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PubMed1988

Slow cardioacceleration mediated by noncholinergic transmission in the stellate ganglion of the cat.

In C1-spinal, pentobarbital-anaesthetized or anemically decerebrated cats, the preganglionic input to the acutely decentralized right stellate ganglion was stimulated with 10- to 30-s strains at 20-40 Hz. Electrical stimulation consistently produced an increase in heart rate in the presence of blocking doses of hexamethonium and atropine or after depletion of acetylcholine from the preganglionic axons by prolonged low frequency stimulation in the presence of hemicholinium. The increase in heart rate had a delayed slow onset, lasted several minutes, and was abolished by propranolol or by section of the inferior cardiac nerve. The magnitude and duration of the heart rate increase were related to intensity, frequency, and duration of preganglionic stimulation. The response to stimulation of a given white ramus was progressively attenuated, and eventually irreversibly lost, during prolonged continuous stimulation of that ramus, while the response to stimulation of a different unstimulated ramus was unchanged. We conclude that the slow cardioacceleration results from a slow and prolonged excitation of postganglionic neurons by a noncholinergic transmitter released by the preganglionic axons.

Animals↗
PubMed1994

Blockade effect of nerve growth factor on GM1 ganglioside-induced activation of transglutaminase in superior cervical sympathetic ganglia excised from adult rat.

The activity of transglutaminase (TG), a Ca(2+)-dependent enzyme indicating tissue degradation or differentiation, showed in isolated adult rat superior cervical ganglia (SCG) a rapid (within 15 to 30 min) and marked (approx. 5- to 8-fold) increase with the addition of either GM1 ganglioside (GM1, 5 nM), which is rich in synapses, or sialyl cholesterol (SC, 20 microM), a synthetic sialic acid-containing compound, to the incubation medium at 37 degrees C. Under the same incubation conditions, addition of GM1 or SC decreased protein kinase C (PKC) activity (-26% to -39%) in the cytosolic fraction of the SCG, but increased the enzymic activity (+39% to +61%) in the particulate (cell membrane) fraction, suggesting that a sialic acid-containing compound (GM1 or SC) promotes PKC translocation from the cytosol to the membrane in ganglionic neurons. By contrast, addition of a promoting factor for survival of sympathetic neurons even in adulthood, nerve growth factor, (NGF, 0.25 micrograms/ml) to the medium significantly decreased ganglionic TG activity (-43%). This inhibition was completely antagonized by the co-addition of NGF-monoclonal antibody (0.75 microgram/ml). An effective blockade of GM1- or SC-induced stimulation of ganglionic TG activity was seen by further addition of NGF to the medium. Also, NGF almost abolished the translocation of ganglionic PKC activity induced by the sialic acid-containing compounds, although either NGF or 12-O-tetradecanoylphorbol ester (TPA) alone stimulated the cytosolic PKC activity (approx. +30%) in the tissue.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1964

ACTIONS OF HEMICHOLINIUM (HC-3) ON NEUROMUSCULAR TRANSMISSION.

Hemicholinium No. 3 (HC-3; alpha,alpha'-dimethylaminoethanol-4, 4'-biacetophenone) produced neuromuscular block of the tibialis anterior muscle-sciatic nerve preparation of the anaesthetized cat which was of slow onset, of long duration and dependent on the nerve stimulus frequency. The failure of the compound to modify the response of the tibialis muscle to close-arterial injections of acetylcholine suggested that the sensitivity of the motor endplate was not changed by it. The neuromuscular block produced by hemicholinium was antagonized by choline but only partly relieved by anticholinesterase drugs. The response to tetanic stimulation of the nerve during the neuromuscular block was well sustained and was followed by a slight posttetanic potentiation. The neuromuscular blocking action of hemicholinium could be relieved by temporary suspension of stimulation. These results suggest that the mode of action of hemicholinium at the neuromuscular junction is different from that of tubocurarine, and indicate that the action of hemicholinium is presynaptic, probably arising from a reduction in acetylcholine released by nerve stimulation.

Acetylcholine↗
PubMed1975

Muscarinic suppression of the nicotinic action of acetylcholine on the isolated, blood-perfused atrium of the dog.

1. The isolated canine right atrium perfused through the sinus node artery at a constant pressure of 100 mm Hg with blood led from a support dog was suspended in a bath filed with blood and kept at constant temperature. This preparation maintained its constant tension development and rate over 5 hrs in all 5 control experiments. 2. A relatively small amount of acetylcholine (ACh) induced a negative inotropic effect at 0.01 mug and a negative chronotropic effect at 0.1 mug. 3. A relatively large dose of ACh induced a biphasic inotropic response, i.e., initially a negative inotropic response and secondarily a long-lasting positive tropic response. These positive chronotropic and inotropic responses were abolished by propranolol, hexamethonium or tetrodotoxin. 6. In the papillary muscle and atrial muscle preparations isolated from one canine heart, ACh caused negative and positive inotropic effect in both paced papillary and atrial muscle preparations. In contrast to the results obtained with atria, the positive inotropic response of the papillary muscle preparation was completely blocked by treatment with propranolol or tetrodotoxin. 7. From these results, it is suggested that in the canine atrium muscarinic mechanisms predominate over nicotinic ones. This may well be due to the known inhibition of nicotinic responses by stimulation of muscarinic receptors.

Acetylcholine↗
PubMed1964

ACTIONS OF MECAMYLAMINE, DIMECAMINE, PEMPIDINE AND THEIR TWO QUATERNARY METHO-SALTS AT THE NEUROMUSCULAR JUNCTION.

Mecamylamine, dimecamine and pempidine differed in neuromuscular-blocking activity on the isolated phrenic nerve-diaphragm preparation of the rat from the corresponding methiodides by a factor of less than two. It was concluded that the active component of each amine was the cation acting extracellularly. The finding that the neuromuscular-blocking activity of mecamylamine at pH 6.7 was similar to the activity at pH 7.7 did not refute this conclusion. Mecamylamine, dimecamine methiodide, dimecamine and pempidine, at concentrations insufficient to cause block, could increase the twitch response of the rat diaphragm; the ability to do this increased in the above order. With pempidine (the most active compound) this effect, on the isolated sartorius muscle of the frog, was a direct action. During steady partial block by each of the compounds, the responses to brief tetanic stimulation, to neostigmine and to an increase in calcium concentration were similar to those observed during block by tubocurarine. From indirect evidence, pempidine methiodide appeared both to enhance the release of acetylcholine from motor-nerve terminals and to cause postsynaptic block.

Abdominal Muscles↗
PubMed2006

A high-performance thin-layer chromatographic technique to screen cocaine in urine samples.

Qualitative identification of cocaine and its metabolites in urine samples is generally carried out by an immunoassay technique followed by a gas chromatographic/mass spectrometric confirmation of presumptive positives. Nevertheless, other chromatographic techniques such as thin-layer chromatography or gas chromatography could also be used to screen several types of drugs of abuse especially for forensic and legal purposes. In the present work, the capability of high performance thin-layer chromatography (HPTLC) to detect cocaine in urine samples and discriminate it from interfering substances (local anaesthetic, caffeine and nicotine) was studied. Twenty urine samples of drug addicts were submitted to the HPTLC method. Unaltered cocaine present in the urine samples and cocaine obtained after methylation of benzoylecgonine (main cocaine metabolite) with diazomethane were detected in all tested samples. In conclusion, the proposed HPTLC method showed to be useful to detect cocaine in biological matrices.

Anesthetics, Local↗
PubMed2005

Rabbit retinal ganglion cells express functional alpha7 nicotinic acetylcholine receptors.

It is well known that cholinergic agents affect ganglion cell (GC) firing rates and light responses in the retinas of many species, but the specific receptor subtypes involved in mediating these effects have been only partially characterized. We sought to determine whether functional alpha(7) nicotinic acetylcholine receptors (nAChRs) contribute to the responses of specific retinal GC classes in rabbit retina. We used electrophysiology, pharmacology, immunohistochemistry, and reverse transcriptase-polymerase chain reaction to determine the pharmacological properties and expression of nAChR subtypes by specific rabbit retinal GC classes. Choline was used as an alpha(7) nAChR agonist. Methyllycaconitine (MLA) was used as a competitive alpha(7) nAChR antagonist. The application of choline before synaptic blockade resulted in changes in retinal GC activity, including increases or decreases in maintained firing and/or enhancement or suppression of light responses. Many physiologically identified GC types, including sustained off, sustained on, transient off, and transient on cells, demonstrated responses to choline application while under synaptic blockade. The choline-induced responses could be blocked with MLA, confirming alpha(7) nAChR activation. Individual choline-responsive GCs displayed mRNA transcripts consistent with the expression of functional alpha(7) nAChRs. Other GCs demonstrated physiological responses and mRNA expression consistent with the expression of both alpha(7) and non-alpha(7) nAChRs. Thus mRNA is present for multiple nAChR subunits in whole retina extracts, and functional alpha(7) nAChRs are capable of modulating the responses of GCs in adult rabbit retina. We also demonstrate through physiological responses that subsets of GCs express more than one nAChR subtype.

Animals↗
PubMed1985

Neurophysiology and pharmacology of long-term potentiation in the rat sympathetic ganglion.

Brief tetanic stimulation of the preganglionic nerve induced a persistent potentiation of nicotinic synaptic transmission in the rat superior cervical sympathetic ganglion. Quantitative measurements of the post-tetanic increase in synaptic efficacy revealed two distinct time courses. The early, rapidly decaying component, termed post-tetanic potentiation (p.t.p.), had a decay time constant of 2-3 min, as reported elsewhere. The duration of the more persistent component, called long-term potentiation (l.t.p.), was extremely temperature dependent, lasting much longer at 32 degrees C than at 22 degrees C. In half of the experiments performed at 32 degrees C, l.t.p. showed no detectable decay over the course of 1 h or more after a brief tetanic stimulation. Other experiments were conducted at 22 degrees C. The induction of l.t.p. was dependent on the extracellular [Ca2+]. Transient elevation of the extracellular [K+] also produced a long-term enhancement of synaptic efficacy, and this effect was also Ca2+ dependent. The tetani that were effective in inducing l.t.p. (5-20 Hz for 5-20 s) were well within the physiological range of preganglionic activity. The magnitude and time course were related to frequency and duration of stimulation. The occurrence of l.t.p. was restricted to those preganglionic fibres that were tetanically stimulated. This lack of heterosynaptic or generalized effects was demonstrated by splitting the preganglionic nerve into two branches that could be independently tested and conditioned. Physiological activation of muscarinic or nicotinic receptors apparently does not play an essential role in causing ganglionic l.t.p., which is expressed as an enhancement of nicotinic transmission. A muscarinic antagonist (2 microM-atropine) did not block l.t.p. Preganglionic stimulation induced l.t.p. even when a high concentration of a nicotinic antagonist (3 mM-hexamethonium) was present during the tetanic stimulation. Furthermore, bath application of a cholinergic agonist (100-1000 microM-carbachol) could not substitute for tetanic stimulation in provoking l.t.p. Activation of adrenergic receptors also appeared not to play an essential role. Neither a beta-adrenergic antagonist (10 microM-sotolol or 1 microM-propranolol) nor an alpha-adrenergic antagonist (1 microM-phentolamine) had any significant effect on the magnitude or duration of l.t.p. The results indicate that ganglionic l.t.p. is a Ca2+- and temperature-dependent process that can be created independently of the activation of nicotinic, muscarinic or adrenergic receptors.

Action Potentials↗
PubMed1998

The influence of lobeline on nucleus accumbens dopamine and locomotor responses to nicotine in nicotine-pretreated rats.

In vivo brain microdialysis was used to investigate the influence of lobeline on dopamine (DA) and dihydroxyphenylacetic acid (DOPAC) overflow in the core of the nucleus accumbens of freely-moving rats pretreated with nicotine (0.4 mg x kg(-1), s.c., once per day for 5 days). Locomotion was also recorded. Lobeline, at doses of 0.7, 4.0 and 10.0 mg x kg(-1), i.p., failed to elicit any significant changes in extracellular dopamine or dihydroxyphenylacetic acid levels during the 60 min following its administration and did not stimulate locomotor. The dopamine responses to nicotine (0.4 mg x kg(-1), s.c.), were abolished (P<0.01) if the nicotine challenge was administered 10 min but not 60 min, after lobeline doses of 4.0 and 10.0 mg kg(-1), i.p., but were unaffected following lobeline at the lowest dose tested (0.7 mg x kg(-1), i.p.) at either time. The increase in locomotor activity was significantly attenuated (P<0.01), to a similar extent, when the nicotine was injected 10 min, but not 60 min, after all three doses of lobeline (0.7, 4.0 and 10.0 mg kg(-1), i.p.) when compared with the saline-treated rats. The results suggest that lobeline is a short-acting antagonist of the nicotinic AChRs which mediate the effects of nicotine on mesolimbic dopamine activity and locomotor stimulation.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1993

Electrophysiological study of relations between the dorsal nerve of the penis and the lumbar sympathetic chain in the rat.

Afferent sensory inputs from the penis are carried by the dorsal nerve of the penis (DNP) to the spinal cord. Sympathetic outflow involved in the control of the urogenital tract is partly conveyed by the lumbosacral sympathetic chain. Our aim was to search for a sympathetic component in the DNP and relations between DNP afferents and sympathetic fibers conveyed by the distal sympathetic chain in anesthetized adult male rats. Stimulation of the lumbar sympathetic chain at the L4-L5 level (LSC4-5) elicited an evoked discharge on the DNP. This discharge was abolished by cutting the sympathetic chain distal to the stimulation site. Ganglionic blockade with hexamethonium and various neural sections revealed the presence of sympathetic postganglionic fibers in the DNP, originating in the sympathetic chain. Stimulation of the DNP evoked a reflex discharge in the LSC. This reflex was spinally mediated since it was abolished by acute spinal cord transection at the L5 level. Acute spinalization at the T8 level significantly reduced the latency of the evoked response. We hypothesize that both spinal and supraspinal control exist over relations of the DNP afferents with sympathetic outflow to the pelvis. Increase in sympathetic tone elicited by activation of penile sensory fibers could play a role in regulation of sexual function.

Afferent Pathways↗
PubMed1981

The distal vagal ganglion of the hen (Gallus domesticus). A histological and physiological study.

The distal vagal ganglion of the hen was examined histologically and physiologically. The number of neurons in the right and left distal vagal ganglia were counted and a mean figure of 6710 neurons obtained. The proportions of the different types of neuron present were determined and their size measured. No multipolar cells with boutons on them were found. Morphologically the ganglion is sensory. Following chronic vagotomy proximal to the distal vagal ganglion the vagus nerves were stimulated and the effect on the heart and gastrointestinal tract monitored. It was found that stimulation of the acutely sectioned nerve caused a drop in heart rate and an increase in gastrointestinal activity. There was no cardiac or gastrointestinal response when the chronically operated nerve was stimulated. Physiologically the ganglion is sensory. The evidence is reviewed for homology between inferior vagal ganglion of the mammal and the distal vagal ganglion of the hen.

Animals↗
PubMed1966

The characteristics of spontaneous and evoked action potentials recorded from the rabbit's uterine nerves.

1. A method is described for recording in vivo the action potentials of afferent and efferent fibres in whole nerves supplying the rabbit's uterus.2. Examination of these nerves under the light microscope and the electron microscope showed them to be composed almost entirely of non-myelinated fibres.3. Two types of spontaneous action potential were observed; one travelled at about 4 m/sec and probably came from the myelinated fibres, the other travelled at 0.4-1.4 m/sec and certainly came from non-myelinated fibres.4. The efferent fibre spikes were shown to be faster and higher than the spikes from uterine afferent fibres, but slower and smaller than spikes from broad ligament afferent fibres.5. Apart from differences in conduction velocity and height, all spikes were basically similar, lasting about 1.5 msec. The height was related to the square of the velocity. Some more complex spikes were also observed.6. The compound action potential evoked by stimulation of the uterine nerve had three peaks, conducted at 1.3, 0.8 and 0.6 m/sec, respectively, and thought to correspond to the fast afferent fibres, the efferent fibres and the slow afferent fibres, respectively. There were also some late peaks due to reflexion of the antidromic action potentials from the ganglion cells.7. Stimulation of the hypogastric nerve also evoked a compound action potential in the uterine nerves. Stimulation of the pelvic nerves had no effect.8. By means of ganglion blocking agents, the uterine ganglia were shown to lie in the pelvic plexus, peripheral to the hypogastric nerve, but central to the uterine nerves.9. It is argued that the spontaneous action potentials came from individual fibres rather than Remak bundles, and that the recording technique used detected the activity of all but the smallest fibres.

Animals↗
PubMed2002

Caffeine potentiates the discriminative-stimulus effects of nicotine in rats.

RATIONALE: Caffeine and nicotine are the main psychoactive ingredients of coffee and tobacco, respectively, with a high frequency of concurrent use in humans. OBJECTIVES: The aim of the present study was to examine the interaction of caffeine and nicotine in rats trained to discriminate nicotine from saline. METHODS: Two groups of male Sprague-Dawley rats ( n=8 per group) were trained to discriminate 0.4 mg/kg nicotine, SC, from saline under a fixed ratio schedule of food presentation. One group of rats was chronically exposed to caffeine (1.0 mg/ml) dissolved in their drinking water whereas the other group was exposed to tap water. Effects of IP injections of caffeine on nicotine-lever selection were subsequently examined. In separate groups of rats exposed to the same caffeine-drinking or water-drinking regimen, effects of caffeine pretreatment on nicotine plasma levels were evaluated. RESULTS: Although caffeine (1.0-30.0 mg/kg) did not generalize to nicotine when administered alone, it markedly potentiated discriminative-stimulus effects of the threshold dose of nicotine (0.05 mg/kg) in both water- and caffeine-drinking rats. Nicotine plasma levels were, however, not affected by acute or chronic caffeine exposure. CONCLUSIONS: Caffeine appears to enhance the discriminative-stimulus effects of the threshold dose of nicotine by a pharmacodynamic rather than a pharmacokinetic interaction. This suggests that caffeine consumption may be a contributing factor in the onset, maintenance of and relapse to tobacco dependence.

Animals↗
PubMed1999

Sympathectomy decreases and adrenergic stimulation increases the release of tissue plasminogen activator (t-PA) from blood vessels: functional evidence for a neurologic regulation of plasmin production within vessel walls and other tissue matrices.

Our recent morphologic studies indicated that peripheral nervous system (PNS) adrenergic neurons synthesize, transport, and store the serene protease, tissue plasminogen activator (t-PA) in axon terminals, many of which innervate vessel walls. Sympathoadrenal stimulation induces a surge of t-PA from vessel walls into the blood. The vascular endothelium, which constitutively secretes t-PA into blood also has long been widely assumed to be the principal source of this stress-induced release, but has not been verified as such. A neurologically regulated release from adrenergic stores could thus augment the known constitutive endothelial release. To functionally test this possibility, we quantitated the effects of guanethidine-induced systemic sympathectomy on the basal and stimulated release of t-PA from isolated vessel explants in superfused organ cultures. Moment-to-moment changes in the release rate were plotted from serial assays of the t-PA free activity. The effects of endothelial and adventitial nerve plexus ablations were also tested. Sympathectomy induced 30-50% reductions in t-PA release from both arterial and microvascular explants. An acute release induced by alpha-1 adrenergic receptor stimulations was also strongly suppressed, as were basal levels of the circulating enzyme in vivo. Adventitial and endothelial ablations from normal large vessel explants produced greater reductions than small vessel endothelial ablations. Ganglion electrical stimulation also induced an acute microvascular release in vivo. These and past morphologic findings indicate a physiological infusion of t-PA into the vessel walls, blood, and other innervated matrices by sympathetic neurons.

Animals↗
PubMed2001

Erection and NO override the vasoconstrictive effect of alpha-adrenergic stimulation in the rat penile vasculature.

Studies in this laboratory are designed to determine the effects of vasoconstrictor agents on the erectile response in rats. We have previously demonstrated that the vasoconstrictor effect of endothelin-1 (ET-1) is sharply reduced by erection and by nitric oxide (NO) administration. The present study was performed to determine if vasoconstriction, resulting from alpha-adrenergic stimulation, is altered by erection and NO. During continuous monitoring of corpus cavernosum pressure (CCP) and mean arterial pressure (MAP), erection was induced by electrical stimulation of the autonomic ganglion for the innervation of the penis. When the alpha-adrenergic agonist methoxamine (METH, 10 microg/kg) was injected before erection (ie, into the non-erect penis), the subsequent erectile response (CCP/MAP) was significantly reduced from 0.68+/-0.03 before METH to 0.34+/-0.08 after METH. Injection of METH into the erect penis (ie, during erection) reduced the vasoconstrictor action of METH; CCP/MAP was 0.74+/-0.02 before METH and 0.55+/-0.05 after METH (P<0.05). The vasoconstrictor action of METH was slightly reduced when given in conjunction with NOR-1, a NO donor drug; CCP/MAP was 0.70+/-0.05 before METH, 0.55+/-0.09 after METH but this change was not significant. These results demonstrate that the response to alpha-adrenergic stimulation is attenuated during erection in response to ganglionic stimulation. Furthermore, it appears that NO, produced during erection, may serve to override agonist-induced vasoconstriction. These results support our hypothesis that NO acts to directly stimulate relaxation of cavernous smooth muscle and to inhibit the vasoconstrictor actions of agents like ET-1 and alpha-adrenergic agonists including norepinephrine.

Adrenergic alpha-Agonists↗