Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Ganglionic Stimulants”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 739 records · Page 41Linked to original sources
PubMed1988

Delayed myocardial ischemia following the cessation of sympathetic stimulation.

A phenomenon entitled "delayed myocardial ischemia" has been described, in which there is a significant degree of coronary malperfusion following the cessation of behavioral stress. The primary objective of the present study was to develop a model for the delayed ischemic response in anesthetized animals to gain insights into the underlying mechanisms. In 15 morphine and chloralose-anesthetized dogs, a moderate degree of stenosis was applied to the left circumflex coronary artery by means of a toroidal balloon occluder. The pulsed Doppler technique was used to monitor coronary flow. After baseline data were obtained, the left stellate ganglion was stimulated for 30 seconds. Heart rate increased (63%), as did systemic blood pressure (41%) and flow in the left circumflex artery (47%). These parameters rapidly returned to control levels when stimulation was terminated. Forty-five to 90 seconds later, coronary flow decreased by 65% and coronary vascular resistance increased by 45%. These hemodynamic changes were accompanied by ECG abnormalities indicative of regional myocardial ischemia. The delayed ischemic response could be prevented by pretreatment with either nifedipine (20 micrograms/kg) or prazosin (0.3 mg/kg). These data indicate that the primary mechanism for the delayed ischemic response is alpha-adrenergically mediated contraction of the smooth muscle in the coronary artery wall.

Animals↗
PubMed1997

Expression of catecholamine-synthesizing enzymes, peptidylglycine alpha-amidating monooxygenase, and neuropeptide Y mRNA in the rat adrenal medulla after acute systemic nicotine.

The expression of catecholamine-synthesizing enzymes in the adrenal medulla is upregulated in parallel by stress and pharmacological treatments. In this study we examined whether a neuropeptide and its processing enzyme are regulated in parallel with catecholamine enzyme genes after drug treatment. Because the main effect of stress on the adrenal medulla is via splanchnic nerve stimulation of nicotinic receptors, we used nicotine to stimulate the medulla and visualized expression of catecholamine enzyme genes, the medullary peptide neuropeptide Y (NPY), and the neuropeptide-processing enzyme peptidylglycine alpha-amidating monooxygenase (PAM) by in situ hybridization quantified by image analysis of autoradiographic images. Rats received a single injection of nicotine (0, 1, or 5 mg/kg sc). Six hours later, rats were transcardially perfused. Free-floating adrenal gland sections were hybridized with 35S-labeled cDNA probes for tyrosine hydroxylase (TH), dopamine beta-hydroxylase (DBH), phenylethanolamine N-methyltransferase (PNMT), PAM, and NPY. Nicotine treatment upregulated the expression of TH, PNMT, and NPY genes in a dose-dependent fashion. Small but nonsignificant increases were observed in DBH and PAM mRNA levels. These results suggest that common transcriptional activation mechanisms may upregulate both catecholamine and neuropeptide synthesis in the adrenal medulla after nicotinic stimulation.

Adrenal Medulla↗
PubMed1989

Neurotransmission in the frog retina: possible physiological and histological correlations.

In the frog retina, extracellular recordings of transient ganglion cells have shown that the inhibitory surround of the receptive field of these cells was mediated by gamma-aminobutyric acid and acetylcholine (through the nicotinic receptors). Histoautoradiographic and immunocytochemical studies for the two respectively have shown that these neurotransmitters can act through horizontal and amacrine cells. The separation of the ON and OFF channels mediated by glutamate at the bipolar cell level may also be obtained by glycine and/or acetylcholine (through muscarinic receptors). Respective histoautoradiographic and immunocytochemical studies indicate that these neurotransmitters act at the amacrine cell level. These data are consistent with the functional separation of spatial and temporal organization of retinal information, with horizontal cells especially responsible for the spatial organization of the ganglion cell responses and amacrine cells involved in both spatial and temporal organization of the responses.

Acetylcholine↗
PubMed1996

Glycine produced pressor responses when microinjected in the pressor areas of pons and medulla in cats.

In 24 cats under chloralose/urethane anesthesia changes of systemic arterial pressure (SAP) and sympathetic vertebral nerve activities (VNA) were induced by microinjection of glycine (Gly, 1.0 M, 50 nl) into the pressor areas of the rostral pons, i.e., locus coeruleus-parabrachial nucleus (LC-PBN), nucleus of gigantocellular tegmental field-lateral tegmental field (FTG-FTL), and dorsomedial (DM) and ventrolateral (VLM) medulla. The effects were compared with those induced by microinjection of sodium glutamate (Glu, 0.25 M, 50 nl) into the same sites. In about 60% of the injections Gly produced increases in SAP and VNA similar to that of Glu. The increase in SAP was greater in VLM, while the increase in VNA was more marked in DM. In the rest of microinjections Gly and Glu produced changes of SAP and VNA in different combinations. The latency of Gly-induced increases in SAP and VNA was 1 to 3 s longer than that induced by Glu. Our findings show that although Gly is classified as an inhibitory transmitter, it often produced excitation of the pressor neurons in the pons and medulla similar to that of Glu. Whether Gly acts through the same cardiovascular neurons that respond to Glu or through activation of different kinds of neurons remains to be elucidated.

Animals↗
PubMed2001

Comparative effects of dextromethorphan and dextrorphan on morphine, methamphetamine, and nicotine self-administration in rats.

The effects of dextromethorphan and its metabolite dextrorphan on morphine, methamphetamine and nicotine self-administration and on responding for a nondrug reinforcer (water) were assessed in rats. Both dextromethorphan and dextrorphan decreased morphine self-administration at 10-30 mg/kg, s.c., decreased methamphetamine self-administration at 20 and 30 mg/kg, s.c., and decreased nicotine self-administration at 5-30 mg/kg, s.c.; doses of both drugs less than 40 mg/kg, s.c. did not affect responding for water. The equal potencies of dextromethorphan and dextrorphan suggest mediation of these effects by a non-NMDA receptor mechanism, possibly involving blockade of alpha3beta4 nicotinic receptors. The results also suggest that dextromethorphan should be tested extensively as a potential treatment for diverse populations of drug-abusing patients.

Analgesics, Opioid↗
PubMed2002

Endogenous neurokinins facilitate synaptic transmission in guinea pig airway parasympathetic ganglia.

Neurokinin-containing nerve fibers were localized to guinea pig airway parasympathetic ganglia in control tissues but not in tissues pretreated with capsaicin. The purpose of the present study was to determine whether neurokinins, released during axonal reflexes or after antidromic afferent nerve stimulation, modulate ganglionic synaptic neurotransmission. The neurokinin type 3 (NK(3)) receptor antagonists SB-223412 and SR-142801 inhibited vagally mediated cholinergic contractions of bronchi in vitro at stimulation voltages threshold for preganglionic nerve activation but had no effect on vagally mediated contractions evoked at optimal voltage or field stimulation-induced contractions. Intracellular recordings from the ganglia neurons revealed that capsaicin-sensitive nerve stimulation potentiated subsequent preganglionic nerve-evoked fast excitatory postsynaptic potentials. This effect was mimicked by the NK(3) receptor agonist senktide analog and blocked by SB-223412. In situ, senktide analog markedly increased baseline tracheal cholinergic tone, an effect that was reversed by atropine and prevented by vagotomy or SB-223412. Comparable effects of intravenous senktide analog on pulmonary insufflation pressure were observed. These data highlight the important integrative role played by parasympathetic ganglia and indicate that activation of NK(3) receptors in airway ganglia by endogenous neurokinins facilitates synaptic neurotransmission.

Animals↗
PubMed2004

Maturation of spiking activity in trout retinal ganglion cells coincides with upregulation of Kv3.1- and BK-related potassium channels.

Developmental changes in membrane excitability and the potassium channel profile were monitored in acutely isolated trout retinal ganglion cells by patch-clamp recording in combination with single-cell RT-PCR. During embryonic development in the egg, a sustained above-threshold stimulation of ganglion cells elicited in most cases only a single spike response. After hatching, the proportion of multiply spiking cells increased strongly and the ability of spike frequency coding was acquired. This was accompanied by the occurrence of a highly tetraethylammonium (TEA)- and quinine-sensitive delayed rectifier current, which gradually masked a rapidly inactivating A-type potassium current that was predominant at earlier stages. Pharmacology of the delayed rectifier current closely matched those of recombinant Traw1, a Kv3.1-related potassium channel in trout. The appearance of this current correlated closely with initial expression of Traw1 and Traw2 channel transcripts, as revealed by multiplex single-cell RT-PCR, whereas mRNA, encoding Shaker-related channel genes in trout (termed Tsha1-Tsha4), were already detectable at early embryonic stages. Iberiotoxin-sensitive, calcium-activated potassium currents (BK) were extremely low before hatching, but increased significantly thereafter. These developmental changes in potassium channel expression occurred after the arrival of retinal fibers in the optic tectum and the initiation of synapse formation in the visual center. It is suggested that early expressed Shaker-related potassium channels could act to influence neuronal differentiation, whereas proper neuronal signaling requires expression of Kv3.1- and BK-related potassium channels.

Aging↗
PubMed1980

Modulatory role of alpha adrenoceptors on the release of [3H]norepinephrine elicited by preganglionic stimulation of the cat superior cervical ganglion.

In the isolated cat superior cervical ganglion labeled in vitro with [3H]norepinephrine ([3H]NE), the overflow of radioactivity evoked by preganglionic stimulation at 10 Hz (80 V, 2 msec duration for 5 min) was reduced to 50% of control values by the alpha adrenoceptor agonists clonidine (0.001 microM) and methoxamine (12.0 microM). The alpha adrenoceptor antagonist phenoxybenzamine (2.9 microM) produced a 2-fold increase in the overflow of [3H]NE elicited by nerve stimulation. Preincubation with drugs that reduce the neuronal uptake of norepinephrine in the isolated ganglion (8.8 microM cocaine and 0.33 microM desipramine) did not modify the release of [3H]NE by preganglionic stimulation. However, a higher concentration of desipramine (3.3 microM) produced a 4-fold increase in the overflow of tritium evoked by stimulation. As this concentration of desipramine produced a shift to the right in the concentration-response curve to methoxamine in the isolated nictitating membrane of the cat, the conclusion is drawn that a feedback mechanism mediated through presynaptic alpha adrenoceptors regulates the release of [3H]NE induced by preganglionic stimulation of the cat superior cervical ganglion. In addition, it is suggested that regulatory mechanisms for norepinephrine release by nerve stimulation are not restricted to nerve terminals but are also present in dendrites of the postganglionic adrenergic neurons.

Adrenergic alpha-Agonists↗
PubMed1992

Additivity of nicotinic and muscarinic cholinergic stimulation of substantia nigra.

Microinjection of cholinergic agonists into the anterior substantia nigra increases behaviours for which there is a pre-existing tendency and a low current rate. Rats received microinjections of carbachol, nicotine or a combination of both into the anterior substantia nigra. Carbachol and nicotine both stimulated consumption of palatable food in a dose-dependent manner (F(3,24) = 3.99, p < 0.02 and F(3,33) = 7.07, p < 0.01 respectively). Addition of carbachol to each dose of nicotine caused a significant increase in feeding compared with nicotine alone (F(1,23) = 7.01, p < 0.015). This suggests muscarinic or nicotinic cholinergic stimulation of the anterior substantia nigra can have behaviourally similar effects and, at the doses used here, the effects of nicotinic and muscarinic stimulation are additive.

Animals↗
PubMed2005

Mild anxiogenic effects of nicotine withdrawal in mice.

Increased anxiety is one of the symptoms of nicotine withdrawal that may lead to relapse. Previous studies have shown that nicotine withdrawal affects anxiety-like behavior in different tests of anxiety in humans and rats. However, relatively few studies have focused on the anxiogenic effect of nicotine withdrawal in mice. The present study investigated the effect of nicotine withdrawal on anxiety-like behavior in DBA/2J and C57BL/6J mouse strains in the light-dark box, acoustic startle response, and prepulse inhibition tests. An initial experiment showed that nicotine administration of 12 or 24 mg/kg/day (free base) for 14 days did not result in significant effects during withdrawal in startle, prepulse inhibition, or light-dark box, but there was a trend towards an anxiogenic effect in the light-dark box 24 h, but not 1 or 4 h, after cessation of nicotine administration. A subsequent study was therefore performed, with minipumps delivering saline, 24 mg/kg/day nicotine, or 48 mg/kg/day nicotine (free base), for 14 days. The pumps were removed, and the mice were tested 24 h after cessation of nicotine administration. Cessation of administration of 48 mg/kg/day nicotine free base in C57BL/6J mice resulted in increased anxiety-like behavior in the light-dark box, while the behavior of DBA/2J mice was unaffected. The acoustic startle response and prepulse inhibition were also unaffected in both strains. In conclusion, the present data show that nicotine withdrawal is mildly anxiogenic in C57BL/6J mice under the conditions used in the present experiments.

Acoustic Stimulation↗
PubMed2000

Synergistic effects of muscarinic agonists and secretin or vasoactive intestinal peptide on the regulation of tyrosine hydroxylase activity in sympathetic neurons.

Cholinergic agonists and certain peptides of the glucagon-secretin family acutely increase tyrosine hydroxylase activity in the superior cervical ganglion in vitro. The present study was designed to investigate possible interactions between these two classes of agonists in regulating catecholamine biosynthesis. Synergistic effects were found between carbachol and either secretin or vasoactive intestinal peptide in the regulation of DOPA (dihydroxyphenylalanine) synthesis. In addition, synergism was found at the level of the accumulation of cyclic adenosine monophosphate, the likely second messenger in the peptidergic regulation of tyrosine hydroxylase activity. The synergism seen with carbachol was blocked by a muscarinic, but not by a nicotinic, antagonist. Synergism was also found between bethanechol, a muscarinic agonist, and secretin, but not between secretin and dimethylphenylpiperazinium, a nicotinic agonist. Since previous immunohistochemical results suggest that vasoactive intestinal peptide and acetylcholine are colocalized in some preganglionic sympathetic neurons, the present data raise the possibility that the two might act synergistically in vivo in regulating catecholamine biosynthesis. Synergistic postsynaptic actions may be a common feature at synapses where peptides of the secretin-glucagon and acetylcholine are colocalized.

Animals↗
PubMed1995

[Influence of stellate ganglion block on respiratory system].

The purpose of this study was to investigate the influence of a stellate ganglion block (SGB) or stellate ganglion electrical stimulation (SGES) on pulmonary resistance, on blood flows of the bronchial, pulmonary and common carotid arteries, and on arterial blood gases. Thirteen mongrel dogs were divided into two groups; a SGB group (n = 8) and a SGES group (n = 5). Anesthesia was induced with pentobarbital 25 mg.kg-1 and the animals were mechanically ventilated to maintain constant PaO2 (90-100 mmHg) and PaCO2 (35-40 mmHg). After a thoracotomy, the SGB with 0.5% mepivacaine 1.5 ml was performed, or the SGES was performed at a strength of 12 volts, and at a frequency of 50 Hz, applied for 30 min. In the SGB group, pulmonary resistance after the block did not significantly differ from the control. No significant change occurred in blood flows of the bronchial and pulmonary arteries, but the common carotid artery flow increased significantly after the SGB. Arterial blood gases did not change significantly after the SGB. In the SGES group, pulmonary resistance after the stimulation did not significantly differ from the pre-value. However, blood flows of the bronchial, pulmonary and common carotid arteries decreased significantly after the SGES. Arterial blood gases did not change significantly after the SGES. These results suggest that the SGB may not influence the respiratory system under normal conditions.

Animals↗
PubMed1989

[Convergence of preganglionic fibers on neurons of the rabbit superior cervical ganglion].

Responses of neurons of the rabbit superior cervical ganglion to stimulation of the fascicles of preganglionic fibres and tonic activity of these neurons were recorded with intracellular electrodes in vitro and in situ, respectively. Marked convergence of preganglionic fibres onto ganglion cells was found: 8.5 +/- 1.2 fibres, on the average, converged on each cell. It was found that each ganglionic neuron received two preganglionic inputs: single and multiple. The single input was formed by a single preganglionic fibre which evoked EPSP strong enough to trigger a postsynaptic spike. The multiple input was formed by two or more converging preganglionic fibres which could trigger a postsynaptic spike only through summation of the EPSPs they evoked. The interspike intervals for these two preganglionic inputs in tonic activity of neurons were described by distributions of different types: Gaussian and Poisonian ones. Those two distributions were typical of single and multiple inputs, respectively.

Action Potentials↗
PubMed2005

The influence of caffeine on nicotine's discriminative stimulus, subjective, and reinforcing effects.

Caffeine may acutely alter the discriminative stimulus and subjective effects of nicotine, perhaps explaining the association of coffee intake with smoking status. In this study, smokers were initially trained to discriminate 20 microg/kg nicotine by nasal spray from placebo (0). Then, generalization of nicotine discrimination was tested, using both 2- and 3-choice ("novel" option) procedures, across a range of doses (0-20 microg/kg) following pretreatment with 0, 2.5, and 5.0 mg/kg caffeine p.o. Nicotine reinforcement was assessed after the end of generalization testing using a choice procedure. Caffeine pretreatment did not alter nicotine discrimination and self-administration. Caffeine and nicotine influenced some subjective and cardiovascular responses, but there were no interaction effects except for diastolic blood pressure. These results do not support the notion that caffeine acutely alters nicotine's discriminative stimulus, subjective, or reinforcing effects.

Administration, Intranasal↗
PubMed2006

Calcium transient evoked by nicotine in isolated rat vagal pulmonary sensory neurons.

It has been shown that inhaled cigarette smoke activates vagal pulmonary C fibers and rapidly adapting receptors (RARs) in the airways and that nicotine contained in the smoke is primarily responsible. This study was carried out to determine whether nicotine alone can activate pulmonary sensory neurons isolated from rat vagal ganglia; the response of these neurons was determined by fura-2-based ratiometric Ca(2+) imaging. The results showed: 1) Nicotine (10(-4) M, 20 s) evoked a transient increase in intracellular Ca(2+) concentration ([Ca(2+)](i)) in 175 of the 522 neurons tested (Delta[Ca(2+)](i) = 142.2 +/- 12.3 nM); the response was reproducible, with a small reduction in peak amplitude in the same neurons when the challenge was repeated 20 min later. 2) A majority (59.7%) of these nicotine-sensitive neurons were also activated by capsaicin (10(-7) M). 3) 1,1-Dimethyl-4-phenylpiperazinium iodide (DMPP; 10(-4) M, 20 s), a selective agonist of the neuronal nicotinic acetylcholine receptors (NnAChRs), evoked a pattern of response similar to that of nicotine. 4) The responses to nicotine and DMPP were either totally abrogated or markedly attenuated by hexamethonium (10(-4) M). 5) In anesthetized rats, right atrial bolus injection of nicotine (75-200 mug/kg) evoked an immediate (latency <1-2 s) and intense burst of discharge in 47.8% of the pulmonary C-fiber endings and 28.6% of the RARs tested. In conclusion, nicotine exerts a direct stimulatory effect on vagal pulmonary sensory nerves, and the effect is probably mediated through an activation of the NnAChRs expressed on the membrane of these neurons.

Animals↗
PubMed1999

Synaptic activation of GABAA receptors induces neuronal uptake of Ca2+ in adult rat hippocampal slices.

Synaptically evoked transmembrane movements of Ca2+ in the adult CNS have almost exclusively been attributed to activation of glutamate receptor channels and the consequent triggering of voltage-gated calcium channels (VGCCs). Using microelectrodes for measuring free extracellular Ca2+ ([Ca2+]o) and extracellular space (ECS) volume, we show here for the first time that synaptic stimulation of gamma-aminobutyric acid-A (GABAA) receptors can result in a decrease in [Ca2+]o in adult rat hippocampal slices. High-frequency stimulation (100-200 Hz, 0.4-0.5 s) applied in stratum radiatum close (</=0.5 mm) to the recording site induced a 0.1- to 0.3-mM transient fall in [Ca2+]o from a baseline level of 1.6 mM. Concomitantly, a 30-40% decrease in the ECS volume was seen. Exposure of drug-naïve slices to the GABAA receptor antagonist picrotoxin (100 microM) first attenuated and only thereafter augmented the Ca2+ shifts. Application of ionotropic glutamate receptor antagonists resulted in a monotonic reduction of the Ca2+ response, but a large Ca2+ shift persisted (60-70% of the original), which was attenuated by a subsequent application of picrotoxin or bicuculline. In the absence of ionotropic glutamatergic transmission, pentobarbital sodium (100 microM), an up-modulator of the GABAA receptor, strongly enhanced the activity-evoked changes in [Ca2+]o. We suggest that the underlying mechanism of GABA-induced Ca2+ transients is the activation of VGCCs by bicarbonate-dependent GABA-mediated depolarizing postsynaptic potentials. Accordingly, stimulation-evoked Ca2+ shifts were inhibited by the membrane-permeant inhibitor of carbonic anhydrase, ethoxyzolamide (50 microM) or in N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid (HEPES)-buffered HCO3-free solution. Neuronal Ca2+ uptake caused by intense synaptic activation of GABAA receptors may prove to be an important mechanism in the modulation of activity-dependent neuronal plasticity, epileptogenesis, and cell survival in the adult brain.

Animals↗