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PubMed1997

[Facial neuralgia (neuralgia n. V). Diagnosis and treatment].

We present evaluation and methods of treatment for "tic douloureux" (trigeminal neuralgia). Angio-Magnetic Resonance seems to be essential in establishment of neuro-vascular compression pathology. Present diagnostic increased number of surgical intervention from suboccipital craniectomy approach in micro-vascular decompression. In patients with contraindications for general surgery other techniques are being used to decrease pain sensation: RF thermocoagulation with the help of stereotactic procedure, percutaneous microcompression of the trigeminal ganglion, radiosurgery, electrical stimulation of the Gasserian ganglion. Current methods of imaging and new therapeutical achievements allow to dramatically reduce pain and discomfort in first days of trigeminal neuralgia.

Humans↗
PubMed1997

Plasma protein extravasation induced in the rat dura mater by stimulation of the parasympathetic sphenopalatine ganglion.

It has been proposed that migraine could result from a neurogenic inflammation of the dura mater. According to this theory, inflammation could be initiated by an axon reflex of nociceptive nerve fibers, but the trigger of this axon reflex remains poorly understood. Previous works have shown that parasympathetic agonists can activate mast cells and/or sensory C-fibers, inducing pain and inflammation. The aim of the present work was to determine whether the activation of intracranial parasympathetic nerve fibers could trigger an inflammatory mechanism within the rat dura mater. Activation of the intracranial parasympathetic system was achieved by electrical stimulation of the sphenopalatine ganglion (SPG). The development of a neurogenic inflammation was estimated either by microscopic examination or by quantitative measurement of plasma protein extravasation (PPE) in the dura. To determine the respective roles of the parasympathetic and sensory innervations, two groups of rats were pretreated either with atropine or with capsaicin. Stimulation of the SPG induced a PPE increase of about 200% in the stimulated side on the dura mater. Extravasated material was mainly concentrated around small blood vessels. This extravasation was significantly reduced by capsaicin pretreatment and completely abolished by atropine. Infusion of carbachol in the common carotid artery induced PPE in the ipsilateral dura comparable to that induced by electrical stimulation of the SPG. This extravasation was also blocked by atropine infusion. These data indicate for the first time that the parasympathetic nervous system can trigger a neurogenic inflammation in the dura via muscarinic cholinergic receptors. Sensory C-fibers seem to play a role in this phenomenon. With respect to the potential autonomic imbalance described in the etiology of various types of vascular headaches, such a mechanism could be important in inducing attacks.

Acetylcholine↗
PubMed1995

Structure and innervation of longitudinal and transverse abdominal muscles of the cricket, Gryllus bimaculatus.

Detailed morphological and physiological studies on the insect abdominal muscles, including their innervation and neuromuscular transmission, are essential for understanding their important role in respiratory movements. There are both longitudinal and transverse muscles in the ventral abdominal segments of the cricket, Gryllus bimaculatus. Muscle 202 was selected as an example of a longitudinal muscle. This muscle is, on average, 1.4 mm long, paired on both sides of the abdomen, and consists of 127 fibers whose mean maximum diameter is 32 microns; the average sarcomere length is 8.1 microns. It is innervated by two ipsilateral motoneurons in the second abdominal ganglion, the axons of which run in the ipsilateral first nerve root of the third abdominal ganglion. Two motor axons run in parallel from the two cell bodies and innervate in close proximity. Accordingly, large and small excitatory junctional potentials (EJPs) are recorded from the same fiber with slightly different thresholds when the first nerve root of the third abdominal ganglion is stimulated. Muscle 203, which is a transverse muscle that extends across the fifth abdominal sternum and is located over the fourth abdominal ganglion and muscle 202 on both sides, is, on average, 2.9 mm long and consists of 86 fibers with a maximum diameter of 33 microns. The average sarcomere length is 7.9 microns. The right or left half of the muscle is innervated mainly by a contralateral motoneuron in the third abdominal ganglion through the ipsilateral first nerve root of the third abdominal ganglion. Nerve branches of the first nerve root also reach muscles 188 and 218. Muscle 203 is additionally innervated by the first nerve roots of abdominal ganglia 1, 2, and 4. These innervations were ascertained both electrophysiologically and histologically. Individual muscle fibers of muscle 203 produced small EJPs in response to stimulation of the first nerve roots of abdominal ganglia 2, 3, and 4 and large EJPs in response to stimulation of the root from the first abdominal ganglion. The large and small EJPs in muscle 203 have properties similar to those in muscle 202.

Abdominal Muscles↗
PubMed1980

Effects of synaptic and antidromic stimulation on tyrosine hydroxylase activity in the rat superior cervical ganglion.

1. The effects of orthodromic and antidromic stimulation of the rat superior cervical ganglion on the specific activity of the enzyme tyrosine hydroxylase have been studied. 2. Orthodromic stimulation of the ganglion via the sympathetic trunk produced an increase in the activity of tyrosine hydroxylase when measured 3 days later while causing no change in the protein content of the ganglion. This increase in the specific activity of tyrosine hydroxylase was blocked by administration of the nicotinic antagonist, hexamethonium. 3. Antidromic stimulation of the superior cervical ganglion by stimulating the internal carotid nerve, the external carotid nerve or both nerves simultaneously produced no change in the specific activity of tyrosine hydroxylase. 4. Parallel increases in tyrosine hydroxylase activity and protein content per ganglion were seen when the internal carotid nerve was stimulated but similar changes were seen in "sham-stimulated" animals. These "non-specific" changes were apparently produced by the trauma involved in the extensive dissection necessary to position electrodes on this nerve trunk. 5. We conclude that an increase frequency of firing in post-ganglionic neurones is not a sufficient stimulus to elevate the specific activity of tyrosine hydroxylase. Rather some other aspect of nicotinic receptor stimulation seems to be required.

Animals↗
PubMed1985

Synthesis and utilization of catecholamines in the rat superior cervical ganglion following changes in the nerve impulse flow.

The nerve impulse flow to the noradrenaline nerve cell body region of the superior cervical ganglion and to the noradrenaline nerve terminals of the salivary glands was decreased and increased by decentralization and pre-ganglionic electrical stimulation, respectively. The concentrations of dopamine, noradrenaline, and their primary deaminated metabolites (DOPAC, DOPEG) in the ganglion were not changed during the first day after the decentralization but were increased following preganglionic stimulation, particularly that of DOPAC. The disappearances of dopamine and noradrenaline after alpha-methyltyrosine and the disappearance of noradrenaline after inhibition of the dopamine-beta-hydroxylase were not changed by decentralization or stimulation. The accumulation of dopamine following inhibition of the dopamine-beta-hydroxylase was somewhat lowered by decentralization and was markedly enhanced by stimulation. In the noradrenaline nerve terminals of the salivary glands, preganglionic sympathetic stimulation decreased and increased the concentration of noradrenaline and dopamine, respectively. Thus, nerve impulses stimulated the tyrosine hydroxylase activity in the cell body region and the axon terminals of the noradrenaline neurons but they increased the utilization of noradrenaline only in the terminals.

Animals↗
PubMed1997

Light exposure stimulates the activity of ganglioside glycosyltransferases of retina ganglion cells.

In chicks submitted to light stimulation, the synthesis of gangliosides of the retina ganglion cell increases with respect to chicks maintained in the dark. In an attempt to elucidate if the activation of glycosyltransferases participates in the establishment of these light-dark differences detected in vivo, we examined the activity of a key ganglioside glycosyltransferase, the GalNAc-T (N-acetylgalactosaminyltransferase) that converts GM3 to GM2, in the retina ganglion cells isolated from light and dark exposed chicks. We found that GalNAc-T and other glycosyltransferases are active in these ganglion cell preparations; the kinetic parameters for GalNAc-T were similar to those previously reported for chick retina. The other glycosyltransferase activities assayed were the galactosyltransferase (Gal-T2) that converts GM2 to GM1 and the N-acetylneuraminyltransferase (Sialyl-T1) that converts lactosylceramide to GM3. The three glycosyltransferase activities were higher in the ganglion cell preparations obtained from chicks exposed to light compared to those maintained in the dark. For the GalNAc-T activity, the differences disappear when the cell preparations are sonicated or if the assays are carried out in the presence of detergents or if the end product of the reaction is added to the incubates. The results indicate that the activation of the glycosyltransferases is part of the phenomenon required for cells to achieve the precise rate of synthesis of gangliosides needed in vivo.

Animals↗
PubMed1992

Role of PGE2 in neurotransmission from pre- to post-ganglionic hypogastric nerves of guinea pigs.

The hypogastric nerve to guinea pig vas deferens was stimulated pre- or post-ganglionically by adjusting the position of the suction electrode. Both stimulations induced a biphasic contraction consisting of a rapid transient phase and a delayed tonic phase. Indomethacin partially inhibited the contraction induced by pre-ganglionic stimulation, but did not inhibit that induced by post-ganglionic stimulation. Prostaglandin (PG) E2 counteracted the inhibitory effect of indomethacin. Mepacrine also inhibited the contraction induced by pre-ganglionic stimulation. Arachidonic acid and PGE2 both reversed the inhibition. The PGE2-receptor antagonist SC-19220 inhibited the contraction induced by pre-ganglionic, but not post-ganglionic nerve stimulation. These results suggested that endogenous PGE2 is important in neurotransmission in the pelvic ganglion of guinea pigs.

Animals↗
PubMed2000

Nitric oxide mediates a therapeutic effect of nicotine in ulcerative colitis.

BACKGROUND: Ulcerative colitis is a condition of nonsmokers in which nicotine is of therapeutic benefit. AIMS: To examine the in vitro effect of nicotine on colonic smooth muscle activity and the role of nitric oxide (NO) as a mediator. METHODS: Nicotine, 1-10 microM, was administered to strips of circular muscle from the distal sigmoid colon of 9 patients with active ulcerative colitis and 18 with colorectal cancer. The effect of electrical field stimulation (EFS) was examined before nicotine was added. Finally L-NAME, a NO synthetase inhibitor, was added before nicotine was administered again. RESULTS: Muscle strips developed similar spontaneous resting tone. In response to EFS, ulcerative colitis tissue developed lower tensions than the controls. Nicotine significantly reduced the resting tone and peak tension after EFS, with a greater effect in controls. With L-NAME, peak tensions were increased more in ulcerative colitis than controls, and nicotine produced a much smaller reduction. CONCLUSIONS: Nicotine reduces circular muscle activity, predominantly through the release of nitric oxide-this appears to be 'up-regulated' in active ulcerative colitis. These findings may explain some of the therapeutic benefit from nicotine (and smoking) in ulcerative colitis and may account for the colonic motor dysfunction in active disease.

Adult↗
PubMed1978

[Bioassay for acetylcholine from the rat cervical sympathetic ganglion (author's transl)].

1. A bioassay for acetylcholine (Ach), with a sensitivity of 0.1 picomoles in 30 microliters (microliter) (Fig. 3), was developed using the powerful musculature of the common leech (Haemopis sanguisuga). 2. Ach was extracted from a pool of ganglia with sodium tetraphenylborate in 3-heptanone and analysed using gas chromatography. The chromatograph confirmed that the "Ach like effect" measured with bioassay was due to acetylcholine and not to one of its derivatives (Fig. 5 and 6). 3. An incubation chamber for perfusing the isolated superior cervical ganglion of the rat is described, with which it is possible to do electrophysiological experiments and to sample the Ach lost or released by the ganglion (Fig. 2). 4. Using this system, the results obtained from the resting or stimulated rat ganglion incubation in-vitro, were similar to those obtained with the cat ganglion perifused in situ. 5. Experiments were also performed to investigate the effect of removing the two precursors of Ach, glucose (Table I) and choline (Fig. 9), from the incubation medium.

Acetylcholine↗
PubMedDate not supplied

Androgenic maintenance of the rat erectile response via a non-nitric-oxide-dependent pathway.

Prior studies have demonstrated that the erectile response in the rat penis is androgen dependent and is mediated by nitric oxide (NO), the neurotransmitter synthesized by the enzyme nitric oxide synthase (NOS). The present studies used L-nitro-L-arginine methyl ester (L-NAME), an inhibitor of NOS, to determine if androgens also regulate alternative pathways leading to the erectile response but not mediated by NO. Castrated rats that were treated with L-NAME (L-NAME CASTRATE) exhibited little or no increase in intracavernosal pressure in response to stimulation of the major pelvic ganglion. This ganglion controls blood flow into the penis and, when stimulated, normally leads to erection. However, when castrated animals were treated with testosterone along with L-NAME (L-NAME TESTO), the animals responded to the ganglionic stimulation with increased intracavernosal pressure. This finding suggests that there are other androgen-dependent pathways that lead to penile erection but are not mediated by NO. Erection occurred in both L-NAME CASTRATE and L-NAME TESTO rats in response to intracavernosal injection of sodium nitroprusside (an NO donor drug), proving that the NO responsive mechanisms were unaffected by the inhibition of NOS activity. To investigate further the nature of this NO independent pathway, L-NAME CASTRATE and L-NAME TESTO rats were treated with either zaprinast (a specific phosphodiesterase 5 inhibitor), which would block the breakdown of cGMP to 5'GMP, or methylene blue (an inhibitor of guanylate cyclase) to prevent the synthesis of cGMP. Zaprinast treatment led to increased erectile response in L-NAME TESTO rats but not in L-NAME CASTRATE rats, demonstrating that androgen-sensitive alternative pathways increased guanylate cyclase activity. Methylene blue inhibited the erectile response in all treatment groups, showing that cyclic GMP is critical to the NO-independent pathway as well as the NO-dependent pathway. Taken together, these results support the hypothesis that androgens maintain the erectile response by alternate pathways, including one that is independent of NO but involves the synthesis of cyclic GMP.

Androgens↗
PubMed2003

Fibroblast growth factor-2 gene delivery stimulates axon growth by adult retinal ganglion cells after acute optic nerve injury.

Basic fibroblast growth factor (or FGF-2) has been shown to be a potent stimulator of retinal ganglion cell (RGC) axonal growth during development. Here we investigated if FGF-2 upregulation in adult RGCs promoted axon regrowth in vivo after acute optic nerve injury. Recombinant adeno-associated virus (AAV) was used to deliver the FGF-2 gene to adult RGCs providing a sustained source of this neurotrophic factor. FGF-2 gene transfer led to a 10-fold increase in the number of axons that extended past 0.5 mm from the lesion site compared to control nerves. Detection of AAV-mediated FGF-2 protein in injured RGC axons correlated with growth into the distal optic nerve. The response to FGF-2 upregulation was supported by our finding that FGF receptor-1 (FGFR-1) and heparan sulfate (HS), known to be essential for FGF-2 signaling, were expressed by adult rat RGCs. FGF-2 transgene expression led to only transient protection of injured RGCs. Thus the effect of this neurotrophic factor on axon extension could not be solely attributed to an increase in neuronal survival. Our data indicate that selective upregulation of FGF-2 in adult RGCs stimulates axon regrowth within the optic nerve, an environment that is highly inhibitory for regeneration. These results support the hypothesis that key factors involved in axon outgrowth during neural development may promote regeneration of adult injured neurons.

Animals↗
PubMed1988

Effects of halothane on acetylcholine release and sympathetic ganglionic transmission.

Depression of synaptic transmission is one of the actions common to many general anesthetics. They appear to act primarily on the chemical transmission process itself without affecting the conduction of impulses in nerve axons. The objective of the present study was to directly examine the effects of halothane on the release of acetylcholine and overall ganglionic transmission. The effects of halothane on ganglionic transmission were studied in the stellate ganglion of the cat in vitro. The preganglionic nerves of the stellate ganglion were stimulated electrically to generate threshold and suprathreshold evoked potentials in the postganglionic nerves. The picomole levels of released acetylcholine in the superfusate were determined with a radioenzymatic method using 32P-ATP following a 5-min preganglionic stimulation before and after the addition of 0.28 and 0.59 mM halothane (vaporizer settings of 1% and 2%, respectively). Halothane at both concentrations: 1) depressed sympathetic ganglionic transmission induced by either threshold or suprathreshold stimulation of the preganglionic nerves; and 2) caused a dose-dependent decrease in acetylcholine release during threshold stimulation with no change in neurotransmitter release during suprathreshold stimulation. In summary, the interruption of synaptic transmission by halothane involves at least two mechanisms: 1) decrease in acetylcholine release during low level of synaptic transmission; and 2) postsynaptic decrease in sensitivity to acetylcholine during low and high levels of synaptic transmission.

Acetylcholine↗
PubMed1982

Physiological studies of canine sympathetic ganglia and cardiac nerves.

Anatomical studies have indicated that the middle cervical ganglion is the primary locus of sympathetic postganglionic neurons which have axons projecting in canine cardiac nerves. Small regions of thoracic sympathetic ganglia were stimulated electrically with bipolar electrodes and the generated compound action potentials were recorded from ipsilateral cardiac nerves. Several procedures were used to distinguish the effects of stimulating preganglionic axons, ganglionic sites and postganglionic axons. Following hexamethonium it was found that only low frequency stimulation (e.g. 1 Hz) of ganglionic sites resulted in the generation of compound action potentials in cardiac nerves. These ganglionic sites were located throughout the middle cervical ganglion, but only in the cranial medial pole of the stellate ganglion. Stimulation of a single locus in a stellate or middle cervical ganglion generated compound action potentials in all major ipsilateral sympathetic cardiac nerves. A ganglion was also identified at the junction of the thoracic vagus and the cranial vagal nerve which may be as important as the right stellate ganglion in cardiac regulation. These results demonstrate that there are discrete loci in thoracic ganglia which contain neurons projecting in several ipsilateral cardiac nerves. Low frequency stimulation of these loci was found to be optimal for generation of compound action potentials.

Animals↗
PubMed2006

Oncomodulin is a macrophage-derived signal for axon regeneration in retinal ganglion cells.

The optic nerve, like most mature CNS pathways, does not regenerate after injury. Through unknown mechanisms, however, macrophage activation in the eye stimulates retinal ganglion cells (RGCs) to regenerate long axons beyond the site of optic nerve injury. Here we identify the calcium (Ca(2+))-binding protein oncomodulin as a potent macrophage-derived growth factor for RGCs and other neurons. Oncomodulin binds to rat RGCs with high affinity in a cyclic AMP (cAMP)-dependent manner and stimulates more extensive outgrowth than other known trophic agents. Depletion of oncomodulin from macrophage-conditioned media (MCM) eliminates the axon-promoting activity of MCM. The effects of oncomodulin involve downstream signaling via Ca(2+)/calmodulin kinase and gene transcription. In vivo, oncomodulin released from microspheres promotes regeneration in the mature rat optic nerve. Oncomodulin also stimulates outgrowth from peripheral sensory neurons. Thus, oncomodulin is a new growth factor for neurons of the mature central and peripheral nervous systems.

Animals↗
PubMed1992

Effects of dopamine receptor and alpha 2-adrenoceptor agonists and antagonists on muscarinic receptor stimulation in cardiac sympathetic ganglia of the dog.

The effects of dopamine (DA)-receptor and alpha 2-adrenoceptor agonists and antagonists on ganglionic muscarinic stimulation were examined in anesthetized dogs. All drugs were injected or infused intra-arterially into the blood supply of the cardiac sympathetic ganglia. The muscarinic agonists McN-A-343 (10, 20, and 30 micrograms) and muscarine (1, 2, and 3 micrograms) increased heart rate. The muscarinic receptor stimulation elicited by McN-A-343 or muscarine was significantly inhibited by infusion of the DA2-receptor agonist quinpirole (3 and 10 micrograms/min) but not by the DA1-receptor agonist SK&F 38393 (10 and 30 micrograms/min). The alpha 2-adrenoceptor agonist BHT 933 (3 and 10 micrograms/min) also inhibited muscarinic receptor stimulation. The DA2-receptor antagonist domperidone (10 micrograms/min) and the alpha 2-adrenoceptor antagonist yohimbine (1 micrograms/min) had no effects on muscarinic receptor stimulation, but they antagonized the inhibitory effects of quinpirole and BHT 933, respectively. The nicotinic transmission elicited by preganglionic cardiac sympathetic nerve stimulation (1 and 2 Hz) was also inhibited by DA-receptor and alpha 2-adrenoceptor agonists and antagonists. These results suggest that DA2-receptors and alpha 2-adrenoceptors suppress muscarinic transmission as well as nicotinic transmission in the cardiac sympathetic ganglia of the dog.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗