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At least 649 records · Page 36Linked to original sources
PubMed1999

A non-pungent triprenyl phenol of fungal origin, scutigeral, stimulates rat dorsal root ganglion neurons via interaction at vanilloid receptors.

1. A [3H]-resiniferatoxin (RTX) binding assay utilizing rat spinal cord membranes was employed to identify novel vanilloids in a collection of natural products of fungal origin. Of the five active compounds found (scutigeral, acetyl-scutigeral, ovinal, neogrifolin, and methyl-neogrifolin), scutigeral (Ki=19 microM), isolated from the edible mushroom Albatrellus ovinus, was selected for further characterization. 2. Scutigeral induced a dose-dependent 45Ca uptake by rat dorsal root ganglion neurons with an EC50 of 1.6 microM, which was fully inhibited by the competitive vanilloid receptor antagonist capsazepine (IC50=5.2 microM). 3. [3H]-RTX binding isotherms were shifted by scutigeral (10-80 microM) in a competitive manner. The Schild plot of the data had a slope of 0.8 and gave an apparent Kd estimate for scutigeral of 32 microM. 4. Although in the above assays scutigeral mimicked capsaicin, it was not pungent on the human tongue up to a dose of 100 nmol per tongue, nor did it provoke protective wiping movements in the rat (up to 100 microM) upon intraocular instillation. 5. In accord with being non-pungent, scutigeral (5 microM) did not elicit a measurable inward current in isolated rat dorsal root ganglion neurons under voltage-clamp conditions. It did, however, reduce the proportion of neurons (from 61 to 15%) that responded to a subsequent capsaicin (1 microM) challenge. In these neurons, scutigeral both delayed (from 27 to 72 s) and diminished (from 5.0 to 1.9 nA) the maximal current evoked by capsaicin. 6. In conclusion, scutigeral and its congeners form a new chemical class of vanilloids, the triprenyl phenols. Scutigeral promises to be a novel chemical lead for the development of orally active, non-pungent vanilloids.

Animals↗
PubMed1982

Exogenously stimulated gastric secretion in dogs after ganglion and sympathetic blockade and antral acidification.

1 In conscious dogs with gastric fistulae, Heidenhain pouches and in some cases, innervated pyloric pouches, ganglionic blockade augmented Heidenhain pouch acid secretion only if the gastric fistula remained closed in animals receiving pentagastrin. 2 Ganglionic blockade depressed methacholine-stimulated acid and pepsin secretion from the Heidenhain pouch whether or not the fistula was open. 3 Acidification of the antral pouch consistently augmented the acid and pepsin secretion from the Heidenhain pouch when either pentagastrin or methacholine was the stimulus. Ganglionic blockade prevented this.

Animals↗
PubMed1975

Study of two acetylcholine analogs with fixed conformations.

Two acetylcholine analogs, compound M (4,4-dimethyl-2-morpholonium) and compound P (1,1-dimethyl-3-acetoxypiperidinium) which contain the N-C-C-O group of acetylcholine fixed in the gauche and trans conformations, respectively, were tested for activity on the terminal ileum of the rat, the rectus abdominis muscle of the frog, and the superior cervical ganglion of the cat. It was found that compound M stimulates the ganglion but has no affinity for receptors in either the ileum or the rectus muscle, while compound P stimulates cholinergic receptors in the ileum and in the fast fibers of the rectus muscle but acts neither on the slow fibers of the rectus muscle nor on the ganglion.

Acetylcholine↗
PubMed1995

[Stellate ganglion block with transcutaneous electric nerve stimulation (TENS): a double-blind study with healthy probands].

OBJECTIVE: Blockade of the stellate ganglion is an established and highly effective diagnostic and therapeutic procedure for management of certain acute and chronic pain syndromes or other disorders. The paratracheal injection of a local anaesthetic is the simplest and most frequently used approach for blocking the cervicothoracic sympathetic nerves (ganglion stellate). However, since serious complications can occur during or following the anterior paratracheal technique including accidental intravenous or intraarterial injection, non-invasive methods for blockade of the stellate ganglion have been suggested. In 1980 Jenkner (15) reported the successful interruption of the sympathetic outflow from the stellate ganglion together with the relief of pain by transcutaneous electrical nerve stimulation (TENS), followed by the development of an "optimal wave form" in 1981 (14). Since we were unable to reproduce Jenkner's results of sympathetic blockade in our patients, this study was designed to investigate the effects of TENS on the sympathetic activity of the stellate ganglion in healthy volunteers. METHODS: 50 healthy volunteers were randomised into two groups (n = 25). In group I the left stellate ganglion was stimulated for 20 min by the mode described by Jenkner (monophasic pulse, small anode, large cathode, frequency 20 Hz), while group II was stimulated by conventional TENS (biphasic pulse, electrodes of identical size, frequency 100 Hz). The method of stimulation was blinded to both the investigator and the subjects investigated. Measurements included cutaneous blood flow of the volar forearm (laser Doppler), skin temperature on two sites of the cheeks (thermistor), pupil diameter and size of the palpebral fissures, sweat production (ninhydrine test) and global sensitivity and pain perception thresholds on both sides (electrical stimulation). Measurements were performed before TENS of the stellate ganglion, after 5, 10, 15 and 20 min of stimulation and 10 min after termination of TENS. Statistical analysis of the obtained data was performed by Friedman-Test and by Mann-Whitney-U-Test. p < 0.05 was assigned statistical significance. MAIN RESULTS: Skin temperature increased in both groups and on both sides by 1.2 degrees C, while skin perfusion rate, pupil size, size of the palpebral fissure and sweat production remained unchanged. Global sensitivity and pain perception thresholds of forehead decreased in both groups and on both sides, while there was no change of both parameters on the hands. CONCLUSION: No signs and symptoms of sympathetic blockade could be demonstrated in any of the groups, neither by TENS of the stellate ganglion as described by Jenkner nor by unspecific TENS. Thus, pain relief by TENS of the stellate ganglion as reported in the literature must involve other mechanisms than sympathetic blockade. In addition, TENS may not replace traditional blockade of the stellate ganglion by local anesthetics, if sympathetic blockade is required for diagnostic and therapeutic purposes.

Adult↗
PubMed1993

Time-dependent blockade of neurogenic plasma extravasation in dura mater by 5-HT1B/D agonists and endopeptidase 24.11.

1. The delayed effects of stimulating the trigeminal ganglion unilaterally in rats and guinea-pigs were assessed by measuring the leakage of radiolabelled albumin from blood into the dura mater at intervals for up to 120 min after a 5 min stimulation period (5 Hz, 0.6 mA, 5 ms). 2. [125I]-albumin (50 microCi kg-1) was injected i.v. as a tracer 0, 20, 50, 80 or 110 min after stimulation and the animals were killed 10 min later. Extravasation of plasma protein developed for up to 90 min poststimulation. 3. To examine the mechanism underlying delayed plasma protein extravasation, CP-93,129 (5-HT1B receptor agonist, 460 nmol.kg-1), sumatriptan (5-HT1B/D receptor agonist, 24 nmol kg-1), or neutral endopeptidase 24.11 (1 nmol kg-1) were administered 45 or 75 min after trigeminal stimulation and 5 min before radiolabelled albumin. The extravasation response was reduced at 45 min. CP-23,129 also blocked extravasation when injected 25 min after capsaicin administration (1 mumol kg-1). 4. If the tracer was injected 5 min prior to electrical trigeminal stimulation, endopeptidase 24.11 (1 nmol kg-1) given 10 min before stimulation blocked the leakage (as reported previously for CP-93,129 or sumatriptan). All three compounds blocked the leakage when administered 30 min (but not 60 min) poststimulation in this paradigm. 5. The data support the previously made contention that neuropeptide release from sensory fibres mediates the plasma extravasation response following trigeminal ganglion stimulation, and that release and plasma leakage continue many minutes beyond the stimulation period. Hence, drugs that inhibit neuropeptide release (CP-93,129, sumatriptan), or enhance breakdown of neuropeptide mediators(endopeptidase 24.11) block the delayed extravasation response. Extravasation developing later than 45 min poststimulation was not neurogenically mediated.

Animals↗
PubMed1982

Effects of stimulation of the chorda tympani in bursts on submaxillary responses in the cat.

1. The effects of continuous preganglionic stimulation of the chorda tympani at 2 Hz for 10 min were compared with those of stimulation at 20 Hz in 1 sec bursts at 10 sec intervals for the same period in cats treated with atropine (0.5 mg/kg). Both the fall in mean submaxillary vascular resistance (s.v.r.) and the rise in mean vasoactive intestinal peptide (VIP) output from the gland were increased significantly (P < 0.01; P < 0.02) when the same total number of impulses were delivered in the form of bursts at the higher frequency.2. Both responses were also consistently increased by stimulating the post-ganglionic innervation in bursts in atropinized cats, or by stimulating the preganglionic innervation in bursts in the absence of atropine.3. The effects of stimulation of the chorda tympani in 1 sec bursts at 10 sec intervals for 2-3 min were investigated over the frequency range 2-160 Hz. The change in mean s.v.r. under these conditions was significantly reduced by administration of atropine at frequencies between 2 and 20 Hz, but not at higher frequencies. In atropinized cats, the fall in mean s.v.r. was linearly related to stimulus frequency (r = 0.993) over the range 2-60 Hz and a maximal response was obtained during stimulation at 80 Hz. In the same experiments the fall in mean s.v.r. was linearly related to log mean VIP output over the frequency range 20-160 Hz (r = 0.998).4. Closely similar changes in mean s.v.r occurred in response to both pre- and post-ganglionic stimulation at all frequencies tested between 2 and 160 Hz in atropinized cats when the stimuli were delivered in bursts. The changes in mean s.v.r. were not significantly affected by varying the duration of individual stimuli over the range 0.1-25.0 msec.5. The flow of submaxillary saliva was also linearly related to stimulus frequency over the range 2-40 Hz (r = 0.997) when the stimuli were delivered in bursts in the absence of atropine and secretion of saliva was maximal at 60 Hz.6. It is concluded that release of VIP from the submaxillary gland of the cat is optimal in response to stimulation of the chorda tympani at relatively high frequencies, when the impulses are delivered in bursts. Flow of saliva which is mediated by acetyl choline, may also be potentiated under the same conditions.

Animals↗
PubMed1981

Effect of chemical sympathectomy and ganglion blockade on angiotensin-stimulated fluid absorption in the rat jejunum.

A study has been made of the effects of chemical sympathectomy and ganglion blockade on the responses of rat jejunum in vivo to intravenous doses of angiotension and noradrenaline capable of stimulating fluid transport. Pretreatment with 6-hydroxydopamine (chemical sympathectomy) or pentolinium tartrate (ganglion blockade) abolished the stimulatory actions of angiotensin II but left the responses to noradrenaline unimpaired. Dopamine, like noradrenaline, stimulated fluid transport but this response required very high dopamine infusion rates, was refractory to the dopamine antagonist sulpiride and was inhibited by the alpha- blocker phentolamine. The possible interaction between angiotensin and the intestinal sympathetics is discussed with reference to control in extracellular fluid volume.

Angiotensin II↗
PubMed2001

Examination of motor output pathways in patients with corticobasal ganglionic degeneration using transcranial magnetic stimulation.

The alien hand sign (AHS) is often encountered in patients with corticobasal ganglionic degeneration (CBGD), revealing a unilateral dysfunction of the motor system of unknown pathophysiology. We examined the possibility of an abnormal cortical representation of hand muscles in 10 patients with probable CBGD and a prominent AHS. Cortical maps were obtained from the responses to magnetic stimuli applied with a figure of eight coil at an intensity of 110% above motor threshold. For comparison, the same study was carried out in 10 normal volunteers, eight patients with Parkinson's disease and eight patients with Alzheimer's disease. AHS patients had a larger extension of the cortical map to stimulation of the hemisphere contralateral to the AHS in comparison with the ipsilateral hemisphere. Furthermore, in six patients, focal stimulation of the hemisphere ipsilateral to the AHS gave rise to ipsilateral responses, delayed by a mean of 7.7 +/- 2.2 ms with respect to those recorded in the same muscle to contralateral stimulation. None of the other patients or control subjects had ipsilateral responses. Our results indicate an enhanced excitability, or reduced inhibition, of the motor area of the hemisphere contralateral to the AHS. The delay of the ipsilateral responses is compatible with a disinhibited transcallosal input.

Aged↗
PubMed1980

Influence of clonidine on experimental hypertension induced by cholinergic stimulation.

Hypertension may be induced by pharmacologic activation of central cholinergic receptors either indirectly, through the injection i.v. of physostigmine, or directly, through the injection of i.v. of arecholine in anesthetized rats. Activation of peripheral preganglionic cholinergic receptors with dimethylphenylpiperazinium iodide (DMPP) also produced a hypertensive response. Pretreatment with various doses of clonidine caused inhibition of the pressor response to central cholinergic stimulation but was without effect on the response to ganglionic cholinergic stimulation.

Animals↗
PubMed1996

Myenteric ganglionic 5-hydroxytryptamine(1P) signal transmission is mediated via Go protein.

The role of G proteins in mediating the signal transduction of the guinea pig myenteric ganglionic 5-hydroxytryptamine (5-HT)1P receptors was examined. Stimulation of ganglionic membranes with 5-HT in the presence of [35S]GTPgammaS or [alpha 32P]GTP increased guanine nucleotide binding to G(alpha)o but not to G(alpha)s, G(alpha)i or G(alpha)q in a concentration-dependent fashion. Pertussis toxin pretreatment markedly reduce this 5-HT induced response. Similarly, the 5-HT1P receptor-mediated slowly developing and long-lasting depolarizing response is potentiated by GTPgammaS and is inhibited by GDPbetaS or pertussis toxin. The activation of G(alpha)o by 5-HT also was mimicked by the 5-HT1P agonist, 5-hydroxyindalpine and was blocked by the selective 5-HT1P antagonist, N-acetyl-5-hydroxytryptophyl-5-hydroxytryptophan amide. These data provide compelling evidence to suggest that transmembrane signaling for the 5-HT1P receptors in isolated myenteric ganglia is transduced by the trimeric Go protein.

Animals↗