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Results for “Ganglionic Stimulants”

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At least 991 records · Page 55Linked to original sources
PubMed1986

Cholecystokinin octapeptide depolarizes guinea pig inferior mesenteric ganglion cells and facilitates nicotinic transmission.

Cholecystokinin octapeptide (CCK-8) applied either by superfusion (0.1-10 microM) or by pressure ejection elicited a slow depolarization in a portion of inferior mesenteric ganglion cells studied in vitro. The depolarization which persisted in a low Ca2+/high Mg2+ solution, or solution containing cholinergic antagonists, was often associated with a small to moderate increase in neuronal input resistance, and the response was reduced by conditioning hyperpolarization. Nicotinic excitatory postsynaptic potentials were consistently augmented during the course of CCK-8-induced depolarization. Our results, together with findings of the presence of CCK-immunoreactive fibers in the prevertebral ganglia, suggest that the peptide may serve to facilitate nicotinic transmission.

Animals↗
PubMed1989

Colchicine effect on B-50/GAP43 phosphoprotein localization in rat dorsal root ganglion explants.

In rat embryonic dorsal root ganglion explants stimulated by nerve growth factor, the neuron-specific phosphoprotein B-50 (GAP43) is primarily localized in the distal portion of outgrowing neurites. Addition of colchicine leads to a decrease in total amount of B-50 and a marked redistribution in the neurons. The data underscore the role of axonal transport in the concentration of B-50 in growth cones of growing neurites.

Animals↗
PubMed1996

Effects of pentylenetetrazol on GABA receptors expressed in oocytes of Xenopus laevis: extra- and intracellular sites of action.

The convulsive agent pentylenetetrazol (PTZ) antagonized gamma-aminobutyric acid (GABA)-induced membrane currents on RNA-injected Xenopus oocytes with both extra- and intracellular applications. With extracellular administration PTZ enters the cell within a few minutes and reaches concentrations in the millimolar range. The permeability of the plasma membrane makes it possible for systemically applied PTZ to elicit its effect on the GABA-induced currents via extra- as well as intracellular sites of action.

Animals↗
PubMed1983

Actions of opiates, substance P, and serotonin on the excitability of primary afferent terminals and observations on interneuronal activity in the neonatal rat's dorsal horn in vitro.

Approximately 5 segments of lumbo-thoracic spinal cord together with connected dorsal root ganglia were removed from 1-11-day-old rats and maintained in vitro. Dorsal root afferents, recorded from the ganglion and stimulated at the root entry zone, had conduction velocities typical of unmyelinated fibers (less than 2 m/s). The spinal terminals of individual afferents showed increased excitability with bath application of substance P and serotonin and decreased excitability with morphine sulfate, [D-ala2]methionine-enkephalinamide, manganese ions and magnesium ions. Naloxone by itself elicited no change in excitability, although it appeared to reduce the ongoing effect of opiates. Neurons recorded extracellularly in the dorsal horn responded to afferent volleys with one or more of 3 distinct phases: an excitation roughly coincident with the volley's arrival, a 50-300 ms period of inhibition, and a late excitation of 150-300 ms latency. The excitability results are accounted for by a model in which substance P, gamma-aminobutyric acid and possibly other depolarizing agents are contained in interneurons which synapse on afferent terminals. These interneurons could receive inhibitory enkephalinergic input, and, in the neonate but not the adult, excitatory serotoninergic input. An alternate scheme would have enkephalin and serotonin acting directly on afferent terminals, although perhaps by non-synaptic diffusion since the appropriate synapses have not been seen in histochemical studies. Such an action for enkephalin might explain the existence of opiate receptor on afferent terminals. The interneuronal responses to afferent volleys are parallel in most aspects to those found in the dorsal horns of adult mammals in vivo.

Afferent Pathways↗
PubMed1993

Nicotinic depolarizations of rat medial pontine reticular formation neurons studied in vitro.

Either muscarinic or nicotinic cholinergic activation of the medial pontine reticular formation evokes a behavioral state, indistinguishable in most respects from that of natural rapid eye movement sleep. However, the presence of physiologically relevant nicotonic receptors has not been described. Intracellular current and single electrode voltage clamp recordings were used to analyse the electrophysiological responses of rat medial pontine reticular formation neurons to nicotinic activation in vitro. In response to the nicotonic agonist, 1,1-dimethyl-4-phenylpiperazinium iodine, depolarization in association with an inward current was observed in 70% of the medial pontine reticular formation neurons. This effect was insensitive to the muscarinic antagonist atropine and the nicotinic ganglionic antagonists mecamylamine and hexamethonium. However, the neuromuscular nicotinic antagonist D-tubocurare and dihydro-beta-erythroidine were effective. This is consistent with a cholinergic activation of medial pontine reticular formation neurons evoking a rapid eye movement sleep-like behavioral state, at least in part, by nicotinic receptors on these neurons.

Animals↗
PubMed1984

A comparison of eel electroplax and snake venom acetylcholinesterase.

The effects of some cholinergic ligands, harmala alkaloids and local anesthetics on the activity of eel electroplax and Naja naja siamensis venom acetylcholinesterase have been studied. In most cases, eel electroplax was found to be more susceptible towards inhibition than the venom acetylcholinesterase. No major difference was observed with respect to the type of inhibition in both enzymes. The activation of the two enzyme preparations by inorganic cations (Ca2+, Mg2+ and Na+) showed a similar pattern. In both preparations, the onset of activation was detectable at much lower concentration with the divalent metal ions than with the monovalent Na+. Antagonism between Ca2+ and decamethonium, tubocurarine and tetracaine in both enzymes approached competitive kinetics. The onset of substrate inhibition is delayed by Ca2+ (30 mM) in both enzymes. It is suggested that the Ca2+ binding site overlaps with the substrate inhibitory site. It is concluded that cobra venom acetylcholinesterase has similar allosteric binding sites to those of eel electroplax.

Acetylcholinesterase↗
PubMed1987

Cholinergic control of the mechanical properties of the catch connective tissue in the holothurian body wall.

Effects of acetylcholine (ACh), ACh-agonists and antagonists were studied on the viscosity of the dermis of the sea cucumber Holothuria leucospilota. ACh and nicotinic agonists caused an early increase in viscosity and late decrease. Muscarinic agonists produced a viscosity decrease. The viscosity increase elicited by nicotine was inhibited by tubocurarine. The viscosity decrease caused by methacholine was suppressed by atropine. The mechanical properties of this connective tissue are very likely controlled by both nicotinic and muscarinic cholinoreceptors.

Acetylcholine↗
PubMed1990

Pharmacological control of muscular activity in the sea urchin larva. III. Role of cyclic nucleotides.

1. The muscular activity of the sea urchin pluteus is strongly affected by dibutyryl-c-AMP, in a stimulatory or inhibitory manner depending on the concentration, the time of exposure, and the spontaneous level of activity. 2. Dibutyryl-c-GMP, like muscarinic agents and the guanylate-cyclase activators biotin and nitrite, keeps the activity low. 3. It is suggested that the effects of muscarinic agents is mediated by c-GMP, the effects of certain monoamines by c-AMP. 4. The two cyclic nucleotides appear to control the cellular influx of Ca2+ in opposite directions. They therefore interfere with the stimulatory and paralytic effects of nicotinic agents.

1-Methyl-3-isobutylxanthine↗
PubMed2004

Cognitive and psychological correlates of smoking abstinence, and predictors of successful cessation.

The neural circuitry implicated in addictive drug use, which appears to be down-regulated in early abstinence, corresponds closely with brain reward pathways. A literature review suggests that responses to incentive stimuli and the ability to inhibit reflexive responses, both of which have been associated with normal functioning in these pathways, might be weakened during acute abstinence from chronic drug use. In an ongoing study, 82 smokers, abstinent overnight before two separate testing occasions, have been assessed after administration of nicotine and placebo lozenges (order of sessions counterbalanced). Nicotine administration is associated with a significant reduction in anhedonia, a near-significant increase in response to financial incentive, enhanced ability to inhibit reflexive eye movements, and increased attentional bias to words with appetitive significance. Fifty-nine participants then initiated a quit attempt and 19 reported relapsing within 7 days. Comparing their performance in the two prequit lozenge assessment sessions, relapsers showed a stronger effect of nicotine on enhancing their ability to inhibit reflexive eye movements and a near-significant trend towards greater nicotine-induced increases in attentional bias toward appetitive words.

Adult↗
PubMed2005

Nicotine induces mitogen-activated protein kinase dependent vascular smooth muscle cell migration.

Cigarette smoke, specifically the nicotine contained within, has been shown to cause ultrastructural changes in vascular endothelium resulting in the development of atherosclerosis. Our study examines the effects of nicotine on vascular smooth muscle cell (VSMC) migration and attempts to eludicidate the cellular mechanisms governing those effects. Bovine aortic VSMC were cultured in 10% fetal bovine serum (FBS) growth media and exposed to 10(-8) nicotine for varying periods of time. Boyden chamber chemotaxis assays and a scrape injury model using confluent cells were used to assess cell motility. Activation of the mitogen-activated protein kinases (MAPK), p38 and p44/42, was assessed using Western blotting methods. Nicotine, itself, did not cause significant VSMC migration. However, augmented migration was seen in nicotine-treated VSMCs (16.6+/-3-fold) and media (17.0+/-4-fold) with 10% FBS as chemoattractant. Inhibitors of p38 and p44/42 diminished this migration by 48.5+/-6% and 29.4+/-2%, respectively. Immunoblotting verified p38 and p44/42 activation with nicotine and inhibition with inhibitors of p38 and p44/42. Nicotine-treated endothelial cell (EC) conditioned media (CM) was shown to increase migration 20.3+/-l.l-fold. This chemotactic effect was diminished both with heat treatment and serial dilution. In conclusion, nicotine enhances the chemoatactiveness of VSMC. This migration is mediated via the MAPKs p38 and p44/42. Nicotine causes EC production of a chemoattractant molecule that enhances VSMC migration.

Animals↗
PubMed2005

Lobelane analogues as novel ligands for the vesicular monoamine transporter-2.

A series of lobelane analogues has been synthesized and their structure-activity relationships at the vesicular monoamine transporter-2 (VMAT2) have been evaluated. The most potent analogues in this series were the cis-2,6-piperidino analogues, 25b, 27b, 28b, and 30b, with K(i) values ranging from 430 to 580 nM.

Animals↗
PubMed2003

Effect of nicotine on the expression of leptin and forebrain leptin receptors in the rat.

We have previously reported that chronic nicotine administration (4.0 mg/kg/day by i.p. injection over 14 days) up-regulates orexin/hypocretin and neuropeptide Y (NPY) mRNA expression and peptide levels within the hypothalamus. Since there exists a coregulation between these neuropeptides and the protein leptin, the present study was undertaken to determine whether nicotine has a regulatory effect on leptin signaling. Under the same experimental regimen used previously, we found that nicotine down-regulates plasma leptin concentration by 48.8% (P<0.001) and leptin RNA level by 11.4% and 12.4%, respectively, in the perirenal and epididymal white adipose tissue (PWAT, EWAT) compared to the saline controls. We also measured an approximately 20% decrease in white and brown adipose tissue (BAT) by weight in nicotine-treated animals relative to saline controls (P<0.05). On the other hand, we found that chronic nicotine administration increased the expression levels of OB-Rb mRNA by 12% and OB-R mRNA by 25% in the medial basal hypothalamus compared to control rats. Subsequent radioligand binding assays indicated that nicotine also significantly increased leptin binding in ventromedial hypothalamic area (VMA), medial basal hypothalamic area (MBA), arcuate nucleus/median eminence, paraventricular nuclei and piriform cortex. Taken together, our results revealed that nicotine is involved in the regulation of leptin signaling, suggesting that leptin and its receptor play a role in the anorectic effects of nicotine on food intake and body weight in rats.

Adipose Tissue↗
PubMed2006

Comprehensive evaluation of variability in nicotine metabolism and CYP2A6 polymorphic alleles in four ethnic populations.

Human cytochrome P450 (CYP) 2A6 metabolizes nicotine to cotinine and is a possible modulator of nicotine addiction. Quantitative and qualitative differences in nicotine addiction have been observed between ethnic groups. However, there are few data on the ethnic influences of the CYP2A6-nicotine metabolism relationship, particularly with regard to black subjects. We determined the nicotine metabolism and CYP2A6 genotype in 176 white subjects and 160 black subjects, comparing them with our previous data from 209 Korean subjects and 92 Japanese subjects. Large interindividual differences were observed in the cotinine/nicotine ratios in plasma calculated as an index of nicotine metabolism in white subjects (range, 0.6-36.5) and in black subjects (range, 0.9-30.4). No ethnic difference in the metabolic ratio was observed among white subjects (mean, 7.2 +/- 5.0), black subjects (mean, 7.1 +/- 4.7), and Korean subjects (mean, 8.7 +/- 11.9), whereas Japanese subjects showed a significantly (P < .005) lower metabolic ratio (mean, 3.8 +/- 3.1) compared with the other populations. Women showed significantly (P < .05) higher metabolic ratios than men in the black population (8.0 +/- 5.3 versus 6.0 +/- 3.7). Obvious ethnic differences in the CYP2A6 alleles were observed among these 4 populations. The combined frequencies of the alleles lacking or showing reduced enzymatic activity (CYP2A6*2, CYP2A6*4, CYP2A6*5, CYP2A6*7, CYP2A6*9, CYP2A6*10, CYP2A6*11, CYP2A6*17, CYP2A6*19, and CYP2A6*20) were 9.1%, 21.9%, 42.9%, and 50.5% in white, black, Korean, and Japanese subjects, respectively. These CYP2A6 alleles were associated with reduced nicotine metabolism. Among the homozygotes of CYP2A6*1, interindividual and ethnic differences in the metabolic ratio were still observed. Thus some factors other than genetic ones might also contribute to the interindividual and ethnic differences. This comprehensive study of 4 populations extends our understanding of nicotine metabolism and the impact of genetic polymorphisms of the CYP2A6 gene.

Adolescent↗