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Results for “Neuroeffector Junction”

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At least 307 records · Page 17Linked to original sources
PubMed1984

Comparison of affinities of muscarinic antagonists to pre- and postjunctional receptors in the guinea-pig ileum.

The myenteric plexus-longitudinal muscle preparation of the guinea-pig ileum was preincubated with [3H]choline, then superfused and stimulated electrically (1 Hz 120 pulses). Oxotremorine reduced the evoked outflow of [3H]acetylcholine in a concentration-dependent manner. Each of the six antagonists (scopolamine, methylatropine, trihexyphenidyl, 4-DAMP, clozapine, pirenzipine) produced parallel shifts of the concentration-response curves for the prejunctional effects of oxotremorine. Similarly, in contraction experiments, the antagonists competitively antagonized the postjunctional responses to oxotremorine. The pre- and postjunctional pA2 values did not differ significantly for any of the antagonists. It is concluded that pre- and postjunctional muscarinic receptors in the guinea-pig ileum are pharmacologically similar.

Acetylcholine↗
PubMed1986

A re-appraisal of the mode of action of 5-HT in inhibiting GABA-induced cholinergic contractions in the guinea-pig ileum.

In the guinea-pig ileum, pretreatment with 5-hydroxytryptamine (5-HT) (5 microM) for 4-5 min inhibited both 5-HT- and gamma-aminobutyric acid (GABA)-induced cholinergic contractions without consistently altering those induced by electrical field stimulation. Cisapride (1 micron) antagonized 5-HT-induced cholinergic contractions but left those induced by GABA or twitch responses unchanged. These results indicate that the 5-HT action in inhibiting GABA-induced cholinergic responses may arise at the interneuronal level, thus suggesting that GABA may also indirectly activate cholinergic terminal neurons. These findings rule out the possibility of 5-HT acting as an intermediate transmitter in this type of response.

Animals↗
PubMed1990

Endothelin modulation of neuroeffector transmission in rat and guinea pig vas deferens.

The effects of endothelin-1 (human, porcine) on contractions induced by transmural nerve stimulation, exogenous ATP or noradrenaline, and on the release of [3H]noradrenaline were studied in guinea pig and rat vas deferens. Endothelin enhanced nerve-induced contractile responses, increased basal muscle tone and increased the contractile response to exogenous ATP in both guinea pig and rat vas deferens. Endothelin did not affect the contractile responses to exogenous noradrenaline. The calcium channel blocker felodipine antagonized the stimulating effects of endothelin in the rat vas deferens, whereas blockade of lipoxygenase and cyclooxygenase pathways by a combination of BW 755C and indomethacin was without effect. In rat vas deferens preparations preincubated with [3H]noradrenaline, endothelin inhibited the 3H overflow induced by transmural stimulation, although the contractile responses were enhanced by endothelin. Pretreatment with forskolin or felodipine did not abolish the endothelin inhibition of radiotracer overflow. In conclusion, endothelin can modulate adrenergic and purinergic neuroeffector transmission in both guinea pig and rat vas deferens via inhibitory prejunctional and stimulant postjunctional mechanisms. The stimulant postjunctional effect seemed to predominate in our experiments.

4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗
PubMed1993

Motor effects of indomethacin, morphine or vagal nerve stimulation on the feline small intestine in vivo.

Some factors known to affect jejunal motility (recorded as volume changes of an intraluminal balloon) were investigated in anaesthetized cats (ether-chloralose) pretreated with guanethidine and atropine. Indomethacin, morphine (both compounds administered systemically) or vagal nerve stimulation elicited jejunal excitatory motor responses. The effect of indomethacin seemed to be independent of cyclooxygenase inhibition and probably did not involve opioid receptors. It is suggested that the spasmogenic stimuli caused jejunal hypermotility by inhibiting tonically active, inhibitory motor neurons that are intrinsic to the gut. Furthermore, when the jenunal tone had been raised by indomethacin or morphine spontaneous relaxations were observed, and these could be mimicked by vagal stimulation. Hexamethonium antagonized these relaxations but did not attenuate the drug-induced jejunal hypermotility.

Animals↗
PubMed1994

Localisation of dopamine D2-like receptors in pulmonary artery of the human and rabbit but not of the rat.

The present study was designed to investigate the presence of dopamine D2-like receptor sites in the main trunk of the human, rabbit and rat pulmonary artery using combined radioligand binding and light microscope autoradiography techniques. [3H]Spiroperidol was used as a ligand. The presence and the localisation of the sympathetic neuroeffector plexus were also studied using catecholamine histofluorescence techniques. Radioligand binding experiments demonstrated the labelling of a population of dopamine D2-like receptors in sections of human and rabbit pulmonary arteries by [3H]spiroperidol. No specific binding occurred in sections of the rat pulmonary artery. Light microscope autoradiography showed the development of specific silver grains within the tunica adventitia, including the adventitia-media border, of the human and rabbit pulmonary arteries. No specific silver grains were found in sections of the rat pulmonary artery. Studies on the pharmacological characterisation of [3H]spiroperidol binding sites in the human and rabbit pulmonary arteries showed that they are sensitive primarily to domperidone, haloperidol, (-)-sulpiride or bromocriptine, and to a lesser extent to n-propylnorapomorphine, quinpirole or clozapine displacement. This suggests that [3H]spiroperidol binding sites in the pulmonary artery probably belong to the dopamine D2 receptor subtype. Catecholamine histofluorescence techniques revealed a rich plexus of fluorescent adventitial and adventitial-medial nerve fibres in the human and to a lesser extent in the rabbit pulmonary artery. Comparison of the localisation of dopamine D2-like receptor sites and of the sympathetic neuroeffector plexus in the pulmonary artery, suggests a possible prejunctional localisation of these sites.

Aged↗
PubMed1994

Effect of omega-agatoxin-IVA on autonomic neurotransmission.

omega-Agatoxin-IVA, a peptide from the venom of the funnel-web spider Agelenopsis aperta and a P type Ca2+ channel inhibitor, was examined for effects on responses to nerve stimulation in isolated autonomic neuroeffector preparations from the rabbit, guinea-pig and rat. Ca(2+)-dependent, tetrodotoxin sensitive, noradrenergic excitatory responses of rabbit pulmonary artery, rat vas deferens, and anococcygeus muscles, and cholinergic guinea-pig myenteric plexus preparations (all highly sensitive to the N type Ca2+ channel inhibitor omega-conotoxin-GVIA) were unaffected by omega-agatoxin-IVA (100 nM). Similarly, the neurogenic response of rat bladder, which has cholinergic, and non-adrenergic non-cholinergic (NANC) excitatory components, and the NANC inhibitory response of rat jejunum (atropine 0.5 microM- and guanethidine 5.0 microM-treated), which are partially sensitive and insensitive to omega-conotoxin-GVIA, respectively, were unaffected by omega-agatoxin-IVA (100 nM). Neurogenic NANC inhibitory responses of the guinea-pig taenia caecum, and rat anococcygeus muscles (atropine- and guanethidine-treated, and tone raised with prostaglandin F2 alpha), were also insensitive to omega-agatoxin-IVA. These results suggest that P type Ca2+ channels, if present, play an insignificant role in supplying the Ca2+ necessary for neurotransmitter release in the peripheral autonomic nervous system.

Animals↗
PubMed1986

Action of the polyamine beta-philanthotoxin on neuromuscular transmission in insects.

The beta-fraction of the venom of the solitary wasp Philanthus triangulum inhibited glutamate-induced potentials in muscle fibres of the locust in a dose-dependent manner (50% block at 2 micrograms/ml). Single channel behaviour and miniature excitatory postsynaptic currents were not affected. The blocking effect disappeared after treatment of the muscle with the lectin concanavalin A which prevents desensitization of glutamate receptors. Block of potentials induced by iontophoretic application of glutamate was strongly dependent on the frequency of stimulation: no block occurred at stimulus intervals of 30 sec or more. The nature of this inhibition is discussed and proposed to be a delay of recovery from desensitization.

Animals↗