 10Linked to original sources
PubMed1988

Stimulation of afferent fibres of the guinea-pig ureter evokes potentials in inferior mesenteric ganglion neurones.

1. Intracellular recordings were made from neurones of the guinea-pig inferior mesenteric ganglion (IMG) maintained in vitro with both ureters and major nerve trunks attached. Afferent fibres in the ureteric nerve were activated by electrical, chemical and mechanical stimuli. 2. Repetitive stimulation of a ureteric nerve branch evoked a non-cholinergic, synaptic slow excitatory potential (slow EPSP) in 48% of neurons. The amplitude of the slow EPSP was dependent on membrane potential and was decreased by membrane depolarization and increased by hyperpolarization. 3. The slow EPSP was attenuated or abolished by capsaicin (1 microM), which itself depolarized IMG neurones. Substance P (2 microM) or neurokinin A (2 microM) also depolarized IMG neurones and in the presence of these tachykinins the slow EPSP was attenuated or abolished. 4. Distension of the ureter evoked a non-cholinergic slow depolarization in 45% of IMG neurones which was abolished by tetrodotoxin (1 microM) and by capsaicin (1 microM). 5. Chemical stimulation of ureteric afferent nerve terminals by intralumenal perfusions of the ureter with capsaicin (1 microM) produced a slow depolarization in the IMG which was prevented by blocking nerve conduction with TTX. 6. These data demonstrate that electrical stimulation of ureteric afferent fibres produces a non-cholinergic slow EPSP in the IMG. Primary afferent (capsaicin-sensitive) C fibres are also activated by distension of the ureter and evoke a slow depolarization in the IMG. The synaptic mediator of these events is likely to be tachykinin(s) released from capsaicin-sensitive C fibres. These fibres may be mechanosensory and/or nociceptive.

Animals↗
PubMed1987

Peripheral effects of opioid drugs on capsaicin-sensitive neurones of the guinea-pig bronchus and rabbit ear.

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 microM). This effect was abolished by naloxone (1 microM). 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 microM) or lofentanil (1 and 10 microM).(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1987

Reserpine-induced depletion of neuropeptide Y in the guinea-pig: tissue-specific effects and mechanisms of action.

The effects of treatment with reserpine (5 mg.kg-1, s.c., 24 h prior to sacrifice) or 6-hydroxydopamine (6-OHDA; 250 mg.kg-1, s.c., for 4 days, one week before sacrifice) on the content of neuropeptide Y (NPY)-like immunoreactivity (LI) and noradrenaline (NA) were compared in a variety of tissues from the guinea-pig. Reserpine and 6-OHDA treatment markedly reduced the NA content of all peripheral organs investigated. Reserpine treatment also caused depletion of the content of NPY-LI in larger blood vessels and in organs containing mainly perivascular nerves. Furthermore, reserpine treatment depleted NPY-LI in the heart, spleen and adrenal gland. In other organs dominated by parenchymal adrenergic innervation such as genital organs (vas deferens, uterus) or iris, treatment with 6-OHDA but not reserpine caused significant depletions of NPY-LI. The urinary bladder and gastrointestinal tract seem to be mainly innervated by non-adrenergic NPY-containing neurons resistant to reserpine and 6-OHDA treatment. The content of NPY-LI was elevated in sympathetic ganglia after reserpine treatment while no increase in axonal transport occurred in the sciatic nerve. Cerebellum was the only studied area in the central nervous system where the NPY content was depleted by reserpine or 6-OHDA treatment suggesting presence of NPY-LI in perivascular nerves. The reserpine-induced depletion of NPY-LI in the spleen, kidney and skeletal muscle was prevented by preganglionic denervation. This suggests that enhanced nerve impulse discharge in sympathetic nerves caused a situation where NPY release exceeded the amount which could be replaced by axonal transport.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Stress induced ACTH release in capsaicin treated rats.

The plasma concentrations of adrenocorticotropic hormone (ACTH) in rats pretreated with capsaicin as neonates were compared with those of control rats pretreated with the capsaicin vehicle. Capsaicin pretreatment has been shown earlier to abolish the increase in plasma ACTH concentration induced by cold stress while not affecting that induced by restraint stress. In the present experiments rats pretreated with capsaicin showed the same increase in plasma ACTH concentration in response to an i.v. infusion of ovine-corticotropin releasing factor as control rats pretreated with the capsaicin vehicle. Intraperitoneal injection of formalin, surgical stress and intravenous infusion of (-)-isoprenaline increased plasma ACTH concentrations in control rats. In capsaicin pretreated rats the increase in plasma ACTH was significantly attenuated. It is concluded that capsaicin-sensitive sensory neurones mediate the activation of pituitary ACTH secretion in response to somatosensory stimuli. The function of the corticotroph cells of the anterior pituitary is not impaired by capsaicin treatment.

Adrenocorticotropic Hormone↗
PubMed1986

Capsaicin sensitive afferent neurons from peripheral glucose receptors mediate the insulin-induced increase in adrenaline secretion.

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. 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. 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. 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. 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. 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. 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.

Adrenal Glands↗
PubMed1986

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.

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 guinea-pig. 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. Injections of AP-2 (20 nmol) and spantide (66 nmol) caused nociceptor stimulation which might in part result from the histamine release. 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 mumol l-1 but not at 2.4 mumol l-1. Spantide (up to 100 mumol l-1) did not inhibit electrically evoked "twitch" responses of the guinea-pig ileum. The local anaesthetic drug procaine (4.2-42 mumol l-1) inhibited these contractions in a concentration-dependent manner. 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.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1986

The influence of capsaicin sensitive neurons on stress-induced release of ACTH.

Changes in the plasma levels of ACTH in response to cold exposure or restraint stress were measured in adult rats which had been pretreated with capsaicin or vehicle as neonates. There was no difference in basal ACTH levels between capsaicin and vehicle pretreated animals. Following restraint stress, ACTH levels rose similarly in vehicle and capsaicin pretreated rats, indicating that the pituitary-adrenal system is not impaired by capsaicin pretreatment. However, following cold exposure ACTH levels rose only in control animals whereas no change was observed in capsaicin pretreated animals. It is concluded that capsaicin-sensitive afferent neurons participate in the cold stress-induced increase of plasma ACTH levels.

Adrenocorticotropic Hormone↗
PubMed1985

In vivo and in vitro actions of mammalian tachykinins.

Recently, two kassinin-like tachykinins have been isolated from mammalian nervous tissue. The potencies of these peptides, substance K (neurokinin alpha) and neuromedin K (neurokinin beta) were compared with those of substance P, eledoisin, and kassinin in various pharmacological systems in vivo and in vitro. In contracting the isolated guinea-pig ileum and rabbit jejunum the potencies of eledoisin, kassinin, substance K, and neuromedin K were 13-80% that of substance P. In the rat vas deferens substance K and neuromedin K potentiated the electrically induced contractions with potencies similar to those of eledoisin and kassinin; they were 46-236 times as potent as substance P. In stimulating salivation in the rat after intravenous injection, eledoisin, kassinin, and substance K were respectively 2.3, 1.3 and 0.33 times as potent as substance P. In contrast, neuromedin K exhibited negligible activity. Each peptide tested led to a short fall in blood pressure after intravenous injection in the rabbit, substance P being 12-250 times as potent as the other peptides. Substance P was 20 times as potent as substance K or neuromedin K in inducing vasodilatation in the rat hind paw in vivo. Of the peptides tested, only substance P (10 nmol/min) significantly increased the release of histamine from the rat isolated hindquarter preparation. The results are discussed with respect to several theories of tachykinin receptor heterogeneity.

Animals↗
PubMedDate not supplied

Activation of primary afferent neurons by thermal stimulation. Influence of ruthenium red.

The effect of thermal stimulation on primary afferent neurons and its modulation by Ruthenium Red (RR) has been investigated in the isolated perfused rabbit ear with intact neuronal connection to the animal. Capsaicin, K(+)-depolarization as well as increasing the temperature of the perfusate to 50 degrees C, increased the amount of substance P-like immunoreactivity (SP-IR) in the outflow in a calcium-dependent manner. High performance liquid chromatography (HPLC) revealed that SP-IR which was released by thermal stimulation consisted of two components, one of which co-eluted with synthetic substance P. The same two components of SP-IR were also present in extracts of the auricular nerve and were released by capsaicin. RR attenuated the effect of capsaicin and thermal stimulation but did not reduce potassium-evoked release of SP-IR. To evaluate an inhibitory action of RR on the excitation of primary afferents, the isolated perfused ear with intact neuronal connection to the anaesthetized rabbit was used. Intraarterial injection of capsaicin or bradykinin as well as superfusion of a skin area of approximately 2 cm2 with water at 53 degrees C for 1 min, produced a depressor reflex. RR attenuated the response to thermal stimulation and to capsaicin, but did not block the bradykinin-induced depressor reflex. These results demonstrate that, in the rabbit ear, thermal stimuli excite primary afferent neurons and evoke the calcium-dependent release of neuropeptides from their peripheral terminals by a mechanism which is sensitive to RR.

Animals↗